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Uterine Carcinosarcoma

A plain-English summary of the published research on Uterine Carcinosarcoma, reviewed and approved by our editors — not a hand-curated clinical overview.

Research summary · reviewed
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Evidence at a glanceHuman trial / meta-analysisMixed results⚠ Studies disagree
33 published studies that name Uterine Carcinosarcoma10 human studies approved & graded (trial, observational, or meta-analysis)28 human clinical studies in the Uterine Carcinosarcoma corpus339 source documents in the Uterine Carcinosarcoma corpus

last checked June 12, 2026

Why this grade?

Human trial / meta-analysisIncludes human trial or meta-analysis evidence.

Computed deterministically from the studies’ types and reported outcomes — not written by AI, and not a claim that anything works.

What the guidelines say

NCI PDQESMONCCNASCO

We link the authoritative guidelines rather than reproduce them. Below, the treatments on this page are split into standard care, guideline or regulatory options, supportive care, and studied but not standard so established care is not mixed with experimental or supportive items.

Studied, not standard - investigational
  • adjuvant chemotherapy
  • adriamycin (doxorubicin)
  • anthracycline
  • carboplatin
  • carboplatin and paclitaxel
  • carboplatin/ifosfamide/mesna
  • carboplatin/paclitaxel
  • carboplatin + paclitaxel
  • carboplatin/paclitaxel/cisplatin/doxorubicin/epirubicin
  • carboplatin plus paclitaxel
  • chemotherapeutic combinations
  • chemotherapy
  • cisplatin
  • cisplatin/ifosfamide
  • doxorubicin
  • ifosfamide
  • paclitaxel
  • paclitaxel and carboplatin
  • paclitaxel and ifosfamide
  • paclitaxel and platinum
  • paclitaxel, ifosfamide, and cisplatin
  • palliative chemotherapy
  • platinum
  • postoperative chemotherapy
  • taxane/platinum doublet
  • topotecan
  • trabectedin
  • anastrozole
  • tamoxifen
  • dostarlimab
  • IL-13Rα2-targeted CAR macrophages
  • lenvatinib plus pembrolizumab
  • PD-L1
  • pembrolizumab
  • pembrolizumab + lenvatinib
  • PRAME
  • ?
  • adjuvant treatment
  • chemoradiotherapy
  • combined chemo-radiotherapeutic approach
  • heterologous component
  • MSI/MMRd
  • NSMP
  • NUCB2
  • POLEmut
  • radiotherapy and chemotherapy
  • URI1 amplification
  • adjuvant multimodal treatment
  • aspiration thrombectomy
  • chemoradiation
  • fine-needle aspiration (aspiration cytology)
  • hysterectomy with bilateral salpingo-oophorectomy and lymphadenectomy
  • lymphadenectomy
  • minimally invasive surgery
  • modified radical hysterectomy
  • para-aortic lymphadenectomy
  • partial (subtotal) surgical resection
  • pelvic lymphadenectomy
  • sentinel lymph node biopsy
  • sequence-based diagnostics
  • subtotal hysterectomy and left salpingo-oophorectomy
  • surgery
  • surgery (hysterectomy / cytoreduction)
  • surgical resection / debulking
  • total abdominal hysterectomy with bilateral salpingo-oophorectomy
  • concurrent chemoradiotherapy
  • cuff brachytherapy
  • external beam irradiation / vaginal brachytherapy / systemic chemotherapy
  • external beam pelvic radiation therapy and HDR brachytherapy
  • external beam radiotherapy and chemotherapy
  • external radiotherapy
  • gamma knife radiation
  • pelvic external beam radiotherapy
  • pelvic radiation
  • radiation
  • radiation and chemotherapy
  • radiochemotherapy
  • radiotherapy
  • stereotactic radiosurgery
  • vaginal brachytherapy
  • whole brain radiotherapy
  • whole-pelvic irradiation
  • adagrasib
  • adavosertib
  • alrizomadlin
  • anti-VEGF / anti-PD-ECGF / anti-PDGFR-β therapy
  • aurora kinase inhibitors
  • avutometinib
  • ceralasertib
  • chemotherapeutic agents with molecular-targeted agents
  • cobimetinib
  • copanlisib
  • COX-2
  • fascin
  • Folate receptor alpha
  • galunisertib
  • HER2
  • histone deacetylase inhibitors (HDACi)
  • lenvatinib and pembrolizumab
  • LY2109761
  • LY2157299
  • MRTX1133
  • olaparib
  • PARP inhibitors
  • pazopanib
  • sacituzumab govitecan
  • SLC1A5
  • SYK
  • trastuzumab
  • trastuzumab deruxtecan
  • VEGF
  • PTC-028
  • 18F-FDG PET/CT
  • MRI (including DWI and MRS)
  • Transvaginal sonography (TVS)
  • Trastuzumab-Deruxtecan (T-Dxd)

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Uterine Carcinosarcoma.

Treatment map: Uterine Carcinosarcoma

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Standard care plus every compound studied in the literature (each cited) and graded by evidence, organized by clinical readiness. A category, not a verdict that anything works — confirm anything here with your oncology team.

125
Interventions
0
Standard of care
28
Tested in people
2
Lab / animal
95
Named in lit.
7
Classes
Standard of care (0) Guideline option (0) Tested in people (28) Lab / animal only (2) Named in the literature (95)

Tested in people, by trial phase: Phase III ×8 · Phase II ×4 · phase not reported ×16

Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
2
18
Radiotherapy
2
16
Chemotherapy
11
22
Targeted therapy
6
2
25
Immunotherapy
7
Hormonal therapy
3
Other
4
7

Columns group into clinical evidence (used in, or tested on, people) and preclinical evidence (lab/animal, or only named in the literature). Cell = number of interventions; a dashed cell means none recorded there.

Investigational & adjunct compounds — detail (125)
Phase II trial (4)
anastrozoleoff-labelceralasertibtrabectedin· Recurrent or later-linetrabectedin
Meta-analysis (10)
adjuvant multimodal treatment· Adjuvant (after surgery)chemoradiation· Adjuvant (after surgery)chemotherapy· Adjuvant (after surgery)HER2· biomarker-selectedheterologous component· Recurrent or later-lineminimally invasive surgeryMSI/MMRd· biomarker-selectedNSMPPOLEmut· Recurrent or later-lineradiotherapy· Adjuvant (after surgery)
Named in the literature
adjuvant chemotherapy· Adjuvant (after surgery)adriamycin (doxorubicin)anthracyclinecarboplatin and paclitaxel· First-line (advanced disease)carboplatin/ifosfamide/mesnacarboplatin/paclitaxel· First-line (advanced disease)carboplatin + paclitaxelcarboplatin/paclitaxel/cisplatin/doxorubicin/epirubicincarboplatin plus paclitaxel· Adjuvant (after surgery) · biomarker-selectedcarboplatin plus paclitaxel· Adjuvant (after surgery)carboplatin and paclitaxel· Adjuvant (after surgery)chemotherapeutic combinationscisplatinoff-label· Adjuvant (after surgery)cisplatin/ifosfamide· Adjuvant (after surgery)doxorubicinoff-label· Recurrent or later-linepaclitaxel and platinum· Recurrent or later-linepaclitaxel, ifosfamide, and cisplatin· Adjuvant (after surgery)palliative chemotherapyplatinum· Adjuvant (after surgery)postoperative chemotherapy· Adjuvant (after surgery)taxane/platinum doublet· Recurrent or later-linetopotecanoff-label· Recurrent or later-linedostarlimaboff-label· MaintenanceIL-13Rα2-targeted CAR macrophageslenvatinib plus pembrolizumabPD-L1pembrolizumaboff-labelpembrolizumab + lenvatinib· Recurrent or later-linePRAME?· Adjuvant (after surgery)adjuvant treatment· Adjuvant (after surgery)chemoradiotherapycombined chemo-radiotherapeutic approachNUCB2radiotherapy and chemotherapy· Adjuvant (after surgery)URI1 amplification· Adjuvant (after surgery)aspiration thrombectomyfine-needle aspiration (aspiration cytology)· Recurrent or later-linehysterectomy with bilateral salpingo-oophorectomy and lymphadenectomylymphadenectomymodified radical hysterectomypara-aortic lymphadenectomypartial (subtotal) surgical resectionpelvic lymphadenectomysentinel lymph node biopsysequence-based diagnosticssubtotal hysterectomy and left salpingo-oophorectomysurgery· First-line (advanced disease)surgery (hysterectomy / cytoreduction)surgical resection / debulkingtotal abdominal hysterectomy with bilateral salpingo-oophorectomyconcurrent chemoradiotherapy· Adjuvant (after surgery)cuff brachytherapy· Adjuvant (after surgery)external beam irradiation / vaginal brachytherapy / systemic chemotherapyexternal beam pelvic radiation therapy and HDR brachytherapyexternal beam radiotherapy and chemotherapyexternal radiotherapygamma knife radiationpelvic external beam radiotherapy· Adjuvant (after surgery)pelvic radiation· Adjuvant (after surgery)radiation· Adjuvant (after surgery)radiation and chemotherapyradiochemotherapy· Adjuvant (after surgery)stereotactic radiosurgeryvaginal brachytherapy· Adjuvant (after surgery)whole brain radiotherapywhole-pelvic irradiation· Recurrent or later-lineadagrasibadavosertib· Recurrent or later-linealrizomadlinanti-VEGF / anti-PD-ECGF / anti-PDGFR-β therapy· Recurrent or later-lineaurora kinase inhibitorsavutometinibchemotherapeutic agents with molecular-targeted agentscobimetinibcopanlisibCOX-2fascinFolate receptor alpha· biomarker-selectedgalunisertibhistone deacetylase inhibitors (HDACi)LY2109761LY2157299MRTX1133olapariboff-label· Maintenance · biomarker-selectedPARP inhibitors· biomarker-selectedpazopanib· Recurrent or later-lineSLC1A5SYKtrastuzumab· Recurrent or later-line · biomarker-selectedVEGFPTC-02818F-FDG PET/CTMRI (including DWI and MRS)Transvaginal sonography (TVS)

"Tested in people" rows show the highest trial phase found in that compound's cited human studies (Phase I–IV; "phase not reported" = a human study with no phase tag). "Studied" = named in the cited literature for this cancer. "FDA ✓" = FDA-approved for this cancer; "off-label" = an FDA-approved drug used outside its approved indications (per openFDA). Not a claim that anything works.

Reported figures

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Answers come only from the cited sources on this page — with the supporting evidence shown. If the sources here don't cover your question, it will say so. Educational information, not medical advice.

10 sections — tap any heading to expand its cited detail. Key points are above.

Overview41 points

Key figures

Survival & outcomes
OutcomeValue95% CI
5-year survival rate, FIGO stage 322%
5-year survival rate, FIGO stage 49%
proportion of uterine tumors5%
share of uterine cancer deaths30%
5-year survival rate35%
Source quotes
  • "patients diagnosed with stages 3 and 4 diseases exhibit 5-year survival rates of 22% and 9%, respectively."
  • uterine carcinosarcomas account for under 5 % of uterine tumors but are responsible for 30 % of uterine cancer deaths
  • UCS has a poor prognosis (∼35% survival rate after 5 years)
  • Uterine carcinosarcoma (also called malignant mixed Müllerian tumor, UCS or MMMT) is a rare, highly aggressive biphasic uterine tumor composed of carcinomatous (epithelial) and sarcomatous (mesenchymal) components. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51]51 sources
  • Uterine carcinosarcoma is described as a rare tumor. [52][53][28][29][30][31][54][55][32][56][35][36][34][57][58][59][60][61][62]19 sources
  • The tumor is described in multiple sources as a rare, aggressive, high-grade endometrial cancer with generally poor outcomes; it often presents at advanced stage and is associated with high rates of metastasis and recurrence, and many patients have extremely poor prognosis despite intensive surgery. [3][15][14][4][5][6][63][7][64][8][9][10][11][12][65]15 sources
  • Sources describe uterine carcinosarcoma as a rare, aggressive biphasic tumor with malignant epithelial and mesenchymal components and generally poor prognosis. [66][67][68][69][70][71][72][73][74][75][76][77][78][79][12]15 sources
  • UCS is associated with poor prognosis and generally worse survival outcomes than endometrial cancer or uterine sarcoma; it is described as difficult to treat. [37][80][38][42][81][82][83][44][84][43][46][48][49][50][51]15 sources
  • Uterine carcinosarcoma (UCS), also referred to as malignant mixed Müllerian tumor (MMMT), is described in the literature as a rare, aggressive, high-grade subtype or invasive variant of endometrial (uterine) cancer. [85][86][87][88][89][90][91][92][93][94][95][96]12 sources
  • Sources describe uterine carcinosarcoma as a rare, aggressive/high-grade uterine neoplasm composed of malignant epithelial (carcinomatous) and mesenchymal/sarcomatous components. [97][98][99][100][101][102][103][104][105]9 sources
  • Uterine carcinosarcoma is described as an aggressive, high-grade endometrial cancer with frequent extra-uterine spread at diagnosis, a high incidence of recurrence after initial treatment, and overall poor outcomes with higher rates of recurrence and mortality than other high-grade endometrial cancers; some studies report poor prognosis even when diagnosed at an early stage. [54][55][32][106][33][57][56][35][62]9 sources
  • The sarcomatous component largely originates from the epithelial component, and UCS is described as a metaplastic carcinoma that often shows a monoclonal epithelial origin or epithelial dedifferentiation/metaplasia. [77][100][101][102][107][103][98]7 sources
  • Uterine carcinosarcomas are biphasic malignant tumors containing carcinomatous (epithelial) and sarcomatous (mesenchymal) components. [108][85][109][110][111][95]6 sources
  • Prognosis is often poor: one review reports that median survival is less than two years, 5-year overall survival has been described as not having changed in decades, and some reports give an estimated 5-year survival of only 30%; overall outcomes have been described as poor with limited treatment options. [112][95][24][19][113]5 sources
  • Many reviews and molecular analyses consider most uterine carcinosarcomas to be metaplastic or dedifferentiated carcinomas arising from a single (monoclonal) malignant clone, with the carcinomatous element driving the tumor; a small proportion are thought to be true collision tumours, which in some instances may have a better prognosis than a similar-stage carcinosarcoma. [58][59][36][35][60]5 sources
  • Sources describe UCS as a biphasic tumor in which the sarcomatous component can arise from the carcinomatous element, with epithelial–mesenchymal transition (EMT) playing a pivotal role in its pathogenesis. [96][108][85][95]4 sources
  • Uterine carcinosarcoma has both epithelial and mesenchymal malignant cell components and historically was considered an endometrial carcinoma with sarcomatoid (sarcomatous) differentiation and therefore staged and treated as a high-grade endometrial carcinoma in prior practice. [109][85][93][86]4 sources
  • The term 'malignant mixed Müllerian tumor (MMMT)' is used for uterine carcinosarcoma in multiple sources. [85][86][109][87]4 sources
  • UCS causes a relatively high proportion of uterine cancer deaths; one review reported it accounts for 16.4% of all deaths caused by uterine malignancies. [102][107][103][104]4 sources
  • Uterine carcinosarcoma predominantly affects elderly postmenopausal women. [37][114][38][51]4 sources
  • Many sources recognize UCS as a uterine carcinoma or as a variant/subtype of high-grade endometrial cancer. [39][41][83][45]4 sources
  • Sources describe uterine carcinosarcoma as a rare, high-grade, aggressive epithelial non-endometrioid endometrial carcinoma. [1][115][11]3 sources
  • Sources note that UCS is biphasic and that the carcinomatous component drives its aggressive nature; EMT-related biology has also been implicated in UCS. [25][26][27]3 sources
  • Uterine carcinosarcoma is usually diagnosed in older women; reported median age at diagnosis ranges from 62 to 67 years. [25][116][117]3 sources
  • Due to the rarity of uterine carcinosarcoma, there is a scarcity of specific treatment guidelines. [118][16][113]3 sources
  • A review describes uterine carcinosarcoma as distinguished by a high likelihood of metastasis and multisite recurrence. [79][119]
  • Sources describe that aspects of the diagnosis and management of uterine carcinosarcoma are controversial, including questions about the efficacy of adjuvant therapy. [103][98]
  • Primary treatment is surgical debulking; multimodal adjuvant therapy (including chemotherapy and radiotherapy) is commonly used, but there is currently no consensus on adjuvant therapy. [109][112]
  • Rare endometrial cancers, including carcinosarcomas, are characterized as high-grade, aggressive malignancies that are often diagnosed at an advanced stage. [120][95]
  • Prior pelvic irradiation has been reported in association with uterine carcinosarcoma (post‑radiation UCS). [117][112]
  • Historically classified with uterine sarcomas, uterine carcinosarcoma was categorized in 2009 by the International Federation of Gynecology and Obstetrics as a variant of endometrial carcinoma rather than a pure sarcoma. [121][60]
  • Most uterine carcinosarcomas are classified as copy-number high/serous-like (p53-abnormal), while a small subset represent other molecular subtypes, including POLE-mutated tumors. [15]
  • The standard or preferred adjuvant chemotherapy regimen and schedule for uterine carcinosarcoma remain uncertain. [14]
  • Clinical guidelines include uterine carcinosarcoma among the diseases they address. [122]
  • A source notes a disproportionate uterine carcinosarcoma disease burden in patients of African ancestry. [8]
  • Uterine carcinosarcoma is treated as a high‑grade endometrial cancer. [123]
  • HER2 has been described as a potential target for novel therapeutic interventions in uterine malignancies, including carcinosarcoma. [124]
  • Uterine carcinosarcoma is described as a rare tumor with gradually increasing incidence that typically affects older women, although some reports note patients have become younger in recent decades. [95]
  • Uterine carcinosarcoma is typically seen in postmenopausal women and is exceptionally uncommon in young adults. [61]
  • Treatment is typically surgical and the ideal adjuvant therapy remains unknown. [57]
  • One review reports that only one-third of patients survive beyond 5 years. [82]
  • The TCGA transcriptomic dataset used for site-of-origin classification included uterine carcinosarcoma (UCS) as one of the cancer sites. [125]
  • A meta-analysis reports that uterine carcinosarcoma has a significantly increased hazard of death compared with serous carcinoma and clear cell carcinoma. [2]
Show 1 lab & early-research finding
  • Sources report that reduced p27 expression is common and p53 overexpression is infrequent in carcinosarcoma, and similar p27/p53 rates in stromal and epithelial elements have been reported to support a monoclonal origin. [5][63][7][126]4 sources
Epidemiology34 points

Key figures

Survival & outcomes
OutcomeValue95% CI
mean age at diagnosis70
mortality rate16%
extrauterine disease56.3%
proportion of uterine tumors5%
share of uterine cancer deaths30%
median age at diagnosis69 months
age distribution34.8%
proportion of ECS among primary ECs1.7%
proportion of ECS among primary ECs5.6%
proportion of ECS among type II ECs6%
proportion of ECS among type II ECs17.5%
percentage of black women with ECS11.9%
percentage of black women with ECS20%
percentage of white women with ECS86%
percentage of white women with ECS60.5%
proportion of UCS during study period4.7%4.6–4.8
recurrence after surgery and adjuvant therapy37%
5-year overall survival vs less than 30%30%
Source quotes
  • The mean age of the patients at diagnosis was 70 years (range 51–95)
  • and a mortality rate of 16%
  • UCS presents with extrauterine disease in 56.3% of cases (p < 0.001), according to a study using the Surveillance Epidemiology and End Result database (1973–2010) [5].
  • uterine carcinosarcomas account for under 5 % of uterine tumors but are responsible for 30 % of uterine cancer deaths
  • The median age at diagnosis was 69 years (range, 26 to 90 years).
  • Gynecologic carcinosarcomas were most prevalent in patients in their 60s (34.8% of uterus, 32.3% of cervix, and 28.2% of ovary).
  • There was a significant rise in the proportion of ECS among primary ECs from 1.7% to 5.6% during this period.
  • the proportion of ECS also increased significantly from 6% to 17.5%; ECS was detected in 11,000 (4.7%) women.
  • The percentage of black women with ECS was elevated from 11.9% to 20%, whereas the proportion of white women decreased from 86% to 60.5%.
  • UCS were seen in 11,000 (4.7%, 95% CI=4.6, 4.8) women during the study period.
  • Recurrence is observed in 37 % to 80 % of patients based on stage following surgery and adjuvant therapy
  • with a 5-year overall survival of less than 30 %
  • Sources report uterine carcinosarcoma comprises under 5% of uterine malignancies, with some analyses showing proportions exceeding 5% in recent years (e.g., up to 5.6%). [85][87][109][127][90][118][25][22][95][128]10 sources
  • Reported proportion of endometrial/uterine cancers that are uterine carcinosarcoma is about 4.1%–6% across sources (individual reports include 4.1%, approximately 5%, about 6%, <5%, over 5%, and a single-center 4.7%). [4][3][115][5][63][7][129][68]8 sources
  • Sources indicate uterine carcinosarcoma mostly affects older, postmenopausal women, often in the seventh decade of life. [42][83][44][45][46][47][40]7 sources
  • One source reports uterine carcinosarcoma accounts for 16.4% of mortality among uterine malignancies. [106][18][32][17][130]5 sources
  • Uterine carcinosarcoma is rare and its reported incidence and demographic patterns vary between data sources and time periods. [87][86][110][25][95]5 sources
  • Sources report a median age around 67 years for uterine carcinosarcoma, and the tumor is usually diagnosed in older women. [111][131][113][86][25]5 sources
  • Uterine carcinosarcoma is an uncommon subtype, reported to account for less than 5% to approximately 5% of uterine (corpus/endometrial) malignancies. [44][84][45][46][132]5 sources
  • Black women have a disproportionately increased risk of uterine carcinosarcoma; one analysis reported the percentage of Black women with ECS increased from 11.9% to 20% while the percentage of White women decreased from 86% to 60.5%. [18][60][62]3 sources
  • Several reviews and series report that many cases are diagnosed at advanced stage and that outcomes are generally poor. [74][133][98]3 sources
  • Small series and registries report that the most common presenting symptom is post-menopausal bleeding (about 80% in one series). [104][103]
  • Some series report that uterine carcinosarcoma represents a growing proportion of endometrial cancers over recent decades. [109][95]
  • Uterine carcinosarcomas have been reported to occur under or after tamoxifen administered in an adjuvant setting. [134][135]
  • The tumor is described as uncommon or rare. [123][136]
  • Sources report uterine carcinosarcoma is more frequent in postmenopausal women. [20][62]
  • Sources describe presenting features including abnormal vaginal bleeding, abdominal pain, and yellowish vaginal discharge. [114][38]
  • Uterine carcinosarcoma and uterine serous carcinoma are reported to account for over 50% of endometrial cancer deaths. [79]
  • In one series, 43% of women with uterine carcinosarcoma presented at stage I/II. [137]
  • One source describes uterine carcinosarcoma as uncommon and reports that about 35% of cases are not confined to the uterus at diagnosis. [138]
  • In a series of POLE-mutated uterine carcinosarcomas the tumors usually presented as FIGO 2009 clinical stage IA or IB. [15]
  • The tumor predominantly appears in the uterine corpus. [128]
  • Uterine carcinosarcoma is described as a rare gynecological malignancy. [16]
  • Uterine carcinosarcomas are considered a high‑risk variant of endometrial adenocarcinoma because they share more similarities in epidemiology, risk factors, and clinical behavior with endometrial carcinoma than with uterine sarcomas. [52]
  • Uterine carcinosarcoma is described as rare in some sources. [34]
  • Metastases from uterine carcinosarcoma most commonly occur in the abdominal wall, lung, and bone. [139]
  • The most common presenting symptom in that series was postmenopausal abnormal uterine bleeding, which occurred in 57.3% of patients. [140]
  • Uterine carcinosarcoma/endometrial carcinosarcoma is reported to account for approximately 2% to 5% of gynecological/uterine carcinomas (other reports state 3–4%, ~4%, <5%, or 5%), and a SEER analysis found it in 11,000 women (4.7%) during the study period. [17][18][31][30][55][32][56][60]8 sources
  • A Korea registry study reported that uterine carcinosarcoma incidence increased over time, with an annual percent change of 13.9%. [72][98][99][103][124]5 sources
  • Population-based analyses report that uterine carcinosarcoma diagnosis/incidence is higher in Black/non-Hispanic Black women than in White women; one US study found the highest incidence among Black women aged 70–74 in the South. [25][141][110]3 sources
  • In one cohort the median age at diagnosis was 67 years. [24][142]
  • In one cohort the most common presentation was abnormal vaginal bleeding (85%); pelvic mass occurred in 45% and abdominal pain in 38%. [142]
  • One surgical cohort reported that 9.1% of women with uterine carcinosarcoma were aged 80 years or older. [21]
  • In a retrospective series from South India, 20 patients were diagnosed over 10 years; the majority were postmenopausal, post-menopausal bleeding was the main presenting complaint in about 80% of patients, and more than two-thirds presented in stage I or stage II. [104]
  • In that cohort CA125 was elevated in 34.9% of the 43 evaluated women and in 60% of those elevated cases the level was below 200 U/ml. [140]
Show 1 lab & early-research finding
  • In a case series, the median length of exposure to tamoxifen was 9 years (5-20) and the median time from initiation of tamoxifen to diagnosis (latency period) was 9 years (7-20). [134]
Key biomarkers94 points

Key figures

Survival & outcomes
OutcomeValue95% CI
p53 immunohistochemistry positivity60%
MMR loss4%
overall molecular classification concordance91%
HER2 overexpression and amplification in UC14%
TROP2 mRNA detected90%
Prognostic factors
FactorEffectHR (95% CI)p
advanced FIGO stage▲ worse1.259=0.517
Source quotes
  • twenty-seven (60%) women were positive for p53 immunohistochemistry
  • 4 cases (4%) showed loss of MLH1/PMS2
  • with an overall molecular classification concordance of 91 %.
  • and 14% of UC patients [11].
  • TROP2 mRNA expression was detected in 64 out of 71 (90%) primary UCSs
  • MSI/MMR-d showed no significant association with advanced FIGO stage (OR = 1.259; p = 0.517)
  • Most uterine carcinosarcomas fall into the TP53-mutant/p53-abnormal or TCGA copy-number-high molecular group; TCGA molecular groups in uterine carcinosarcoma were assessed in five studies with 263 patients. [1][143][144][12][8][145]6 sources
  • In a UCS cohort, HER2 high expression (IHC 2+/3+) was observed in 50 of 148 cases; another study found HER2 overexpression in 26.6% of uterine carcinosarcomas and that HER2 amplification was associated with shorter overall survival. [79][72][124][123][76]5 sources
  • PIK3CA mutations were identified in 15% of uterine malignant mixed mesodermal tumors in one study. [18][146][30]3 sources
  • Mutations in chromatin-remodeling genes including ARID1A and CHD4 were common in molecular studies; one review reported ARID1A and mixed-lineage leukemia 3 mutations in 36% and 27% of uterine carcinosarcoma, respectively; mutations previously identified in uterine and ovarian carcinomas include TP53, PIK3CA, PPP2R1A, KRAS, PTEN, CHD4, and BCOR; one review reported an excess of mutations in genes encoding histone H2A and H2B. [30][147][33]3 sources
  • Gene-expression and pan-cancer analyses have examined mRNA expression of hub genes in uterine carcinosarcoma alongside other gynecologic tumors; specific findings reported include that COMP expression could predict uterine carcinosarcoma with an AUC of 0.769 and that EBNA1BP2 showed no significant differential expression in uterine carcinosarcoma compared with adjacent normal tissues. [148][149][150]3 sources
  • Recurrent alterations in PI3K-pathway genes such as PIK3CA and PTEN are common in uterine carcinosarcoma. [8][15][145]3 sources
  • In some cohorts, higher PD-L1 expression (including PD-L1_E and PD-L1_S) and PD1_E expression were associated with a significantly lower risk of progression or death or with longer survival; one study reported PD-L1 expression in tumor tissue as an independent good prognostic factor for overall survival. [25][151]
  • p16 expression has been observed in both the epithelial and mesenchymal components in uterine carcinosarcoma. [18][31]
  • Most carcinosarcomas are described as metaplastic carcinomas in which the sarcomatous component is derived from the carcinomatous component through transdifferentiation; most ECS are similar to serous-like, copy-number high endometrial cancers; a small percentage of ECS probably represent molecularly biclonal collision tumors; shared expression of p16, p53, and PAX8 in both malignant components has been reported, supporting the monoclonal theory. [18][31]
  • PD-L1 expression was reported in 33 of 41 uterine carcinosarcoma cases in one review and in 25% of cases in another study. [152][151]
  • TROP2 (Trop-2) is frequently expressed in primary uterine carcinosarcomas: TROP2 protein was reported by IHC in the majority of primary tumors, TROP2 mRNA was detected in 64 of 71 primary tumors, and expression was reported to be restricted to the carcinoma component of cases; however, one study found no significant association between Trop-2 or FRα expression and progression-free survival. [153][67]
  • One study reported HER2 overexpression in 26.6% of uterine carcinosarcomas, and HER2 overexpression or amplification was associated with shorter overall survival. [72][76][72]
  • A reported uterine carcinosarcoma case had a pathogenic POLE mutation present in both histologic components, supporting a clonal origin. [41][154]
  • In one cohort, the three-year progression-free survival rate was 21.2% and the three-year overall survival rate was 29.4%. [25]
  • Reduced p27 expression was observed in 77.8% of the stromal component and 66.7% of the epithelial component of carcinosarcoma in one comparative study. [126]
  • VEGF is strongly expressed in both the epithelial and spindle (sarcomatous) components of uterine carcinosarcoma. [155]
  • ERBB2 alterations have been reported in uterine carcinosarcoma. [79]
  • Sarcoma dominance was independently associated with decreased overall survival. [156]
  • FIGO stage was an independent prognostic factor for disease-free survival and overall survival. [156]
  • Patients with higher CA 125 levels, sarcoma dominance, cervical involvement, advanced stage, no lymphadenectomy, and residual tumour had a significantly higher risk of recurrence. [156]
  • At 240 months, the actuarial recurrence rate was 34.3%. [156]
  • Five-year disease-free survival and overall survival were 67% and 77%, respectively. [156]
  • In one study of proliferation markers, Ki67 expression was higher in the carcinomatous component than in the sarcomatous component; Ki67 reactivity in the epithelial component was related to FIGO stage and histological grade; PCNA positivity in the carcinomatous component was associated with omental metastases; and MCM3 staining and topoIIα positivity in the epithelial/carcinomatous component were related to clinical stage and omental metastasis. [111]
  • High PD-L1 expression was seen in 12 of 41 uterine carcinosarcoma cases in one review. [152]
  • MMR-deficient carcinosarcomas were more likely to have high-level PD-L1, but this difference did not reach statistical significance in the reported series. [152]
  • The review authors suggested that PD-L1 may be additive to MMR testing as a predictive biomarker for checkpoint inhibitor vulnerability in carcinosarcomas. [152]
  • Genomic profiling of uterine carcinosarcoma identified recurrent mutations in TP53, PIK3CA, FBXW7, PTEN, KRAS, and PPP2R1A. [113]
  • PAX8 positivity was noted in 73% of epithelial components and 13% of stromal components in one immunohistochemical study. [31]
  • COX-2 is expressed in a high percentage of uterine carcinosarcoma, but it was not associated with prognostic factors or survival in the cited study. [157]
  • MSI/MMR-deficient uterine carcinosarcomas were associated with endometrioid, undifferentiated/dedifferentiated, and clear cell carcinoma components and inversely associated with serous carcinoma component, heterologous sarcoma component, TP53-mutation/p53-abnormal expression, and recurrence; MSI/MMR-d showed no significant association with advanced FIGO stage in that series. [158]
  • One molecular comparison study found a 3.6-fold increase in DNA repair capacity and increased expression of DNA repair genes in uterine carcinosarcoma versus uterine papillary serous carcinoma, and the authors suggested possible vulnerability to agents targeting DNA damage repair such as PARP inhibitors. [159]
  • CD47 positivity was detected in 26 of 42 uterine carcinosarcoma tissue samples in one study. [13]
  • Uterine carcinosarcoma is characterized by a high frequency of copy number alterations. [75]
  • Biopsy-based molecular classification showed high concordance with hysterectomy specimens and effectively stratified recurrence risk, with POLE-mutated tumors showing the most favorable outcomes and p53-abnormal tumors the poorest. [160]
  • Abnormal β-catenin expression was reported in some uterine carcinosarcomas classified in the p53-abnormal category. [161]
  • TCGA/GTEx analysis reported LINC01087 was significantly upregulated in uterine carcinosarcoma. [162]
  • In a review of carcinosarcoma samples, Signature-3, described as a homologous recombination deficiency (HRD)-related signature, was identified in 25% of uterine carcinosarcoma samples. [163]
  • ERBB2 (HER2) gene amplification was observed among gynecologic malignancies and uterine carcinosarcoma had an ERBB2 amplification incidence of 7.9%. [164]
  • URI1 amplification was detected in 40% of primary uterine carcinosarcomas in one study. [56]
  • ESR1 gene amplification occurs in 7% of uterine carcinosarcoma (TCGA UCS dataset). [154]
  • In a phase II study of ARID1A-deficient solid tumors, one patient with uterine carcinosarcoma had stable disease with the ATR inhibitor ceralasertib. [165]
  • A germline MITF(E318K) analysis observed an association with uterine carcinosarcoma in TCGA sporadic samples (OR 9.24; 95% CI 2.08–37.17; p=0.024). [166]
  • In POLE-mutated uterine carcinosarcoma, frequent co-occurring somatic mutations reported included PIK3CA, PTEN, RB1, ARID1A, ATM, PIK3RA, and FBXW7; two POLE-mutated tumors demonstrated loss of mismatch repair protein expression (one with subclonal loss). [15]
  • In three tumors originally diagnosed as uterine rhabdomyosarcoma, pathogenic TP53 mutations and high genomic instability were found; one tumor harbored an FBXW7 hotspot mutation and another a PPP2R1A hotspot mutation. [145]
  • HER2 positivity was associated with worse survival in endometrial endometrioid carcinoma and improved survival in serous endometrial carcinoma, but HER2 status showed no survival difference in uterine carcinosarcoma in that analysis. [167]
  • One analysis found BRCA1 and BRCA2 to be most frequently mutated in carcinosarcoma among the endometrial carcinoma histologies studied and reported carcinosarcoma among the least altered for PI3K/Akt/mTOR pathway dysregulation. [168]
  • LILRB4 expression was reported to be associated with survival in uterine carcinosarcoma in a pan-cancer analysis. [169]
  • PRAME mRNA expression was reported as highest in uterine carcinosarcoma among the gynecologic malignancies discussed; PRAME is described as a cancer antigen with limited expression in normal tissues and as a diagnostic and immunotherapeutic target. [170]
  • Elevated GTSF1 expression was reported to be significantly correlated with reduced disease-free survival in uterine carcinosarcoma patients. [129]
  • Recurrent PPP2R1A hotspot mutations (e.g., P179R, S256F) occur exclusively within high-grade subtypes of uterine cancer (USC/UCS). [171]
  • ESRG was reported as significantly upregulated in uterine carcinosarcoma in a pan-cancer analysis. [172]
  • GRB7 expression was reported as significantly elevated in uterine carcinosarcoma in a pan-cancer analysis. [173]
  • MYL6B was reported as highly expressed in uterine carcinosarcoma tissues in a pan-cancer analysis. [174]
  • NUCB2 expression was significantly higher in sarcomatous compared with carcinomatous components in UCS tissues. [175]
  • In a pan-cancer analysis, NRP1 expression was significantly decreased in uterine carcinosarcoma compared with matched healthy tissues; low NRP1 expression was linked to longer overall survival in some cancers but to shorter overall survival in KIRC only. [176]
  • An analysis reported that four newly discovered alternative splicing factors could help reveal the molecular mechanism of uterine carcinosarcoma and act as potential drug targets and prognostic biomarkers. [88]
  • SLC1A5 expression was reported as increased in UCS compared with normal tissue in a pan-cancer analysis, and an SLC1A5 missense mutation at position 330 was found in UCS and could be associated with poor prognosis in UCS. [177]
  • In one study of paired primary and metastatic uterine carcinosarcoma, HER2 scores differed between primary and metastatic lesions, and HER2 discordance between primary and metastatic tumors was reported as a poor prognostic factor. [178]
  • SATB2, cyclin D1, SALL4, and BCOR can be expressed in uterine carcinosarcoma and their expression must be interpreted in context. [179]
  • TET2 was included in analyses of uterine carcinosarcoma in The Cancer Genome Atlas (TCGA) datasets. [180]
  • ADA1 expression was reported as significantly increased in uterine carcinosarcoma in a pan-cancer analysis. [181]
  • APOE expression was reported as upregulated in uterine carcinosarcoma in a GEO-based pan-cancer analysis. [182]
  • FBXW7 was reported as one of the most deregulated ubiquitin–proteasome system proteins in uterine carcinosarcoma. [183]
  • Common somatic mutations reported in uterine carcinosarcoma include TP53, PIK3CA, FBXW7, PTEN, and ARID1A, and UCS tumors have been characterized as serous-like. [95]
  • Epithelial–mesenchymal transition (EMT) is reported to play a pivotal role in the pathogenesis of sarcomatous dedifferentiation in uterine carcinosarcoma, and heterologous sarcoma is associated with a higher EMT signature than homologous sarcoma. [95]
  • In clinical samples, S100A4 score was higher in sarcomatous than in carcinomatous components of UCS and was positively correlated with ALDH1, Slug, and vimentin scores and inversely correlated with Ki-67 labeling indices. [184]
  • High expression of phospho-aurora kinase A and aurora kinase B was a prognostic factor for progression-free survival in one small study. [29]
  • High expression of fascin was associated with extrapelvic disease, higher stage, larger tumor size, shorter progression-free interval, and reduced estrogen receptor-alpha expression in one study. [185]
  • High nestin was more common in uterine carcinosarcoma than in type I cancers; nestin was inversely correlated with ER, PR, and TFF3, and correlated with p53 and IMP3. [186]
  • In uterine carcinosarcoma patient samples, c-Myc mRNA levels were elevated in the recurrent group compared to the non-recurrent group. [32]
  • A study using a genetically engineered model identified Fbxw7 as a key driver of uterine carcinosarcoma, with tumors undergoing epithelial–mesenchymal transition. [19]
  • ER-β expression, increased serum CA-125, increased CRP, and thrombocytosis were reported as significant prognostic factors in one clinicopathologic study. [187]
  • In one immunohistochemical study, none of the tested markers was statistically significantly associated with survival of carcinosarcoma patients. [188]
  • The presence of ALT-associated PML bodies (APBs) was found to be a poor prognostic factor for disease-free survival and overall survival. [189]
  • ALT positivity was negatively correlated with human telomerase reverse transcriptase reactivity in one study. [189]
  • Reduced membranous expression of E-cadherin and β-catenin may contribute to the biphasic morphology of uterine carcinosarcoma. [190]
  • MMR status was reported as proficient in all five patients with uterine carcinosarcoma who were treated with lenvatinib plus pembrolizumab in one report. [191]
  • CD133+ cells have been identified in uterine carcinosarcomas and are described as having cancer stem‑cell–like properties including differentiation into both epithelial and stromal lineages and chemotherapy resistance. [192]
  • Sources describe TP53 as frequently mutated in uterine carcinosarcoma; for example, one cohort detected TP53 mutation in 8 of 19 tumors. [18][20][19][24][30][106][193][31]8 sources
  • POLE-mutant tumors are uncommon (reported as 2.7% in one molecular study), and MSI/MMR-deficient or MSI-high tumors are uncommon overall (reported rates across studies include 4% MMR deficiency and 7.4% MSI-H); a meta-analysis found the POLE and MSI subgroups to be less common in uterine carcinosarcoma. [144][194][143]3 sources
  • In a retrospective cohort, all uterine carcinosarcoma cases were mesothelin-positive, and 33.9% showed high mesothelin expression; HER2-high tumors had higher mesothelin expression than HER2-negative tumors. [97]
  • L1CAM, CDX2, p53, and microsatellite instability (MMR) status were evaluated in a cohort of uterine carcinosarcoma; in that cohort, mismatch repair deficiency (dMMR) occurred in 5.3% of cases, aberrant p53 expression in 26.3%, and CDX2 positivity in 5.3%. [108]
  • Mismatch repair deficiency was reported as rare in that genomic profiling cohort. [113]
  • A multi-institution retrospective review reported mismatch repair deficiency in 4% of uterine carcinosarcomas, noted that all MMR-deficient carcinosarcomas identified were due to somatic MLH1 hypermethylation, and recommended that universal screening include uterine carcinosarcoma. [194]
  • TSC2 loss was significantly associated with recurrence in one retrospective cohort. [75]
  • In one uterine carcinosarcoma cohort, HER2 IHC scores were negative in 41/148 (27.7%), 1+ in 57/148 (38.5%), and 2+/3+ in 50/148 (33.8%); FISH testing was performed in 72 patients. [123]
  • In a cohort of gynecologic tumors, lymphovascular invasion (LVI) was reported as highest among uterine carcinosarcoma cases at 5/11 (45%). [195]
  • A retrospective study reported folate receptor alpha (FRα) expression in all uterine carcinosarcoma specimens, with FRα-high status present in 20% of patients; among HER2-negative cases, 34% exhibited FRα-high status, and no significant association was observed between FRα status and clinicopathological characteristics or prognosis. [196]
  • In a UCS cohort, HER2-positive cases all had serous morphology and aberrant p53 expression; those HER2-positive cases showed only minimal PD-L1 expression and none had mismatch repair (MMR) loss. [197]
Show 5 lab & early-research findings
  • HER2/ERBB2 alterations and expression occur in a subset of uterine carcinosarcomas, with higher expression in the carcinomatous component than in the sarcomatous component; ERBB2 gene alterations have been evaluated and might have a biologic role; HER2 overexpression or amplification has been reported in individual cases and may be present in invasive or metastatic components; HER-2 and c-KIT have been described as poor therapeutic targets. [43][198][199][155]4 sources
  • One small series reported p53 overexpression in 27.8% of carcinosarcomas by immunohistochemistry. [126][12]
  • In patient-derived xenografts from uterine carcinosarcoma, HER2 expression was reported as 1+ in all xenografts studied. [92]
  • FGFR1 amplification was identified in a recurrent uterine carcinosarcoma case report. [84]
  • One case report described HER2 staining and HER2 amplification in myometrial invasion, myometrial lymphovascular invasion, and pelvic lymph node metastasis but not in the surface tumor. [43]
Biology & pathways47 points

Key figures

Survival & outcomes
OutcomeValue95% CI
p53 protein overexpression concordance85%
TP53 gene mutation concordance96%
Source quotes
  • The carcinomatous and sarcomatous components show a concordance of 85% for the p53 protein overexpression and 96% for the TP53 gene mutation
  • Sources describe molecular and EMT findings supporting a monoclonal/metaplastic model in which the sarcomatous component arises from an epithelial clone via epithelial–mesenchymal transition. [37][38][61][41][40][83][200][201][60]9 sources
  • Epithelial–mesenchymal transition (EMT) is described as a central mechanism in UCS pathogenesis: the sarcomatous component is reported to arise via dedifferentiation of the carcinoma, and EMT is linked to poor prognosis, therapy resistance and a mesenchymal/cancer stem cell–like phenotype, sometimes evident prior to metastasis. [26][20][19][184][21][106][33][54]8 sources
  • Uterine carcinosarcoma is a biphasic tumor composed of carcinomatous (epithelial) and sarcomatous (mesenchymal) components, with the carcinomatous component driving biphasic growth; it is biologically considered an endometrial (epithelial) carcinoma that secondarily exhibits mesenchymal differentiation. [202][2][203][5][79][7][3]7 sources
  • Epithelial–mesenchymal transition (EMT) is described as the mechanism of sarcomatous dedifferentiation in uterine carcinosarcoma, is characterized as central to the disease (a model of EMT/cellular plasticity), and is linked to enhanced migratory capabilities and facilitation of metastasis. [202][5][6][8][11][67]6 sources
  • Sources note that UCS presents an admixture of epithelial and mesenchymal tumor cells and exhibits a typical epithelial-to-mesenchymal transition gene expression profile. [108][96][16][204][25]5 sources
  • Uterine carcinosarcoma (malignant mixed Müllerian tumor) is a biphasic tumor characterized by malignant epithelial (carcinomatous) and mesenchymal (sarcomatous) components and is considered an epithelial cancer with sarcomatous dedifferentiation. [37][38][51][135][205]5 sources
  • Multiple sources state that the carcinomatous (epithelial) element is the driving force in uterine carcinosarcoma and that tumors may originate from an endometrial tumor clone that subsequently undergoes metaplastic differentiation; on this basis UCS has been considered a form of metaplastic carcinoma. [79][103][133][98]4 sources
  • Multiple molecular alterations have been associated with EMT and cancer stem cell–like properties in UCS, including an S100A4/NMII‑related signaling cascade, methylation‑associated silencing of the miR‑200 family (with reported therapeutic relevance of the miR‑200 family), and increased EMT marker expression after stable mutant H2A/H2B expression. [184][30][106][33]4 sources
  • The sarcomatous component may be homologous or heterologous; reported heterologous elements include cartilage (chondrosarcoma), adipose tissue (liposarcoma), and bone (osteosarcoma). [37][114][38][83]4 sources
  • Sources describe UCS as a biphasic tumor composed of malignant epithelial and sarcomatous components, and heterologous sarcomatous elements are reported in some cases. [72][98][89]3 sources
  • Epithelial-to-mesenchymal transition (EMT) is described as central to or a hallmark of UCS and is implicated in differentiation of the sarcomatous portion; mechanisms reported to contribute to EMT include repression of the miR-200 family, TGFβ signaling (which promotes EMT and a cancer stem cell phenotype), TGF-β1–induced changes (including increased NUCB2 and ZEB1 expression), and influences from the tumor microenvironment. [119][99][175]3 sources
  • Sources report that EMT is implicated in uterine carcinosarcoma, with ZEB1 showing higher nuclear expression in sarcomatous components, and that UCS lesions can exhibit loss of E‑cadherin consistent with EMT. [200][201][83]3 sources
  • Heterologous mesenchymal components have been associated with worse prognosis, including worse disease-free survival and overall survival in at least one study. [98][89]
  • The carcinomatous component tends to spread via lymphatics while the sarcomatous component tends to spread loco‑regionally. [18][206]
  • Cancer stem cells are associated with chemotherapy resistance and recurrence in uterine carcinosarcoma; a mechanism involving CCL1, M1 macrophage chemotaxis, and IL-6 secretion has been reported to amplify cancer stemness. [203][129]
  • Uterine carcinosarcoma is a high‑grade, biphasic neoplasm with epithelial and mesenchymal components; it shows molecular heterogeneity, aneuploidy and a high frequency of copy‑number variations, features that have been noted as opening opportunities for targeted therapies. [18]
  • Sources describe that primary UCS tumors show EMT, mTORC1, and glycolytic programs, while metastases show enhanced TNFα–NFκB signaling linked to invasion; UCS is characterized by epithelial–mesenchymal plasticity and a complex microenvironment. [8]
  • A study reported increased expression of immune-exhaustion and immune-evasive genes in uterine carcinosarcoma, alongside evidence that the immune system was activated in response to increased DNA damage. [159]
  • A small genomic series reported a likely oncogenic YTHDF2–FOXR1 fusion in one tumor and found that uterine carcinosarcoma and three adult uterine tumors intermingled on hierarchical clustering based on somatic mutations and copy-number alterations. [145]
  • The source notes that UCS shares the same FIGO 2009 staging system as endometrial carcinoma. [7]
  • Wee1 kinase inhibition has been identified as a potential therapeutic strategy in uterine carcinosarcoma. [69]
  • Sources report that recurrent PPP2R1A (PP2A Aα) mutants in USC/UCS enhanced tumor-initiating capacity, promoted a hybrid epithelial–mesenchymal plasticity phenotype, and increased IGFBP2 secretion, with PP2A regulating IGFBP2 via NF-κB. [171]
  • A genomic study reported commonly altered pathways in uterine carcinosarcoma including TP53, RTK/RAS, PI3K, and cell cycle pathways. [207]
  • Sources describe SLC16A3 as a highly expressed H+-coupled symporter that facilitates lactate transport and contributes to acidosis. [208]
  • Sources state that NRP1 is a membrane-bound co-receptor for vascular endothelial growth factor and semaphorin family members. [176]
  • Some studies report that p53 mutations are frequent in high-grade non-endometrioid endometrial cancers, including uterine carcinosarcoma. [209]
  • One review states that TP53 is related to immunological function based on different mutation classification in various cancers. [210]
  • Sources describe TIPE2 (TNFAIP8L2) as a negative regulator of immunity and a potential checkpoint, with expression associated with increased macrophage and dendritic cell infiltration. [211]
  • One review reported that SHCBP1 was correlated with an immunosuppressive tumor microenvironment and that SHCBP1 may function as an emerging onco-immunological biomarker and is expected to become a therapeutic target for tumor immunotherapy. [212]
  • The FBXW7 review states that alteration in FBXW7 leads to aberration in signaling pathways and substrate binding ability. [183]
  • The LINC01087 review states that in silico analyses revealed a potential role for LINC01087 in carcinogenesis through regulation of gene products that sense or exchange extracellular molecules. [162]
  • Sources characterize 40 BRCAness-related genes across cancers and identify uterine carcinosarcoma as a potential target for PARP inhibitor therapy. [213]
  • A TCGA-based study of uterine carcinosarcoma identified survival-related alternative splicing events; JUP was significantly correlated with RALGPS1-87608-AT, which was associated with distant metastasis, and pyrimidine metabolism was the key pathway coexpressed with RALGPS1. [118]
  • Tumors with URI1 amplification showed decreased transcription of genes encoding tumor suppressors and apoptotic regulators and increased expression of genes regulating oncogenesis, survival, and metastasis. [56]
  • Alternative lengthening of telomeres (ALT) is described as a prevalent mechanism in uterine sarcomas and carcinosarcomas and has been associated with tumor aggressiveness and progression. [189]
  • Sources report that matrisome gene expression was profiled in CESC, UCEC, and UCS, identifying distinct matrisome-associated gene sets characterizing each cohort. [127]
  • Reported molecular alterations in uterine carcinosarcoma include mutations in KRAS, PIK3CA, PTEN and ARID1A in a UCS cell line; in a separate case, both epithelial and mesenchymal components shared an identical pathogenic POLE mutation, supporting a clonal origin. [83][205][214][41][201]5 sources
  • The carcinomatous and sarcomatous components show high concordance for p53 protein overexpression and TP53 gene mutation, and several studies report that the carcinomatous and sarcomatous elements derive from a common precursor (supporting a monoclonal origin in which the carcinomatous component can be the driving force). [18][33][62][54]4 sources
  • TGFβ signaling promotes EMT and aggressive behaviors in UCS: TGFβ1/TGFβ‑I activates canonical and non‑canonical pathways (including Smad2/3), promotes cell proliferation, migration, clonal growth, invasion and EMT in UCS models, and TGFβ1 activation engaged AKT and p70S6 kinase (which were inhibited by galunisertib or combined with cisplatin); in one cell line TGFβ‑I also induced nuclear NFAT‑1 and c‑Myc expression. [26][32]
  • Two molecular subtypes have been reported: subtype I is enriched for cell‑cell adhesion, antigen processing and presentation, and apoptosis pathways, while subtype II is enriched for myogenesis/muscle development and transcriptional activation pathways. [17][28]
  • HER2 overexpression has been reported in uterine carcinosarcoma. [203]
  • Dysregulation of apoptosis pathways is described as a hallmark of cancer. [215]
  • Sources describe SLC1A5 as a major glutamine transporter and indicate it may influence cell proliferation by affecting DNA synthesis. [177]
  • Aurora kinases A and B are highly expressed in UCS (with dominant cytoplasmic expression of A and B and nuclear localization of the phosphorylated forms); phosphorylated aurora kinase A and aurora kinase B show higher expression in the carcinomatous component, phosphorylated aurora A expression was associated with lymphatic metastasis (including positive pelvic lymph node and omental involvement), and aurora kinase B overexpression was related to vascular invasion. [29]
  • UCS shares mutational spectra with endometrial cancers, including frequent mutations in loci encoding PI3K pathway components; in a mouse model, combined loss of Fbxw7 and Pten acted synergistically in endometrial carcinogenesis. [19]
  • Preclinical work in a UCS‑derived cell line (CS99) suggests BMI1 inhibition with the agent PTC‑028 increased apoptosis, decreased cell viability in vitro, and delayed tumor growth in vivo. [192]
  • Accidental surgical implantation of endometrioid cells has been suggested as a pathogenic mechanism for an extra-uterine Müllerian carcinosarcoma in a reported case. [216]
Standard management43 points

Key figures

Prognostic factors
FactorEffectHR (95% CI)p
HR for adjuvant chemoradiation and OS▼ better0.1–0.22all p < 0.001
Source quotes
  • adjuvant chemoradiation was consistently selected as an independent prognostic factor for OS (hazard ratio [HR] 0.10-0.22, all p < 0.001) and PFS (HR 0.12-0.23, all p < 0.001)
  • Primary treatment is surgery; initial management typically includes total hysterectomy and bilateral salpingo-oophorectomy with evaluation of lymph nodes and collection of pelvic washings, and staging procedures often include pelvic and para-aortic lymphadenectomy, peritoneal cytology and omentectomy. [21][117][24][217][28][53][218][55][219][36][35][34][220]13 sources
  • Surgery is described as the cornerstone or primary therapy for uterine carcinosarcoma, and multimodal therapy is described as offering the best prognosis. [98][100][99][107][104][89][221][222][85][109][87]11 sources
  • Adjuvant therapy commonly includes cytotoxic chemotherapy and radiotherapy. In a multicenter cohort, combined chemoradiation improved progression-free and overall survival versus chemotherapy alone across stages; in early-stage cohorts, combined modality treatment was associated with longer survival. [122][2][3][14][223][13][224][6][7][11]10 sources
  • Adjuvant treatments after primary surgery may include chemotherapy, radiotherapy, or chemoradiotherapy; adjuvant therapy is indicated for patients in stages IB-IV and has been reported to be closely associated with overall survival. [109][100][89][107][104][85][108][221][222]9 sources
  • Carboplatin and paclitaxel (paclitaxel‑carboplatin) and other platinum doublets are commonly used after surgery and are considered the standard or regimen of choice in adjuvant and palliative settings. [99][100][102][108][221][85]6 sources
  • Published clinical series and database analyses report mixed effects of adjuvant therapy on recurrence and survival: some cohorts found adjuvant treatment was not associated with changes in recurrence or survival, while other retrospective series reported adjuvant chemoradiation as an independent prognostic factor for overall and progression‑free survival and a SEER analysis found receipt of radiotherapy was associated with an overall survival benefit. [156][225][226][131][27]5 sources
  • Sources describe surgery as the primary treatment for uterine carcinosarcoma. [38][39][42][83][44]5 sources
  • Some retrospective studies and cohorts support adjuvant chemoradiotherapy after surgery, but the role of postoperative radiotherapy is uncertain and retrospective data show conflicting findings for progression‑free and overall survival; vaginal brachytherapy is increasingly used in practice. [227][12][77][70][72]5 sources
  • Surgery is the standard/cornerstone treatment and surgical resection is the best curative option for localized disease; non‑metastatic UCS is managed with complete surgical staging including total hysterectomy, bilateral salpingo‑oophorectomy, peritoneal staging with biopsies (including omentum) and lymph node evaluation, a step recommended by the American Radium Society guideline. [93][94][131][16][22]5 sources
  • For advanced‑stage disease, cytoreductive (debulking) surgery is recommended, with removal of suspicious lymph nodes and the aim of complete tumor resection when feasible. [69][70][133][97][98]5 sources
  • In cohorts described in the literature UCS is typically treated with surgery followed by adjuvant chemotherapy; one reported postoperative regimen is carboplatin and paclitaxel every 3 weeks for six cycles, radiotherapy has been delivered as external beam pelvic radiation and high‑dose‑rate brachytherapy, and some reviews describe offering adjuvant chemotherapy followed by radiotherapy or as a sandwich regimen. [226][25][116][228][27]5 sources
  • Postoperative adjuvant therapy is widely considered and most patients are described as candidates for adjuvant chemotherapy; adjuvant approaches reported include chemotherapy (commonly ifosfamide/paclitaxel‑based), radiotherapy, or multimodality combinations following complete surgical staging. [219][117][36][62][34]5 sources
  • Multiple reviews recommend complete surgical staging followed by consideration of multimodal adjuvant therapy in both early and advanced disease, and note that the optimal management strategy for uterine carcinosarcoma is not yet established. [34][36][35][219][24]5 sources
  • Sources describe that standard treatments include surgery with adjuvant chemotherapy, and retrospective data report adding trastuzumab to carboplatin/paclitaxel for advanced-stage HER2-overexpressing uterine carcinosarcoma. [12][72][77][124]4 sources
  • Total hysterectomy with bilateral salpingo-oophorectomy and surgical staging (often including lymphadenectomy) is the first-line/initial treatment for patients without distant metastasis. [46][47][229][50]4 sources
  • Guideline-consistent management typically includes surgery followed by adjuvant platinum-based chemotherapy — usually carboplatin plus paclitaxel — with or without radiotherapy; platinum-based regimens are the usual first-line systemic therapy. [230][205][46][45]4 sources
  • Lymphadenectomy is recommended for staging in tumors apparently confined to the uterus, and lymphadenectomy has been reported as an independent predictor of survival and to prolong survival even for early‑stage disease. [219][220][231]3 sources
  • Surgical resection and traditional cytotoxic chemotherapy remain described as standard of care in several reviews and series. [27][16][25]3 sources
  • Uterine carcinosarcoma is staged as endometrial cancer under the revised FIGO 2009 system; staging categories include stage I (limited to the corpus), stage II (cervical stromal invasion), stage III (metastasis to proximal tissues such as para-aortic lymph nodes) and stage IV (extra‑pelvic metastasis such as bladder and bowel mucosa). [117][220][130]3 sources
  • Some reviews and guidelines state that adjuvant treatment for uterine carcinosarcoma should probably follow approaches used for aggressive high‑grade endometrial carcinomas rather than sarcoma‑based regimens. [58][59][21]3 sources
  • FIGO stage is the most important prognostic factor for survival, followed by myometrial invasion, lymphovascular space invasion, lymph node metastasis and adnexal spread; positive peritoneal cytology is associated with poor prognosis, there appears to be no significant survival difference between positive pelvic versus para‑aortic lymph nodes, and prognosis is worse in patients with stage IIIC disease with other evidence of extrauterine spread. [55][231]
  • For unresectable, advanced, or widely metastatic disease, systemic chemotherapy is the main treatment and surgery is usually palliative or may be omitted in favor of systemic therapy. [122][9]
  • There remains a paucity of specific, widely agreed guidelines for uterine carcinosarcoma management and some reviews state that no existing standard guidelines for adjuvant therapy exist, in part because the disease is rare. [4][11]
  • Comprehensive surgical staging can identify extrauterine disease, and surgery is described as the principal treatment in early or locally advanced disease. [36][35]
  • Some sources state uterine carcinosarcoma generally requires more aggressive management than typical endometrial cancer, though it is often staged and treated according to endometrial cancer guidelines; one review notes that de‑escalation of adjuvant treatment may be a valid option in POLE‑mutated carcinosarcoma. [38][41]
  • In a matched cohort analysis of stage I uterine carcinosarcoma, omission of lymphadenectomy was associated with decreased median survival; in the same analysis multiagent chemotherapy and vaginal brachytherapy were associated with decreased hazard of death and the highest 5‑year survival in stage I was observed following brachytherapy combined with multiagent chemotherapy. [232]
  • A randomized phase III trial concluded that paclitaxel plus carboplatin was not inferior to paclitaxel plus ifosfamide and should be standard treatment for uterine carcinosarcoma. [233]
  • In one surgical series minimally invasive surgery was used in 52% of cases and there was no difference in recurrence‑free survival or overall survival between open surgery and minimally invasive surgery groups. [91]
  • In the same surgical series 93% of patients received adjuvant therapy in the form of chemotherapy and/or radiation therapy. [91]
  • Uterine carcinosarcoma is described as an aggressive malignancy with few treatment options; the same review notes a recent trial showing increased progression‑free survival with anti‑HER2 therapies in HER2‑positive serous endometrial carcinomas and suggests HER2‑positive UCS may be less susceptible to immune checkpoint inhibition because they uncommonly show MMR deficiency and/or strong PD‑L1 expression. [197]
  • Palliative chemotherapy is described as the treatment of choice in the metastatic setting. [16]
  • Use of lymphadenectomy, chemotherapy and brachytherapy has increased over the past few decades. [95]
  • Long‑term surveillance is indicated because many women with uterine carcinosarcoma may experience recurrence. [22]
  • Endometrial sampling may not accurately diagnose uterine carcinosarcoma and definitive diagnosis is often based on pathology after hysterectomy. [42]
  • A 2002 review recommended that prospective studies be performed to determine whether adjuvant therapies are more effective than traditional sarcoma‑based therapies for uterine carcinosarcoma. [59]
  • Aspiration cytology (fine-needle aspiration) has diagnostic utility in the investigation of clinically suspicious post-surgical recurrent lesions of uterine carcinosarcoma. [51]
  • Transvaginal sonography (TVS) characteristics combined with clinical features can indicate the presence of UCS and contribute to clinical decision‑making. [140]
  • Reviews describe that multimodal adjuvant approaches (chemotherapy, radiotherapy, brachytherapy, lymphadenectomy) are commonly used in uterine carcinosarcoma, but the optimal adjuvant strategy remains unsettled. Level 3 evidence for early-stage disease is lacking, though retrospective data suggest adjuvant therapy may be warranted. The American Radium Society advises considering adjuvant multimodality therapies. [93][95][27][131][234][22]6 sources
  • Adjuvant pelvic radiotherapy may reduce locoregional recurrences, but evidence is mixed: some retrospective series and reviews report no reduction in recurrence or no significant improvement in outcome with systemic adjuvant therapy. [219][218][142][57][24]5 sources
  • In one retrospective single‑institution series all patients underwent staging laparotomy; in that series patients with good performance status received adjuvant concurrent chemoradiotherapy and chemotherapy. [104][87]
  • A retrospective analysis reported that lymphadenectomy was not independently associated with improved survival in uterine carcinosarcoma, and noted that its role remains uncertain. [100]
Show 2 lab & early-research findings
  • A case report described a BRCA1-mutated uterine carcinosarcoma treated with paclitaxel/carboplatin followed by durvalumab, achieving a complete radiologic response, with maintenance durvalumab plus olaparib thereafter. [61]
  • A case reported new pulmonary nodules during pembrolizumab for recurrent uterine carcinosarcoma that proved to be a sarcoidosis-like reaction; pembrolizumab was continued and the patient remained disease-free three years after completing treatment. [235]
Treatments & compounds studied120 treatments

Chemotherapy

  • adjuvant chemotherapy: Adjuvant (after surgery)A small retrospective uterine carcinosarcoma cohort reported that adjuvant chemotherapy was associated with better overall survival. [85]
    adjuvant chemotherapy and OS 0.24 (95% CI 0.09–0.65), p=0.005 vs no adjuvant chemotherapy
    Source quote
    • The significant independent factors for OS were FIGO stage III (HR, 2.33; 95% CI, 1.03–5.27; P=0.042), FIGO stage IV (HR, 5.91; 95% CI, 2.35–14.86; P<0.001), and adjuvant chemotherapy (HR, 0.24; 95% CI, 0.09–0.65; P=0.005)
  • anthracycline: Anthracycline use was reported as an independent predictor for improved progression-free survival in high-grade/heterologous disease. [206]
  • carboplatin · 9 findings
    • First-line (advanced disease)Sources describe carboplatin/paclitaxel as a standard-of-care first-line systemic therapy for uterine carcinosarcoma and show its use in cohorts and preclinical models. [69][70][77][99][100][26][44][236]8 sources
      response rate 50% vs older regimensmedian overall survival 37 months vs ifosfamide armmedian overall survival 29 months vs carboplatin arm
      Source quotes
      • Response rates to this combination are on the order of 50%–60%
      • "The carboplatin arm showed greater overall survival than the ifosfamide arm (37 vs. 29 months)."
      • "The carboplatin arm showed greater overall survival than the ifosfamide arm (37 vs. 29 months)."
    • Platinum-based or combination chemotherapy such as carboplatin + paclitaxel is described across stages as an indicated option for disease control. [49][131][95][118]
      Contradicting evidence: Some sources report improved progression-free survival or preference for carboplatin‑paclitaxel versus comparators, while another source reports no significant effect on progression survival rate. (the more authoritative source is [95]).
      4 sources
      response rate 50% vs older regimenscarboplatin-paclitaxel use among chemotherapy recipients 85%
      Source quotes
      • Response rates to this combination are on the order of 50%–60%
      • Carboplatin-paclitaxel (CP) regimen was administered to 227 patients (85.0%).
    • In a retrospective series, the carboplatin/ifosfamide/mesna (CIM) group had a median progression-free survival of 35 months and median overall survival of 47 months and reported no neurotoxicity or other grade 3 or 4 toxicities in the CIM group while the comparison group had grade 3 neutropenia, peripheral sensory neuropathy, and treatment deferrals. [237]
      progression-free survival 35 months vs other regimensoverall survival 47 months, p=0.001 vs other regimensgrade 3 neutropenia 3% vs CIMperipheral sensory neuropathy 4% vs CIMtreatment deferred due to toxicities or allergic reaction to paclitaxel 6% vs CIMprogression-free survival 27.48 months vs CIMoverall survival 30 months, p=0.001 vs CIM
      Source quotes
      • the progression-free survival (PFS) and OS for patients treated with adjuvant or palliative CIM was 35 months [95% confidence interval (CI) =0.26-0.43] and 47 months (95% CI=0.38-0.56; log-rank, p=0.001) respectively
      • the progression-free survival (PFS) and OS for patients treated with adjuvant or palliative CIM was 35 months [95% confidence interval (CI) =0.26-0.43] and 47 months (95% CI=0.38-0.56; log-rank, p=0.001) respectively
      • 3/38 patients in group 2 experienced grade 3 neutropenia
      • 4/38 had peripheral sensory neuropathy
      • 6/38 patients had treatment deferred due to toxicities or allergic reaction to paclitaxel
      • for group 2 patients treated with other regimens, PFS was 27.48 months (95% CI=0.20-0.33) and OS was 30 months (95% CI=0.21-0.38; log-rank, p=0.001)
      • for group 2 patients treated with other regimens, PFS was 27.48 months (95% CI=0.20-0.33) and OS was 30 months (95% CI=0.21-0.38; log-rank, p=0.001)
    • In the same retrospective series, the other-regimen group (including carboplatin/paclitaxel/cisplatin/doxorubicin/epirubicin) had a median progression-free survival of 27.48 months and a median overall survival of 30 months. [237]
      progression-free survival 35 months vs other regimensoverall survival 47 months, p=0.001 vs other regimensgrade 3 neutropenia 3% vs CIMperipheral sensory neuropathy 4% vs CIMtreatment deferred due to toxicities or allergic reaction to paclitaxel 6% vs CIMprogression-free survival 27.48 months vs CIMoverall survival 30 months, p=0.001 vs CIM
      Source quotes
      • the progression-free survival (PFS) and OS for patients treated with adjuvant or palliative CIM was 35 months [95% confidence interval (CI) =0.26-0.43] and 47 months (95% CI=0.38-0.56; log-rank, p=0.001) respectively
      • the progression-free survival (PFS) and OS for patients treated with adjuvant or palliative CIM was 35 months [95% confidence interval (CI) =0.26-0.43] and 47 months (95% CI=0.38-0.56; log-rank, p=0.001) respectively
      • 3/38 patients in group 2 experienced grade 3 neutropenia
      • 4/38 had peripheral sensory neuropathy
      • 6/38 patients had treatment deferred due to toxicities or allergic reaction to paclitaxel
      • for group 2 patients treated with other regimens, PFS was 27.48 months (95% CI=0.20-0.33) and OS was 30 months (95% CI=0.21-0.38; log-rank, p=0.001)
      • for group 2 patients treated with other regimens, PFS was 27.48 months (95% CI=0.20-0.33) and OS was 30 months (95% CI=0.21-0.38; log-rank, p=0.001)
    • Recurrent or later-linePaclitaxel plus carboplatin (TC) is described as the most frequently used regimen for gynecological malignancies and is often reused at relapse. [238]
    • First-line (advanced disease)Sources report carboplatin plus paclitaxel being used as systemic chemotherapy, including as a standard regimen in cohort reports and initiated for metastatic disease. [239][13][9][136][240][25][116]7 sources
      response rate 50% vs older regimens
      Source quote
      • Response rates to this combination are on the order of 50%–60%
    • Adjuvant (after surgery)Carboplatin and paclitaxel were used as adjuvant chemotherapy in a retrospective uterine carcinosarcoma series and a number of cohort reports describe adjuvant use of the combination. [240][25][116][13]4 sources
    • Adjuvant (after surgery)Carboplatin and paclitaxel were used as postoperative chemotherapy in a reported cohort where all patients received postoperative carboplatin plus paclitaxel. [108][205]
      progression-free survival (PFS) 13 monthsoverall survival (OS) 37 months
      Source quotes
      • A phase III trial reported that carboplatin plus paclitaxel resulted in progression-free survival (PFS) of 13 months and OS of 37 months (Miller et al., 2020).
      • A phase III trial reported that carboplatin plus paclitaxel resulted in progression-free survival (PFS) of 13 months and OS of 37 months (Miller et al., 2020).
    • Adjuvant (after surgery) · biomarker-selectedCarboplatin plus paclitaxel was used as frontline chemotherapy in a HER2‑overexpressing uterine carcinosarcoma cohort and as postoperative chemotherapy in another cohort. [124][108][94]3 sources
      most common chemotherapy regimen administered 81% vs ifosfamide-containing chemotherapy regimens
      Source quote
      • Carboplatin plus paclitaxel doublet therapy was the most common chemotherapy regimen administered (81%) followed by ifosfamide containing chemotherapy regimens (12%).
  • chemotherapeutic combinations: Various trials of chemotherapeutic combinations have reported differing response rates. [220]
  • chemotherapy: Adjuvant (after surgery)Chemotherapy is reported across retrospective cohorts, meta-analyses, and reviews as an adjuvant or relapse treatment for uterine carcinosarcoma, with some studies or meta-analyses reporting associations with improved progression-free survival and 5-year overall survival and other series finding no significant survival benefit. [241][3][242][104][89][93][131][21][217][24][53][36][35][243][142][83]16 sources
    5-year recurrence-free survival 67.6% (95% CI 55.3–82.5), p=0.08 vs no adjuvant chemotherapy5-year overall survival 78.1% (95% CI 66.8–91.5), p=0.07 vs no adjuvant chemotherapymPFS with combination chemotherapy 6.7 months (95% CI 5.1–8.5), p < 0.001 vs monotherapymPFS with monotherapy 2.2 months (95% CI 1.9–2.9), p < 0.001 vs combination chemotherapyPFS, chemotherapy-treated vs untreated 0.91 (95% CI 0.69–1.19), p = 0.4809 vs untreated patientsPFS, adjuvant chemotherapy vs no adjuvant chemotherapy in stage IA 0.44 (95% CI 0.2–0.95), p = 0.0310 vs no adjuvant chemotherapyOS, adjuvant chemotherapy vs no adjuvant chemotherapy in stage IA 0.32 (95% CI 0.11–0.91), p = 0.0249 vs no adjuvant chemotherapymPFS at first relapse, UCS 4.1 months (95% CI 3.1–5.2)PFS HR with postoperative chemotherapy in aged ≥80 group 0.44, p=0.021 vs no postoperative chemotherapyCSS HR with postoperative chemotherapy in aged ≥80 group 0.55, p=0.13 vs no postoperative chemotherapy
    Source quotes
    • 5-year RFS was 67.6% (95% CI, 55.3–82.5%) in those who received adjuvant chemotherapy and 51.7% (95% CI, 35.1–76.0%) in those who did not receive adjuvant chemotherapy (P=0.08, Figure 2C).
    • Similarly, 5-year OS was higher in those who received adjuvant chemotherapy compared to those who did not receive adjuvant chemotherapy, 78.1% (95% CI, 66.8–91.5%) vs 61.0% (95% CI, 45.0–82.5%), respectively (P=0.07, Figure 2D).
    • mPFS with a combination of chemotherapy was 6.7 months (95% CI 5.1–8.5) versus 2.2 months (95% CI 1.9–2.9) with monotherapy, p < 0.001.
    • mPFS with a combination of chemotherapy was 6.7 months (95% CI 5.1–8.5) versus 2.2 months (95% CI 1.9–2.9) with monotherapy, p < 0.001.
    • there was no significant difference in PFS between chemotherapy-treated (n = 161) and untreated patients (n = 140) (mPFS 15.6 months (95% CI 13.1–18.3) and 14.0 months (95% CI 10.9–17.8), respectively; HR 0.91 (0.69–1.19) p = 0.4809, logrank test)
    • median PFS for patients treated with adjuvant chemotherapy (n = 24) was not reached (NR) (95% CI 22.2–NR), while mPFS for patients who did not receive adjuvant chemotherapy (n = 62) was 19.9 months ((95% IC 13.9–72.9), HR 0.44 (0.20–0.95) p = 0.0310, logrank test)
    • with a hazard ratio of 0.32 (0.11–0.91) for patients with chemotherapy, p = 0.0249, logrank test
    • The median PFS (mPFS) at the first relapse was 4.2 months (95% CI 3.5–5.3); 4.8 months (95% CI 2.8–8.5) in OCS and 4.1 months (95% CI 3.1–5.2) in UCS, respectively.
    • Postoperative chemotherapy was associated with improved PFS in the aged ≥80 group (HR 0.44, P = 0.021) and also improved CSS in the aged ≥80 group but did not demonstrate statistical significance (HR 0.55, P = 0.13).
    • Postoperative chemotherapy was associated with improved PFS in the aged ≥80 group (HR 0.44, P = 0.021) and also improved CSS in the aged ≥80 group but did not demonstrate statistical significance (HR 0.55, P = 0.13).
  • cisplatin · 2 findings
    • Adjuvant (after surgery)A report describes switching from carboplatin to cisplatin after hypersensitivity in recurrent uterine carcinosarcoma. [10][54][238]3 sources
    • Adjuvant (after surgery)One review reports cisplatin/ifosfamide, ifosfamide/paclitaxel, and paclitaxel/carboplatin have been used as adjuvant treatment options and notes that an effective targeted therapy has not been found. [219]
  • doxorubicin: Recurrent or later-lineDoxorubicin is among the major chemotherapy regimens reported for uterine carcinosarcoma and has been used historically in first-line therapy for advanced or recurrent endometrial cancer; a study on doxorubicin and gemcitabine resistance in uterine carcinosarcoma was retracted and is not considered a reliable source. [7][244][78][245][99][100]6 sources
    use among adjuvant therapy regimens 11 vs other regimens
    Source quote
    • The major CT regimens comprised paclitaxel-carboplatin (n=30), ifosfamide-cisplatin (n=9), doxorubicin (n=11), and others (n=4).
  • ifosfamide · 2 findings
    • A Cochrane review found that ifosfamide-based combination chemotherapy reduced the risk of death and progression compared with single-agent ifosfamide; other studies reported subtype-specific associations (e.g., ifosfamide with improved PFS in low‑grade/homologous disease), and trials have combined ifosfamide with cisplatin or paclitaxel with noted toxicities. [138][99][109][94][131][26][21][206][237][205]10 sources
      cell death in DMSO-treated cultures 10.539% vs DMSO-treated culturescell death in gemcitabine-treated cultures 34% vs DMSO-treated culturesifosfamide-containing chemotherapy regimens 12% vs carboplatin plus paclitaxel doublet therapyifosfamide-based combination use 2.6%
      Source quotes
      • Of the six drugs used, gemcitabine induced the most cell death, increasing cell death from 10.539% in DMSO-treated to 34% in gemcitabine-treated cultures ( Figures 7B vs. 7E ).
      • Of the six drugs used, gemcitabine induced the most cell death, increasing cell death from 10.539% in DMSO-treated to 34% in gemcitabine-treated cultures ( Figures 7B vs. 7E ).
      • Carboplatin plus paclitaxel doublet therapy was the most common chemotherapy regimen administered (81%) followed by ifosfamide containing chemotherapy regimens (12%).
      • Only 7 patients (2.6%) received a combination based on ifosfamide.
    • Recurrent or later-lineIfosfamide has been studied either alone or combined with paclitaxel as first-line therapy for stage III/IV persistent or recurrent uterine carcinosarcoma. [132]
      overall survival hazard ratio 0.69 (95% CI 0.49–0.97), p=0.03 vs ifosfamide aloneprogression hazard ratio 0.71 (95% CI 0.51–0.97), p=0.03 vs ifosfamide alone
      Source quotes
      • That group demonstrated a 31 % decrease in the risk of death (hazard ratio [HR] 0.69; 95 % confidence interval [CI] 0.49 60.97; P = 0.03) and a 29 % decrease in the risk of progression (HR 0.71; 95 % CI 0.51 60.97; P = 0.03), favoring the combination arm. Nevertheless, toxicity was also increased with combination therapy [7].
      • That group demonstrated a 31 % decrease in the risk of death (hazard ratio [HR] 0.69; 95 % confidence interval [CI] 0.49 60.97; P = 0.03) and a 29 % decrease in the risk of progression (HR 0.71; 95 % CI 0.51 60.97; P = 0.03), favoring the combination arm. Nevertheless, toxicity was also increased with combination therapy [7].
  • paclitaxel · 5 findings
    • Adjuvant (after surgery)One molecular classification study suggested that uterine carcinosarcoma subtypes may differ in their response to paclitaxel. [109][246][37][132]4 sources
      overall survival hazard ratio 0.69 (95% CI 0.49–0.97), p=0.03 vs ifosfamide aloneprogression hazard ratio 0.71 (95% CI 0.51–0.97), p=0.03 vs ifosfamide alone
      Source quotes
      • That group demonstrated a 31 % decrease in the risk of death (hazard ratio [HR] 0.69; 95 % confidence interval [CI] 0.49 60.97; P = 0.03) and a 29 % decrease in the risk of progression (HR 0.71; 95 % CI 0.51 60.97; P = 0.03), favoring the combination arm. Nevertheless, toxicity was also increased with combination therapy [7].
      • That group demonstrated a 31 % decrease in the risk of death (hazard ratio [HR] 0.69; 95 % confidence interval [CI] 0.49 60.97; P = 0.03) and a 29 % decrease in the risk of progression (HR 0.71; 95 % CI 0.51 60.97; P = 0.03), favoring the combination arm. Nevertheless, toxicity was also increased with combination therapy [7].
    • Paclitaxel and ifosfamide was used as an active regimen and served as the comparator arm in randomized phase III trials (including GOG‑0261), where it was compared with paclitaxel/carboplatin. [233][131][97][77]4 sources
      median OS 37 months vs paclitaxel and ifosfamide regimensmedian OS 29 months vs paclitaxel and carboplatin regimens
      Source quotes
      • "paclitaxel and carboplatin regimens were not inferior to paclitaxel and ifosfamide regimens, with a median OS of 37 vs. 29 months."
      • "paclitaxel and carboplatin regimens were not inferior to paclitaxel and ifosfamide regimens, with a median OS of 37 vs. 29 months."
    • Recurrent or later-linePaclitaxel and carboplatin was not inferior to paclitaxel and ifosfamide in a randomized phase III trial, was highlighted as contributing valuable information toward treatment strategy for uterine carcinosarcoma, and was described as standard-of-care first-line chemotherapy for metastatic or recurrent disease in one source. [233][27][154]3 sources
      median overall survival 37 months, p < .01 for noninferiority, P > .1 for superiority vs paclitaxel and ifosfamidemedian progression-free survival 16 months, p < 0.01 for noninferiority, P < .01 for superiority vs paclitaxel and ifosfamide
      Source quotes
      • The median OS was 37 versus 29 months (HR = 0.87; 90% CI, 0.70 to 1.075; P < .01 for noninferiority, P > .1 for superiority).
      • The median progression-free survival was 16 versus 12 months (HR = 0.73; P = < 0.01 for noninferiority, P < .01 for superiority).
    • Recurrent or later-linePaclitaxel and platinum regimens were frequently used as salvage therapy and, in a retrospective cohort, were reported with a median PFS of 23.1 months and median OS of 28.7 months compared with 4.9 and 9.5 months for ifosfamide‑platinum. [109][14]
      median PFS 23.1 months, p = 0.04 vs ifosfamide-platinummedian OS 28.7 months, p = 0.06 vs ifosfamide-platinum
      Source quotes
      • The median PFS was 4.9 months, ranging from 3.8 months to 36.5 months in patients treated with IP, and 23.1 months, ranging from 9.3 months to 121 months in patients treated with PP, with statistically significant difference (p = 0.04).
      • The median OS was 9.5 months (ranging from 3.8 months to 36.5 months) and 28.7 months (ranging from 10.3 months to 121 months) in patients treated with IP and PP, respectively (Fig. 3).
    • Adjuvant (after surgery)The triplet paclitaxel–ifosfamide–cisplatin (TIP) has been studied as an adjuvant regimen; in a retrospective study five‑year DFS and OS did not differ significantly between TIP and paclitaxel–carboplatin, with a reported trend toward DFS benefit in advanced stage III but higher rates of grade 3–4 toxicities with TIP. [4]
      5-year DFS 38.2%, p=0.118 vs paclitaxel plus carboplatin5-year overall survival 49%, p=0.306 vs paclitaxel plus carboplatingrade 3/4 toxicities TIP 54.5%, p=0.012 vs paclitaxel plus carboplatin
      Source quotes
      • Five-year DFS and overall survival for TIP versus PC was 38.2% versus 35.9% (P = 0.118) and 49% versus 50.3% (P = 0.306), respectively
      • Five-year DFS and overall survival for TIP versus PC was 38.2% versus 35.9% (P = 0.118) and 49% versus 50.3% (P = 0.306), respectively
      • Grade 3 and 4 toxicities were seen in 54.5% patients of TIP chemotherapy group and in 13.3% patients of the PC chemotherapy (P = 0.012)
  • palliative chemotherapy: Palliative chemotherapy is reported as the treatment of choice in the metastatic setting. [16]
  • platinum: Adjuvant (after surgery)Platinum agents were commonly used postoperatively in elderly cohorts; analyses report platinum as an independent predictor for improved PFS in high‑grade/homologous disease, while studies in low‑grade carcinoma did not show an effect on PFS. [206][21]
  • postoperative chemotherapy: Adjuvant (after surgery)Sources report that postoperative chemotherapy was associated with improved progression-free survival in women aged ≥80 with uterine carcinosarcoma and, on multivariate analysis in a larger cohort, was an independent predictor for improved PFS. [21][206]
  • taxane/platinum doublet: Recurrent or later-lineIn retrospective analyses a taxane/platinum doublet as first‑line salvage therapy was associated with improved survival after recurrence compared with non‑taxane/platinum regimens, though reviews note no clinical trial has demonstrated superiority of a taxane/platinum regimen over others. [54]
    overall response rates 54%overall response rates 67%2-year SAR rate 55.5%, p < 0.001 vs non-taxane/platinum regimens2-year SAR rate 34.8%, p < 0.001 vs taxane/platinum doubletmedian SAR time 72.4 months, p < 0.001 vs non-taxane/platinum regimensmedian SAR time 12 months, p < 0.001 vs taxane/platinum doublet
    Source quotes
    • A combination regimen of paclitaxel with carboplatin has been reported to be effective for women with uterine carcinosarcoma in multiple clinical trials, with overall response rates ranging from 54% to 67%.
    • A combination regimen of paclitaxel with carboplatin has been reported to be effective for women with uterine carcinosarcoma in multiple clinical trials, with overall response rates ranging from 54% to 67%.
    • women who received a taxane/platinum doublet had superior SAR compared to women who received non-taxane/ platinum regimens (2-year SAR rate 55.5% versus 34.8%, median SAR time 72.4 versus 12.0 months, HR 0.49, 95% CI 0.32 to 0.75, P < 0.001; Fig. 1A).
    • women who received a taxane/platinum doublet had superior SAR compared to women who received non-taxane/ platinum regimens (2-year SAR rate 55.5% versus 34.8%, median SAR time 72.4 versus 12.0 months, HR 0.49, 95% CI 0.32 to 0.75, P < 0.001; Fig. 1A).
    • women who received a taxane/platinum doublet had superior SAR compared to women who received non-taxane/ platinum regimens (2-year SAR rate 55.5% versus 34.8%, median SAR time 72.4 versus 12.0 months, HR 0.49, 95% CI 0.32 to 0.75, P < 0.001; Fig. 1A).
    • women who received a taxane/platinum doublet had superior SAR compared to women who received non-taxane/ platinum regimens (2-year SAR rate 55.5% versus 34.8%, median SAR time 72.4 versus 12.0 months, HR 0.49, 95% CI 0.32 to 0.75, P < 0.001; Fig. 1A).
  • topotecan: Recurrent or later-lineTopotecan has been used as a therapy in patients with recurrent disease. [132]
  • trabectedin · 2 findings
    • Recurrent or later-lineIn a phase II trial of recurrent ovarian or uterine carcinosarcomas after up to two prior chemotherapy lines, trabectedin (1.3 mg/m2 every three weeks) produced an objective response rate of 11.9%, median PFS of 2.01 months, and median OS of 4.64 months. [247]
      objective response rate 11.9%median progression-free survival 2.01 months (95% CI 1.78–2.3)median overall survival 4.64 months (95% CI 3.19–8.29)
      Source quotes
      • The ORR was 11.9% (90% CI: 6-23) and included two patients with a complete response and three with a partial response.
      • Median progression-free survival was 2.01 months (95% CI: 1.78-2.30) and median overall survival was 4.64 months (95% CI: 3.19-8.29).
      • Median progression-free survival was 2.01 months (95% CI: 1.78-2.30) and median overall survival was 4.64 months (95% CI: 3.19-8.29).
    • Trabectedin was associated with grade 3 to 5 neutrophil count decreases and transaminase increases, with two patients dying due to trabectedin-related grade 5 hematological toxicity, and a review notes it did not meet prespecified activity criteria. [247]
Show 1 lab & early-research entry
  • adriamycin (doxorubicin): Adriamycin (doxorubicin) was included with cisplatin in a chemotherapy regimen in a reported case after carboplatin hypersensitivity. [238]

Targeted therapy

  • adavosertib: Recurrent or later-lineIn a small phase II trial of TP53-mutated recurrent or persistent UCS (n=9), adavosertib monotherapy produced 2 partial responses (ORR 22.2%) with median PFS 2.7 months; treatment-related adverse events occurred in 8 of 9 patients, most commonly diarrhea and fatigue. [69]
    partial response rate 22.2% (95% CI 2.8–60) vs all enrolled patientsmedian progression-free survival 2.7 months vs all enrolled patientstreatment-related adverse events 88.9% vs all treated patientsgrade 3 or higher diarrhea 33.3% vs all treated patientsgrade 3 or higher fatigue 22.2% vs all treated patients
    Source quotes
    • 2 patients (22.2 %; 95 % CI 2.8–60 %) had a partial response (1 confirmed and 1 unconfirmed).
    • Median PFS was 2.7 months (95 % CI 0.9 to not reached).
    • Treatment-related AEs (TRAEs) occurred in 8 (88.9 %) patients.
    • The most common Grade 3 or higher TRAEs included diarrhea (33.3 %), fatigue (22.2 %), anemia (22.2 %), and platelet count decreased (22.2 %).
    • The most common Grade 3 or higher TRAEs included diarrhea (33.3 %), fatigue (22.2 %), anemia (22.2 %), and platelet count decreased (22.2 %).
  • anti-VEGF / anti-PD-ECGF / anti-PDGFR-β therapy: Recurrent or later-lineA review states that combination anti-VEGF and anti-PD-ECGF or anti-PDGFR-β therapy would be expected in advanced or recurrent uterine carcinosarcoma. [187]
  • aurora kinase inhibitors: Aurora kinase inhibitors are proposed as a prospective therapeutic option for uterine carcinosarcoma. [29]
  • ceralasertib: Ceralasertib monotherapy showed confirmed objective responses in an ARID1A-deficient solid-tumor phase II study (responses occurred in endometrioid endometrial carcinoma or ovarian clear-cell carcinoma rather than uterine carcinosarcoma) and was given at 160 mg twice daily on days 1 to 14 every 28 days in the reported study. [165]
    confirmed objective response rate 14%
    Source quote
    • The confirmed objective response rate (ORR) was 14% among the 29 efficacy-evaluable patients.
  • chemotherapeutic agents with molecular-targeted agents: The emergence of combinations of chemotherapeutic agents with molecular-targeted agents was noted as a potentially promising approach. [220]
  • COX-2: COX-2 has been examined as a potential therapeutic target, but one study found no significant association with stage, grade, depth of myometrial invasion, lymphovascular involvement, or survival. [157]
  • fascin: Fascin has been identified as a possible target for future therapies. [185]
  • Folate receptor alpha: biomarker-selectedFolate receptor alpha has been described as a potential therapeutic target in gynecologic carcinosarcoma. [196]
  • histone deacetylase inhibitors (HDACi): Histone deacetylase inhibitors (HDACi) have been identified as a promising approach that may target epigenetics and EMT in uterine carcinosarcoma. [201]
  • lenvatinib and pembrolizumab: Recurrent or later-lineSources describe lenvatinib plus pembrolizumab as an effective treatment for advanced or recurrent endometrial cancer, with a multicenter observational cohort (including uterine carcinosarcoma cases) evaluating outcomes after prior platinum-based chemotherapy. [78][69][248][9]4 sources
    Overall median progression-free survival 3 months
    Source quote
    • The overall median progression-free survival was 3.0 months
  • SLC1A5: SLC1A5 expression is reported to be increased in uterine carcinosarcoma and a mutation was associated with poor prognosis, leading authors to discuss SLC1A5 as a potential therapeutic target. [177]
  • trastuzumab: Recurrent or later-line · biomarker-selectedSources report that adding trastuzumab to carboplatin–paclitaxel was associated with longer overall survival versus chemotherapy alone in HER2-positive uterine serous carcinoma and carcinosarcoma, and reviews note a randomized trial demonstrating trastuzumab efficacy in uterine serous carcinoma with potential benefit in carcinosarcoma; reported adverse events included increased rates of hypertension, diarrhea, and left ventricular systolic dysfunction. [69][79][72][124][249][105][221][118][250][18][199][43]12 sources
    median overall survival 41 months, p=0.002 vs carboplatin and paclitaxelmedian overall survival 41.7 months, p < 0.0001 vs carboplatin and paclitaxeloverall survival hazard ratio 0.39 (95% CI 0.221–0.56), p < 0.0001 vs carboplatin and paclitaxelmedian overall survival 38.7 months, p=0.04 vs carboplatin and paclitaxeloverall survival hazard ratio 0.56 (95% CI 0.294–0.869), p=0.04 vs carboplatin and paclitaxelhypertension incidence 25%, p=0.002 vs carboplatin and paclitaxeldiarrhoea incidence 9%, p=0.007 vs carboplatin and paclitaxelmedian PFS 8 months vs carboplatin-paclitaxel-trastuzumab vs carboplatin-paclitaxelHR for PFS 0.44 (95% CI 0.26–0.76), p=0.005 vs carboplatin-paclitaxel-trastuzumab vs carboplatin-paclitaxelmedian OS 24.4 months, p=0.041 vs trastuzumab vs controlHR for OS 0.49 (95% CI 0.25–0.97), p=0.041 vs trastuzumab vs controlobjective response rate 54.5% vs IHC 1+ scoresobjective response rate 70% vs IHC scores of at least 2+overall response rate 54.5% vs HER2-low groupoverall response rate 70% vs HER2-high groupORR HER2-high 54.5% (95% CI 32.2–75.6) vs HER2-low cohortORR HER2-low 70% (95% CI 45.1–86.1) vs HER2-high cohortdisease control rate 100% vs HER2-high vs HER2-low cohorts
    Source quotes
    • The median OS times were significantly different between the CP (25.2 months) and CP + T groups (41 months) (hazard ratio [HR]: 0.51, 95% confidence interval [CI] 0.345–0.784, p = 0.002) (Fig. 1).
    • This resulted in a notable contrast in the median OS time between the CP (16.8 months) and the CP + T groups (41.7 months) for uterine carcinosarcoma, with an HR of 0.39 (95% CI 0.221–0.560, p < 0.0001) (Fig. 2).
    • This resulted in a notable contrast in the median OS time between the CP (16.8 months) and the CP + T groups (41.7 months) for uterine carcinosarcoma, with an HR of 0.39 (95% CI 0.221–0.560, p < 0.0001) (Fig. 2).
    • Within the uterine serous carcinoma subgroup, the median OS time significantly differed between the CP (27.1 months) and the CP + T groups (38.7 months), with an HR of 0.56 (95% CI 0.294–0.869, p = 0.04) (Fig. 3).
    • Within the uterine serous carcinoma subgroup, the median OS time significantly differed between the CP (27.1 months) and the CP + T groups (38.7 months), with an HR of 0.56 (95% CI 0.294–0.869, p = 0.04) (Fig. 3).
    • the CP + T group had a higher incidence of hypertension (8% vs. 25%, p = 0.002), diarrhoea (3% vs. 9%, p = 0.007), and left ventricular systolic dysfunction (2% vs. 9%, p < 0.001) than those of the CP group (Table 2).
    • the CP + T group had a higher incidence of hypertension (8% vs. 25%, p = 0.002), diarrhoea (3% vs. 9%, p = 0.007), and left ventricular systolic dysfunction (2% vs. 9%, p < 0.001) than those of the CP group (Table 2).
    • They reported a median PFS of 8.0 months for the control arm, versus 12.6 months (p = 0.005; HR 0.44; 90% CI, 0.26 to 0.76).
    • They reported a median PFS of 8.0 months for the control arm, versus 12.6 months (p = 0.005; HR 0.44; 90% CI, 0.26 to 0.76).
    • median survival of 24.4 months in the control arm vs. not reached in the trastuzumab arm (HR 0.49; 90% CI, 0.25–0.97; p = 0.041).
    • median survival of 24.4 months in the control arm vs. not reached in the trastuzumab arm (HR 0.49; 90% CI, 0.25–0.97; p = 0.041).
    • the STATICE trial demonstrated that T-DXd has efficacy in uterine serous carcinoma, with an objective response rate of 54.5% in cases with IHC scores of at least 2+ and 70% in cases with IHC 1+ scores.
    • the STATICE trial demonstrated that T-DXd has efficacy in uterine serous carcinoma, with an objective response rate of 54.5% in cases with IHC scores of at least 2+ and 70% in cases with IHC 1+ scores.
    • The ORR was 54.5% for the HER2-high group and 70% for the HER2-low group
    • The ORR was 54.5% for the HER2-high group and 70% for the HER2-low group
    • The authors report an overall response rate (ORR) of 54.5% (95% CI, 32.2 to 75.6) in the HER2-high cohort, and 70% (95%CI 45.1 to 86.1) in the HER2-low group.
    • The authors report an overall response rate (ORR) of 54.5% (95% CI, 32.2 to 75.6) in the HER2-high cohort, and 70% (95%CI 45.1 to 86.1) in the HER2-low group.
    • Both groups demonstrated a 100% disease control rate.
  • VEGF: VEGF has been examined as a potential therapeutic target in uterine carcinosarcoma, and one study concluded that the results warrant further study of anti-angiogenic agents. [155]
Show 17 lab & early-research entries
  • adagrasib: Adagrasib was included among combinations with apoptosis pathway targeted agents in a spheroid model that included uterine carcinosarcoma cell lines. [215]
  • alrizomadlin: Alrizomadlin was evaluated in a spheroid model that included uterine carcinosarcoma cell lines alongside pelcitoclax and dasminapant. [215]
  • avutometinib: Avutometinib, combined with FAK inhibition or VS-4718, showed promising in vitro and in vivo anti-tumor activity and superior tumor growth inhibition and longer survival than single agents in xenograft models. [251]
  • cobimetinib: Cobimetinib was included among combinations with apoptosis pathway targeted agents in a spheroid model that included uterine carcinosarcoma cell lines. [215]
  • copanlisib: Copanlisib was included among combinations with apoptosis pathway targeted agents in a spheroid model that included uterine carcinosarcoma cell lines. [215]
  • galunisertib: In UCS models, the TGFβR1 inhibitor galunisertib reduced viability, invasion, clonal growth and differentiation, and sensitized cells to chemotherapy in vitro and in an in vivo preclinical model. [26]
    Median survival, CT treated group 16 vs vehicleTumor doubling time, vehicle 1.9 vs CT treated groupTumor doubling time, CT treated group 3.4 vs vehicle
    Source quotes
    • In the CT treated group median survival was 16 days whereas, more than 50% of the mice survived beyond 20 days in the GLT+CT treated group
    • Compared to the vehicle (TDT= ~1.9 days) or CT (TDT= ~3.4 days) treated group
    • Compared to the vehicle (TDT= ~1.9 days) or CT (TDT= ~3.4 days) treated group
  • HER2: biomarker-selectedHER2 (ERBB2) has been examined as a potential therapeutic target in uterine carcinosarcoma: reports describe variable prevalence of overexpression and amplification (e.g., 3 of 48 with strong IHC expression and 7 of 48 with amplification), evidence of overexpression in cell and tissue studies, high concordance between gastric and breast IHC scoring algorithms with some discordance, and inter-organoid heterogeneity in HER2 expression and sensitivity to HER2 inhibitors. [155][203][167][197][17][252][43][253]8 sources
    HER-2 expression in epithelial component 6%HER2 overexpression 29.2%concordance HER2-positive 95% vs breast criteria vs gastric criteriaconcordance HER2-negative 88% vs breast criteria vs gastric criteriastrong HER2 IHC expression 6% vs all UCS casesHER2 amplification by chromogenic in situ hybridization 15% vs all UCS cases
    Source quotes
    • In the epithelial component, expression of HER-2, VEGF, c-KIT, COX-2, and EGFR were detected in 2 (6%), 30 (100%), 0 (0%), 21 (70%), and 9 (30%) cases, respectively
    • HER2 overexpression in seven of 24 CS cases (29.2%), tested by immunohistochemistry.
    • Concordance between scoring algorithms was high for HER2-positive (95 %) and HER2-negative (88 %) cases.
    • Concordance between scoring algorithms was high for HER2-positive (95 %) and HER2-negative (88 %) cases.
    • Three of 48 UCS (6%) had strong (3+) HER2 IHC expression, and 3 cases (6%) were equivocal (2+).
    • Seven cases (15%) had HER2 amplification by chromogenic in situ hybridization, including all 3 with overexpression and 2 that were equivocal by IHC.
  • LY2109761: In uterine carcinosarcoma cell lines, TGFβR-I and TGFβR-I/II inhibitors attenuated TGFβ-I–induced Smad2/3 phosphorylation, migration, and EMT; notably, the TGFβR-I/II inhibitor enhanced proliferation in the absence of exogenous TGFβ. [32]
  • LY2157299: A TGFβ receptor I inhibitor attenuated TGFβ-I–induced Smad2/3 phosphorylation and migration and blocked TGFβ-I–induced c-Myc expression and proliferation in uterine carcinosarcoma cell lines. [32]
  • MRTX1133: MRTX1133 was included among combinations with apoptosis-pathway–targeted agents in a spheroid model that included uterine carcinosarcoma cell lines. [215]
  • olaparib: Maintenance · biomarker-selectedOlaparib was reported among prior therapies received by some patients and was described as used for PARP inhibitor maintenance in a cohort, and in preclinical carcinosarcoma models olaparib was more active in HRD-signature-3 models than in HRP models both in vitro and in vivo. [69][249][163]3 sources
    Overall median progression-free survival 3 monthsmean IC50 in HRD vs HRP cell lines 2.94, p=0.02 vs HRP cell lines
    Source quotes
    • The overall median progression-free survival was 3.0 months
    • [mean IC50 ± SEM = 2.94 μM ± 0.07 vs mean ± SEM = 23.3 μM ± 0.09, (p = 0.02), respectively].
  • PARP inhibitors: biomarker-selectedPARP inhibitors were reported to suppress carcinosarcoma cell growth through G2/M arrest and to cause more apoptosis in HRD than HRP primary tumors. [163]
    mean IC50 in HRD vs HRP cell lines 2.94, p=0.02 vs HRP cell lines
    Source quote
    • [mean IC50 ± SEM = 2.94 μM ± 0.07 vs mean ± SEM = 23.3 μM ± 0.09, (p = 0.02), respectively].
  • pazopanib: Recurrent or later-lineA case report described off-label pazopanib for recurrent uterine carcinosarcoma with FGFR1 amplification, recommended by a tumor board, and it was reported effective, maintaining quality of life for a period. [26][84][132]3 sources
    lung metastasis size reduction on day 26 28%
    Source quote
    • A 28% reduction in the size of lung metastases was observed on day 26 of treatment, and the reduction was maintained thereafter (Fig. 1).
  • sacituzumab govitecan: Recurrent or later-lineSacituzumab govitecan (a TROP2 antibody-drug conjugate) was studied in uterine carcinosarcoma organoids and in two patient-derived xenograft models, where it reduced tumor volume. [153][221]
  • SYK: Subtype I tumors were reported to overexpress SYK and the review noted SYK-specific inhibitors as potential agents for that subtype. [28]
  • trastuzumab deruxtecan: Recurrent or later-line · biomarker-selectedTrastuzumab deruxtecan showed clinical activity in previously treated patients with advanced or recurrent uterine carcinosarcoma regardless of HER2 status in the STATICE trial (with reported objective responses), caused marked tumor shrinkage in patient-derived xenografts, demonstrated preclinical antitumor activity including bystander killing, and was associated with grade ≥3 adverse events in 61% of patients with pneumonitis/interstitial lung disease observed (including grade 3 events); a complete response in a single HER2-positive stage IVB uterine carcinosarcoma case has also been reported. [102][92][254][199]4 sources
    overall response rate, HER2-high group by central review 54.5% (95% CI 32.2–75.6)overall response rate, HER2-high group by investigator assessment 68.2% (95% CI 45.1–86.1)overall response rate, HER2-low group by central review 70% (95% CI 34.8–93.3)overall response rate, HER2-low group by investigator assessment 60% (95% CI 26.2–87.8)median duration of response, HER2-high group 6.9 months (95% CI 4.1–12.6)median duration of response, HER2-low group 8.1 months, p not reached [NR]median progression-free survival, entire efficacy cohort 6.7 months (95% CI 5.4–8.8)grade ≥3 adverse events 61% vs treated patientstumor shrinkage in PDXs 67%objective response 39%median PFS 4.3 months
    Source quotes
    • In the HER2-high group (n = 22), the ORR by central review (primary end point) was 54.5% (95% CI, 32.2 to 75.6).
    • The ORR was 68.2% (95% CI, 45.1 to 86.1) in the HER2-high group (n = 22) by investigator assessment.
    • The ORRs in the HER2-low group in an exploratory analysis were 70.0% (95% CI, 34.8 to 93.3) by central review (n = 10) and 60.0% (95% CI, 26.2 to 87.8) by investigator assessment (n = 10).
    • The ORRs in the HER2-low group in an exploratory analysis were 70.0% (95% CI, 34.8 to 93.3) by central review (n = 10) and 60.0% (95% CI, 26.2 to 87.8) by investigator assessment (n = 10).
    • The median DoRs was 6.9 months (95% CI, 4.1 to 12.6) in the HER2-high group (n = 22) and 8.1 months (95% CI, 2.8 to not reached [NR]) in the HER2-low group (n = 10).
    • The median DoRs was 6.9 months (95% CI, 4.1 to 12.6) in the HER2-high group (n = 22) and 8.1 months (95% CI, 2.8 to not reached [NR]) in the HER2-low group (n = 10).
    • The median PFS was 6.7 months (95% CI, 5.4 to 8.8) in the entire efficacy cohort (n = 32)
    • Grade ≥ 3 AEs occurred in 20 patients (61%), with the most common being decreased neutrophil count (nine [27%]), anemia (eight [24%]), and decreased lymphocyte count (seven [21%] patients).
    • Remarkable tumor shrinkage after T-DXd administration was observed in four of the six PDXs (67%), comparable with the response rate (70%) of HER2 1+ patients in the STATICE trial.
    • Of the 13 patients with endometrial cancer, 5 showed an objective response (39%), with a median PFS of 4.3 months.
    • Of the 13 patients with endometrial cancer, 5 showed an objective response (39%), with a median PFS of 4.3 months.
  • PTC-028: Preclinical UCS models (CS99 cell line) reported that the BMI1 inhibitor PTC-028 increased apoptosis, decreased cell viability in vitro, and delayed tumor growth in vivo. [192]

Immunotherapy

  • dostarlimab: MaintenanceA stage IVB uterine carcinosarcoma patient developed neurologic symptoms while on maintenance dostarlimab, which was subsequently omitted from treatment. [255]
  • IL-13Rα2-targeted CAR macrophages: iPSC-derived IL-13Rα2-targeted CAR macrophages were studied in uterine carcinosarcoma specimens and in solid tumor models. [256]
  • lenvatinib plus pembrolizumab: In a series of five uterine carcinosarcoma patients treated with lenvatinib plus pembrolizumab, the overall response rate was 40% (2 partial responses, 1 stable disease, 2 progressive), no grade ≥3 adverse events were reported, and median PFS and OS were 9.1 and 10.2 months, respectively. [191]
    overall response rate 40%median progression-free survival 9.1 monthsmedian overall survival 10.2 monthsresponse rate in cited report 25%
    Source quotes
    • “The overall response rate (ORR) was 40 %, with a partial response (PR) in two, stable disease (SD) in one, and PD in two patients”
    • “the median PFS was 9.1 (0.16 to NA) months, and the median OS was 10.2 (1.41 to NA) months”
    • “the median PFS was 9.1 (0.16 to NA) months, and the median OS was 10.2 (1.41 to NA) months”
    • “Another had response and clinical benefit rates of 25 % (3 out of 12) and 58.3 % (7 out of 12), respectively”
  • PD-L1: PD-L1 was studied as a biomarker related to checkpoint inhibitor therapies in uterine carcinosarcoma. [152]
  • pembrolizumab · 2 findings
    • Pembrolizumab was reported in institutional, literature-derived, and real-world uterine carcinosarcoma cases—sometimes combined with lenvatinib or given with radiotherapy—with outcomes ranging from progression to partial or complete responses and disease control in some cases, and in one real-world series an objective response rate of 37.5% and a disease control rate of 67.5%. [64][136][72][77][109][128][47][9]8 sources
      Objective response rate 37.5%Disease control rate 67.5%
      Source quotes
      • Objective response rate (ORR) was 37.5 % and disease control rate (DCR) was 67.5 %
      • Objective response rate (ORR) was 37.5 % and disease control rate (DCR) was 67.5 %
    • Recurrent or later-lineIn a retrospective single-institution series of seven patients with advanced or recurrent uterine carcinosarcoma treated in the recurrent or later-line setting, pembrolizumab plus lenvatinib produced no complete or partial responses and had a median progression-free survival of 2.6 months and median overall survival of 2.8 months. [230]
      median progression-free survival (pembrolizumab + lenvatinib) 2.6 months (95% CI 0.9–11.2)median overall survival (pembrolizumab + lenvatinib) 2.8 months
      Source quotes
      • PFS was 2.6 months (95% CI, 0.9–11.2 months) with 6-month progression free survival of 28.6% (95% CI, 0.0, 62.0).
      • Furthermore, OS was 2.8 months (95% CI, 2.4-NE) with 6-month overall survival of 42.9% (6.2, 79.5)
  • PRAME: PRAME was reported as a potential immunotherapeutic target in uterine carcinosarcoma. [170]

Hormonal therapy

  • anastrozole: Anastrozole was evaluated in an ER/PR-positive uterine carcinosarcoma cohort in a single-arm phase 2 trial, in which the 3-month clinical benefit rate was 43%, no objective responses were observed, and median progression-free survival was 2.7 months; a review also notes this single-arm study. [257][77]
    3-month clinical benefit rate 43% (95% CI 16–75)median progression-free survival 2.7 months (95% CI 1.1–8.2)clinical benefit rate at 3 months 43% vs none statedduration of clinical benefit 5.6 months vs none statedmedian PFS 2.7 months vs none stated
    Source quotes
    • For the UCS cohort CBR at 3 months was 43% (95% CI: 16-75%)
    • The median progression-free survival was 2.7 months (95% CI, 1.1-8.2).
    • "At 3 months, CBR was 43%, and the duration of clinical benefit was 5.6 months; median PFS was 2.7 months."
    • "At 3 months, CBR was 43%, and the duration of clinical benefit was 5.6 months; median PFS was 2.7 months."
    • "At 3 months, CBR was 43%, and the duration of clinical benefit was 5.6 months; median PFS was 2.7 months."
  • tamoxifen · 2 findings
    • Tamoxifen exposure was studied in uterine carcinosarcoma with one study reporting no association with progression-free or disease-specific survival, another reporting less deep myometrial invasion in tamoxifen-related cases, and a review mentioning tamoxifen as a possible inducer of carcinogenesis in some patients. [63][62][18]3 sources
    • Adjuvant (after surgery)Reports describe uterine carcinosarcomas occurring under or after adjuvant tamoxifen exposure and suggest a possible causal role for prolonged tamoxifen. [134][135]

Radiotherapy

  • chemoradiation: Adjuvant (after surgery)Adjuvant chemoradiation has been reported in systematic reviews and retrospective series with trends or associations toward improved disease control, progression-free survival, and overall survival, although selection bias and non-randomized treatment allocation were noted as limitations. [258][259][225][243]4 sources
    HR for adjuvant chemoradiation and OS 0.1, p all p < 0.001 vs adjuvant chemotherapy or other modeled comparators
    Source quote
    • adjuvant chemoradiation was consistently selected as an independent prognostic factor for OS (hazard ratio [HR] 0.10-0.22, all p < 0.001) and PFS (HR 0.12-0.23, all p < 0.001)
  • concurrent chemoradiotherapy: Adjuvant (after surgery)Concurrent chemoradiotherapy has been reported as an adjuvant approach and in one retrospective series was described as possibly improving local control and delaying recurrence but showing little survival advantage. [104]
  • cuff brachytherapy: Adjuvant (after surgery)Cuff brachytherapy was included as an adjuvant option in an early-stage cohort alongside other modalities such as pelvic radiation and chemotherapy. [24]
  • external beam irradiation / vaginal brachytherapy / systemic chemotherapy: External beam irradiation or vaginal brachytherapy together with systemic chemotherapy have been described as part of multimodal therapy after complete surgical staging. [34]
  • external beam pelvic radiation therapy and HDR brachytherapy: External beam pelvic radiation therapy and HDR brachytherapy were used in one cohort. [116]
  • external beam radiotherapy and chemotherapy: A combination of external beam radiotherapy and chemotherapy was reported as used in a retrospective cohort. [11]
    adjuvant radiotherapy proportion 42.8% vs no adjuvant radiotherapy
    Source quote
    • Adjuvant radiotherapy was subsequently performed in 24 patients (42.8%).
  • external radiotherapy: In a population-based analysis, external radiotherapy alone did not show a survival improvement for patients who did not undergo lymphadenectomy and for those with lymph node metastasis. [260]
  • pelvic external beam radiotherapy: Adjuvant (after surgery)Pelvic external beam radiotherapy was used in cohorts (reported delivered at 4500-5040 cGy in 25-28 fractions in one series), and in one retrospective cohort adjuvant chemotherapy plus pelvic external beam radiotherapy was associated with improved progression-free survival compared with radiotherapy alone. [261][217]
    3-year PFS 78.7%, p=0.01 vs RT alone
    Source quote
    • For the CT + EBRT, CT + VBT, and RT-alone groups, median follow up was 93.5, 50.2, and 143.0 months, and 3-year PFS was 78.7 %, 67.6 %, and 58.2 %, respectively.
  • pelvic radiation: Adjuvant (after surgery)Adjuvant pelvic radiation has been reported to decrease the risk of pelvic recurrence and to possibly delay distant recurrence in early-stage and primary advanced disease in a review. [72]
  • radiation: Adjuvant (after surgery)Radiation has been studied in uterine carcinosarcoma but the ideal adjuvant treatment remains unknown. [57]
  • radiation and chemotherapy: Combined radiation and chemotherapy was associated with longer median survival than single treatment or no treatment in one study. [56]
    median survival with combined radiation and chemotherapy 2043, p =0.0016 vs single treatment or no treatmentmedian survival with single treatment 597, p =0.0016 vs combined radiation and chemotherapymedian survival with no treatment 317, p =0.0016 vs combined radiation and chemotherapy
    Source quotes
    • Combined radiation and chemotherapy improved patient survival (median survival=2043 days) compared to single (median survival=597 days) or no treatment (median survival=317 days, P=0.0016).
    • Combined radiation and chemotherapy improved patient survival (median survival=2043 days) compared to single (median survival=597 days) or no treatment (median survival=317 days, P=0.0016).
    • Combined radiation and chemotherapy improved patient survival (median survival=2043 days) compared to single (median survival=597 days) or no treatment (median survival=317 days, P=0.0016).
  • radiochemotherapy: Adjuvant (after surgery)Adjuvant radiochemotherapy was related to overall survival in a retrospective cohort. [53]
  • radiotherapy: Adjuvant (after surgery)Radiotherapy has been reported widely as an adjuvant or palliative modality in uterine carcinosarcoma cohorts and studies, with some retrospective studies and reviews reporting associations with improved progression-free or overall survival and other reviews or meta-analyses reporting no survival benefit. [241][138][14][242][227][66][262][261][100][99][89][104][108][85][87][93][131][226][128][21][53][36][35][220][263]
    Contradicting evidence: Some sources report that adjuvant radiotherapy is associated with improved progression-free or overall survival, whereas other reviews and meta-analyses report no survival benefit. (the more authoritative source is [241]).
    25 sources
    3-year PFS 78.7%, p=0.01 vs RT alonemean OS with adjuvant radiotherapy 39.9 months (95% CI 30.9–48.8), p =0.044 vs those who did notmean OS without adjuvant radiotherapy 26.6 months (95% CI 19.6–33.6), p =0.044 vs patients receiving adjuvant radiotherapyadjuvant radiotherapy proportion 42.8% vs no adjuvant radiotherapyMedian OS with RT vs without RT 41 months vs without RTMedian OS with RT vs without RT after IPTW adjustment 46 months vs without RTPFS HR with postoperative radiotherapy in aged ≥80 group 0.41, p=0.06 vs no postoperative radiotherapyCSS HR with postoperative radiotherapy in aged ≥80 group 0.29, p=0.044 vs no postoperative radiotherapymedian time to development of abscopal effect 2 monthsmedian duration of abscopal effect 6 months (95% CI 0.7–14)median progression-free survival 2.7 months vs all enrolled patients
    Source quotes
    • For the CT + EBRT, CT + VBT, and RT-alone groups, median follow up was 93.5, 50.2, and 143.0 months, and 3-year PFS was 78.7 %, 67.6 %, and 58.2 %, respectively.
    • Kaplan-Meier analysis demonstrated significantly longer OS in patients receiving adjuvant radiotherapy compared to those who did not (mean OS: 39.9 months, 95%CI=30.9-48.8 vs. 26.6 months, 95%CI=19.6-33.6; log-rank p=0.044).
    • Kaplan-Meier analysis demonstrated significantly longer OS in patients receiving adjuvant radiotherapy compared to those who did not (mean OS: 39.9 months, 95%CI=30.9-48.8 vs. 26.6 months, 95%CI=19.6-33.6; log-rank p=0.044).
    • Adjuvant radiotherapy was subsequently performed in 24 patients (42.8%).
    • On UVA, RT improved median and 5-year OS from 41 to 87 months and 43-55%, respectively (HR 0.65, 95% CI 0.56-0.77) (p < 0.001).
    • After IPTW adjustment, RT improved median and 5-year OS from 46 to 65 months and 46-53%, respectively (HR 0.74, 95% CI 0.63-0.87) (p < 0.001).
    • There was a trend towards an improvement in PFS with postoperative radiotherapy in the aged ≥80 group (HR 0.41, P = 0.06) and a significant benefit for CSS (HR 0.29, P = 0.044).
    • There was a trend towards an improvement in PFS with postoperative radiotherapy in the aged ≥80 group (HR 0.41, P = 0.06) and a significant benefit for CSS (HR 0.29, P = 0.044).
    • The median time to the development of the abscopal effect and its duration were reported 2 (0-24 months) and 6 months (0.7-14 months), respectively [8].
    • The median time to the development of the abscopal effect and its duration were reported 2 (0-24 months) and 6 months (0.7-14 months), respectively [8].
    • Median PFS was 2.7 months (95 % CI 0.9 to not reached).
  • stereotactic radiosurgery: For solitary CNS metastases from uterine carcinosarcoma, surgical resection or stereotactic radiosurgery followed by whole brain radiotherapy has been described among treatment options. [49]
  • vaginal brachytherapy: Adjuvant (after surgery)Postoperative vaginal brachytherapy was used in retrospective series of UCS; in one early-stage cohort, CT+EBRT improved PFS versus RT alone, while CT+VBT showed similar time to progression as RT alone. [3][261][86][45]4 sources
    3-year PFS 67.6%, p=0.22 vs RT aloneVBT use 15.8% vs ovarian carcinosarcoma
    Source quotes
    • For the CT + EBRT, CT + VBT, and RT-alone groups, median follow up was 93.5, 50.2, and 143.0 months, and 3-year PFS was 78.7 %, 67.6 %, and 58.2 %, respectively.
    • Vaginal brachytherapy (VBT) was performed more frequently for carcinosarcoma, other than ovarian carcinosarcoma (uterus, 15.8%; cervix, 14.3%).
  • whole brain radiotherapy: Whole brain radiotherapy has been used following surgical resection or stereotactic radiosurgery for CNS metastases from uterine carcinosarcoma. [49]
  • whole-pelvic irradiation: Recurrent or later-lineWhole-pelvic irradiation added to surgery in a small series of stage I-II uterine carcinosarcoma showed a trend toward fewer pelvic recurrences but no difference in distant recurrence or survival. [264]
    2-year Kaplan-Meier survival estimate with whole-pelvic irradiation 79%, p=0.84 vs surgery alone
    Source quote
    • There was also no difference in the 2- and 5-year Kaplan-Meier survival estimates for the patients receiving WPI (79 and 59%, respectively) compared to those who did not receive WPI (60 and 60%, respectively) (P = 0.84).
Show 1 lab & early-research entry
  • gamma knife radiation: Gamma knife radiation was administered to brain lesions in one reported case. [221]
    adjuvant radiotherapy proportion 42.8% vs no adjuvant radiotherapy
    Source quote
    • Adjuvant radiotherapy was subsequently performed in 24 patients (42.8%).

Procedures & devices

  • adjuvant multimodal treatment: Adjuvant (after surgery)A systematic review of FIGO I-II UCS reported a trend toward improved disease control and survival with adjuvant multimodal treatment, although statistical significance was often not reached. [258]
  • aspiration thrombectomy: Aspiration thrombectomy was reported for a UCS tumor thrombus extending into the inferior vena cava and right atrium. [265]
  • fine-needle aspiration (aspiration cytology): Recurrent or later-lineFine-needle aspiration (aspiration cytology) has been used to diagnose recurrent uterine carcinosarcoma in clinically suspicious lesions. [51]
  • lymphadenectomy: Lymphadenectomy (general) has been associated with improved overall survival in a retrospective cohort and has been reported to prolong survival even for early-stage disease. [53][220]
  • minimally invasive surgery: Minimally invasive surgery and open surgery had similar disease-free survival and overall survival in patients with high-risk endometrial cancer, including uterine carcinosarcoma, in a reported series. [266]
  • para-aortic lymphadenectomy: In one elderly cohort, para-aortic lymphadenectomy was not associated with survival in women aged 80 years or older. [21]
    PFS HR with para-aortic lymphadenectomy in aged ≥80 group 1.22, p=0.61 vs no para-aortic lymphadenectomyCSS HR with para-aortic lymphadenectomy in aged ≥80 group 1.3, p=0.53 vs no para-aortic lymphadenectomyPFS HR with pelvic lymphadenectomy in aged ≥80 group 0.82, p=0.5 vs no pelvic lymphadenectomyCSS HR with pelvic lymphadenectomy in aged ≥80 group 0.91, p=0.77 vs no pelvic lymphadenectomy
    Source quotes
    • In the aged ≥80 group, para-aortic lymphadenectomy was not associated with survival (PFS, HR 1.22, P = 0.61; and CSS, HR 1.30, P = 0.53) whereas this procedure was associated with improved survival in other two groups (HR ranges: PFS 0.71 and CSS 0.56–0.65).
    • In the aged ≥80 group, para-aortic lymphadenectomy was not associated with survival (PFS, HR 1.22, P = 0.61; and CSS, HR 1.30, P = 0.53) whereas this procedure was associated with improved survival in other two groups (HR ranges: PFS 0.71 and CSS 0.56–0.65).
    • In the aged ≥80 group, pelvic lymphadenectomy was not associated with survival (PFS, HR 0.82, P = 0.50, Fig. 1A; and CSS, HR 0.91, P = 0.77).
    • In the aged ≥80 group, pelvic lymphadenectomy was not associated with survival (PFS, HR 0.82, P = 0.50, Fig. 1A; and CSS, HR 0.91, P = 0.77).
  • partial (subtotal) surgical resection: Partial (subtotal) surgical resection has been reported to improve or resolve tumor-related hypoglycemia when complete resection is not possible. [267]
  • pelvic lymphadenectomy: In one elderly cohort, pelvic lymphadenectomy was not associated with survival in women aged 80 years or older but was associated with improved survival in younger groups. [21]
    PFS HR with para-aortic lymphadenectomy in aged ≥80 group 1.22, p=0.61 vs no para-aortic lymphadenectomyCSS HR with para-aortic lymphadenectomy in aged ≥80 group 1.3, p=0.53 vs no para-aortic lymphadenectomyPFS HR with pelvic lymphadenectomy in aged ≥80 group 0.82, p=0.5 vs no pelvic lymphadenectomyCSS HR with pelvic lymphadenectomy in aged ≥80 group 0.91, p=0.77 vs no pelvic lymphadenectomy
    Source quotes
    • In the aged ≥80 group, para-aortic lymphadenectomy was not associated with survival (PFS, HR 1.22, P = 0.61; and CSS, HR 1.30, P = 0.53) whereas this procedure was associated with improved survival in other two groups (HR ranges: PFS 0.71 and CSS 0.56–0.65).
    • In the aged ≥80 group, para-aortic lymphadenectomy was not associated with survival (PFS, HR 1.22, P = 0.61; and CSS, HR 1.30, P = 0.53) whereas this procedure was associated with improved survival in other two groups (HR ranges: PFS 0.71 and CSS 0.56–0.65).
    • In the aged ≥80 group, pelvic lymphadenectomy was not associated with survival (PFS, HR 0.82, P = 0.50, Fig. 1A; and CSS, HR 0.91, P = 0.77).
    • In the aged ≥80 group, pelvic lymphadenectomy was not associated with survival (PFS, HR 0.82, P = 0.50, Fig. 1A; and CSS, HR 0.91, P = 0.77).
  • sentinel lymph node biopsy: Sentinel lymph node biopsy alone was feasible in patients with uterine carcinosarcoma and did not show a difference in progression-free survival or overall survival compared with systematic lymphadenectomy in one retrospective study. [94]
  • sequence-based diagnostics: Sequence-based diagnostics have been proposed to direct patients with uterine carcinosarcoma to targeted therapy. [30]
  • surgery: First-line (advanced disease)Surgery is described as part of the initial management framework and as the primary treatment approach for uterine carcinosarcoma in multiple guideline and cohort sources. [122][242][118][22][21][220]6 sources
    PFS HR with para-aortic lymphadenectomy in aged ≥80 group 1.22, p=0.61 vs no para-aortic lymphadenectomyCSS HR with para-aortic lymphadenectomy in aged ≥80 group 1.3, p=0.53 vs no para-aortic lymphadenectomyPFS HR with pelvic lymphadenectomy in aged ≥80 group 0.82, p=0.5 vs no pelvic lymphadenectomyCSS HR with pelvic lymphadenectomy in aged ≥80 group 0.91, p=0.77 vs no pelvic lymphadenectomy
    Source quotes
    • In the aged ≥80 group, para-aortic lymphadenectomy was not associated with survival (PFS, HR 1.22, P = 0.61; and CSS, HR 1.30, P = 0.53) whereas this procedure was associated with improved survival in other two groups (HR ranges: PFS 0.71 and CSS 0.56–0.65).
    • In the aged ≥80 group, para-aortic lymphadenectomy was not associated with survival (PFS, HR 1.22, P = 0.61; and CSS, HR 1.30, P = 0.53) whereas this procedure was associated with improved survival in other two groups (HR ranges: PFS 0.71 and CSS 0.56–0.65).
    • In the aged ≥80 group, pelvic lymphadenectomy was not associated with survival (PFS, HR 0.82, P = 0.50, Fig. 1A; and CSS, HR 0.91, P = 0.77).
    • In the aged ≥80 group, pelvic lymphadenectomy was not associated with survival (PFS, HR 0.82, P = 0.50, Fig. 1A; and CSS, HR 0.91, P = 0.77).
  • surgery (hysterectomy / cytoreduction): Surgical cytoreduction (including hysterectomy and omentectomy) is described as the primary procedural approach for uterine carcinosarcoma and is used for staging and initial treatment. [46]
  • surgical resection / debulking: Surgical debulking or resection is often used for uterine carcinosarcoma and may resolve paraneoplastic hypoglycemia when the tumor is the cause. [267]
  • 18F-FDG PET/CT: 18F‑FDG PET/CT showed superior diagnostic accuracy versus MRI for pelvic and para‑aortic nodal metastases and facilitated identification of distant metastasis in uterine carcinosarcoma. [268]
    sensitivity for pelvic LN areas (FDG PET/CT) 63.2%, p = 0.016 vs MRI
    Source quote
    • The sensitivity, specificity, and accuracy of FDG PET/CT versus MRI were as follows: 63.2% (12/19) versus 26.3% (5/19), 100% (35/35) versus 100% (35/35), and 87.0% versus 74.0%, respectively, for pelvic LN areas (p = 0.016);
  • MRI (including DWI and MRS): Magnetic resonance imaging (MRI) including diffusion-weighted imaging and MR spectroscopy has been described to show characteristic features in UCS such as relatively high mean ADC, low choline concentration, and frequent high lipid peak. [269]
    incidence of high lipid peak in carcinosarcomas on MRS 91% vs endometrial carcinomas (24%)
    Source quote
    • High lipid peak was observed in 91% of carcinosarcomas and in 24% of endometrial carcinomas.
  • Transvaginal sonography (TVS): Transvaginal sonography (TVS) has been reported to demonstrate lesion characteristics that can indicate the presence of UCS and assist clinical decision‑making. [140]
Show 4 lab & early-research entries
  • hysterectomy with bilateral salpingo-oophorectomy and lymphadenectomy: A case report describes a patient who underwent total laparoscopic hysterectomy with bilateral salpingo-oophorectomy, infra-colic omentectomy, and pelvic lymphadenectomy for stage IA uterine carcinosarcoma. [229]
  • modified radical hysterectomy: A case report described a modified radical hysterectomy with bilateral pelvic lymphadenectomy and omentectomy for cytoreduction. [239]
  • subtotal hysterectomy and left salpingo-oophorectomy: One case report describes subtotal hysterectomy and left salpingo-oophorectomy performed for bowel obstruction associated with a migrated intrauterine device. [10]
  • total abdominal hysterectomy with bilateral salpingo-oophorectomy: Total abdominal hysterectomy with bilateral salpingo-oophorectomy has been performed for uterine carcinosarcoma in reported cases. [50]

Other

  • ?: Adjuvant (after surgery)Multiple retrospective analyses reported stage-related differences in recurrence and survival and associations of chemoradiation or postoperative radiotherapy with improved progression-free or overall survival in certain subgroups, with stage III disease deriving the greatest survival benefit from chemoradiation. An organoid study showed heterogeneity in sensitivity to cytotoxic agents, and an analysis proposed alternative splicing factors as potential drug targets and prognostic biomarkers. [259][224][5][69][245][252][88][104][253][196][89][177][85][87][109][234][25][17][217][54][81][83]22 sources
    recurrence frequency stage I 64%, p <0.001 vs stage II, stage III, and stage IVmedian progression-free survival 15 months vs chemotherapy alonemedian overall survival 26 months vs chemotherapy alonepostoperative radiotherapy and PFS 0.49, p all, P < 0.05 vs no postoperative radiotherapypostoperative radiotherapy and CSS 0.37, p all, P < 0.05 vs no postoperative radiotherapyadding radiotherapy to chemotherapy and PFS 0.49, p all, P < 0.05 vs chemotherapy aloneadding radiotherapy to chemotherapy and CSS 0.36, p all, P < 0.05 vs chemotherapy aloneno adjuvant therapy 43.7% vs radiotherapy only / chemotherapy only / chemoradiation groupsradiotherapy only 24.8% vs no adjuvant therapy / chemotherapy only / chemoradiation groupschemotherapy only 19.7% vs no adjuvant therapy / radiotherapy only / chemoradiation groups
    Source quotes
    • Stage I disease recurred less frequently (64%) versus stage II (83%), stage III (85%), and stage IV (90%) (p<0.001).
    • The median progression-free survival favored chemoradiation over chemotherapy (15 vs 11 months, respectively), as did the median overall survival (26 vs 20 months, respectively).
    • The median progression-free survival favored chemoradiation over chemotherapy (15 vs 11 months, respectively), as did the median overall survival (26 vs 20 months, respectively).
    • when tumors had SD, postoperative radiotherapy was significantly associated with improved PFS (adjusted-HR: 0.49 for homo/dominance, and 0.36 for hetero/dominance) and CSS (adjusted-HR: 0.37 for homo/dominance, and 0.35 for hetero/dominance) regardless of sarcoma types (all, P < 0.05; Table 4).
    • when tumors had SD, postoperative radiotherapy was significantly associated with improved PFS (adjusted-HR: 0.49 for homo/dominance, and 0.36 for hetero/dominance) and CSS (adjusted-HR: 0.37 for homo/dominance, and 0.35 for hetero/dominance) regardless of sarcoma types (all, P < 0.05; Table 4).
    • adding radiotherapy to chemotherapy was significantly associated with improved PFS (adjusted-HR: homo/dominance 0.49, and hetero/dominance 0.45) and CSS (adjusted-HR: 0.36 for homo/dominance, and 0.31 for hetero/dominance) compared to chemotherapy alone (all, P < 0.05; Table 5);
    • adding radiotherapy to chemotherapy was significantly associated with improved PFS (adjusted-HR: homo/dominance 0.49, and hetero/dominance 0.45) and CSS (adjusted-HR: 0.36 for homo/dominance, and 0.31 for hetero/dominance) compared to chemotherapy alone (all, P < 0.05; Table 5);
    • 43.7% (n = 330) received no adjuvant therapy, 24.8% (n = 187) received RT only and 19.7% (n = 149) received chemo only.
    • 43.7% (n = 330) received no adjuvant therapy, 24.8% (n = 187) received RT only and 19.7% (n = 149) received chemo only.
    • 43.7% (n = 330) received no adjuvant therapy, 24.8% (n = 187) received RT only and 19.7% (n = 149) received chemo only.
  • adjuvant treatment: Adjuvant (after surgery)A 102-patient surgical series reported that adjuvant treatment was not found to affect recurrence or survival. [156]
  • chemoradiotherapy: In a population-based analysis, chemoradiotherapy showed a survival advantage over radiotherapy alone or chemotherapy alone in subgroup analyses. [260][227]
    mean PFS with combined chemoradiotherapy 39.1 months (95% CI 25.9–52.2), p =0.02 vs radiotherapy alonemean PFS with radiotherapy alone 21.2 months (95% CI 7.7–34.6), p =0.02 vs combined chemoradiotherapy
    Source quotes
    • PFS was significantly improved in patients treated with combined chemoradiotherapy compared to radiotherapy alone (mean PFS: 39.1 months, 95%CI=25.9-52.2 vs. 21.2 months, 95%CI=7.7-34.6; Breslow p=0.02).
    • PFS was significantly improved in patients treated with combined chemoradiotherapy compared to radiotherapy alone (mean PFS: 39.1 months, 95%CI=25.9-52.2 vs. 21.2 months, 95%CI=7.7-34.6; Breslow p=0.02).
  • combined chemo-radiotherapeutic approach: A review reported that a combined chemo-radiotherapeutic approach has shown a survival benefit. [220]
  • heterologous component: Recurrent or later-linePresence of a heterologous component was associated with worse overall survival but not clearly associated with recurrence-free or disease-free survival in a review. [202]
    overall survival 1.81 (95% CI 1.15–2.85), p=0.017 vs homologous componentrecurrence-free survival / disease-free survival 1.79 (95% CI 0.85–3.77), p=0.186 vs homologous component
    Source quotes
    • For carcinosarcomas of the uterus and ovary, the presence of a heterologous component was associated with worse OS (HR=1.81; 95% CI=1.15–2.85; p=0.017) (Fig. 2A).
    • In contrast, pooled analysis of RFS and DFS revealed that the presence of a heterologous component was not associated with prognosis (HR=1.79; 95% CI=0.85–3.77; p=0.186) (Fig. 2B).
  • MSI/MMRd: biomarker-selectedMSI/MMRd UCS showed better progression-free survival than TP53mut/p53abn cases in a meta-analysis, while overall survival was not significantly different. [1]
    progression-free survival vs TP53mut/p53abn 0.19 (95% CI 0.08–0.46), p < 0.001 vs TP53mut/p53abn casesoverall survival vs TP53mut/p53abn 0.91 (95% CI 0.44–1.87), p = 0.788 vs TP53mut/p53abn casesoverall survival vs TP53mut/p53abn 1.51 (95% CI 0.76–2.99), p = 0.240 vs TP53mut/p53abn cases
    Source quotes
    • In UCS, MSI/MMRd cases showed significantly better PFS than TP53mut/p53abn cases, with an HR of 0.19 (95% confidence interval [CI] 0.08–0.46; P < 0.001), but no significant difference was found between NSMP and TP53mut/p53abn cases (HR 1.02, 95% CI 0.59–1.78; P = 0.936).
    • In UCS, MSI/MMRd and NSMP cases showed similar OS to the TP53mut/p53abn cases, with HR of 0.91 (95% CI 0.44–1.87; P = 0.788) and 1.51 (95% CI 0.76–2.99; P = 0.240), respectively.
    • In UCS, MSI/MMRd and NSMP cases showed similar OS to the TP53mut/p53abn cases, with HR of 0.91 (95% CI 0.44–1.87; P = 0.788) and 1.51 (95% CI 0.76–2.99; P = 0.240), respectively.
  • NSMP: NSMP UCS showed no significant difference in progression-free survival or overall survival compared with TP53mut/p53abn cases. [1]
    progression-free survival vs TP53mut/p53abn 0.19 (95% CI 0.08–0.46), p < 0.001 vs TP53mut/p53abn casesoverall survival vs TP53mut/p53abn 0.91 (95% CI 0.44–1.87), p = 0.788 vs TP53mut/p53abn casesoverall survival vs TP53mut/p53abn 1.51 (95% CI 0.76–2.99), p = 0.240 vs TP53mut/p53abn cases
    Source quotes
    • In UCS, MSI/MMRd cases showed significantly better PFS than TP53mut/p53abn cases, with an HR of 0.19 (95% confidence interval [CI] 0.08–0.46; P < 0.001), but no significant difference was found between NSMP and TP53mut/p53abn cases (HR 1.02, 95% CI 0.59–1.78; P = 0.936).
    • In UCS, MSI/MMRd and NSMP cases showed similar OS to the TP53mut/p53abn cases, with HR of 0.91 (95% CI 0.44–1.87; P = 0.788) and 1.51 (95% CI 0.76–2.99; P = 0.240), respectively.
    • In UCS, MSI/MMRd and NSMP cases showed similar OS to the TP53mut/p53abn cases, with HR of 0.91 (95% CI 0.44–1.87; P = 0.788) and 1.51 (95% CI 0.76–2.99; P = 0.240), respectively.
  • POLEmut: Recurrent or later-linePOLEmut UCS had no recurrences or deaths in the meta-analysis. [1]
    progression-free survival vs TP53mut/p53abn 0.19 (95% CI 0.08–0.46), p < 0.001 vs TP53mut/p53abn casesoverall survival vs TP53mut/p53abn 0.91 (95% CI 0.44–1.87), p = 0.788 vs TP53mut/p53abn casesoverall survival vs TP53mut/p53abn 1.51 (95% CI 0.76–2.99), p = 0.240 vs TP53mut/p53abn cases
    Source quotes
    • In UCS, MSI/MMRd cases showed significantly better PFS than TP53mut/p53abn cases, with an HR of 0.19 (95% confidence interval [CI] 0.08–0.46; P < 0.001), but no significant difference was found between NSMP and TP53mut/p53abn cases (HR 1.02, 95% CI 0.59–1.78; P = 0.936).
    • In UCS, MSI/MMRd and NSMP cases showed similar OS to the TP53mut/p53abn cases, with HR of 0.91 (95% CI 0.44–1.87; P = 0.788) and 1.51 (95% CI 0.76–2.99; P = 0.240), respectively.
    • In UCS, MSI/MMRd and NSMP cases showed similar OS to the TP53mut/p53abn cases, with HR of 0.91 (95% CI 0.44–1.87; P = 0.788) and 1.51 (95% CI 0.76–2.99; P = 0.240), respectively.
  • radiotherapy and chemotherapy: Adjuvant (after surgery)In a population-based analysis, radiotherapy and chemotherapy were associated with improved cancer-specific survival and overall survival in UCS without distant metastasis after surgery. [260]
  • URI1 amplification: Adjuvant (after surgery)URI1 amplification was associated with poor response to adjuvant treatment in one study. [56]
Show 1 lab & early-research entry
  • NUCB2: NUCB2 knockout reduced cell proliferation and migration in endometrial carcinoma cells, whereas NUCB2 overexpression had the opposite effect. [175]
Staging & risk28 points

Key figures

Survival & outcomes
OutcomeValue95% CI
upstage shifts17
Advanced/recurrent disease mortality within two years80%
FIGO stage IA at diagnosis67%
MRI staging accuracy rate70%
Source quotes
  • A total of 17 upstage shifts (37.7%) occurred between the 2009 and 2023 FIGO staging system.
  • 80% of patients with advanced/recurrent disease succumb within two years.
  • The majority of patients were FIGO stage IA (67%) at diagnosis.
  • MRI has a 70% staging accuracy rate [15].
  • Sources indicate that some studies used FIGO staging (e.g., FIGO 2009), and TNM stages were also referenced in analyses. [74][76][97][98][100][107][108][85][109][254][222][93]12 sources
  • Multiple retrospective studies identified stage as an independent prognostic factor in uterine carcinosarcoma: advanced FIGO stages III–IV were associated with worse overall and disease‑free survival, and FIGO stage was an independent factor for overall survival in a nomogram study. [98][240][107][100][103][85][87]7 sources
  • Uterine carcinosarcoma is staged using the 2009 International Federation of Gynecology and Obstetrics (FIGO) system and is categorized with endometrial carcinomas rather than as another uterine sarcoma. [21][54][218][220][117][111]6 sources
  • Uterine carcinosarcoma shares the same FIGO staging system as endometrial carcinoma. [1][7][70][12][78]5 sources
  • Reviews note that uterine carcinosarcoma commonly presents with extrauterine or distant disease at diagnosis. [111][26][36][35]4 sources
  • Guidelines include an algorithm for treatment of uterine carcinosarcoma. [122][270]
  • FDG PET/CT showed superior diagnostic accuracy compared to MRI for detecting pelvic and para‑aortic lymph node metastasis in uterine carcinosarcoma. [268]
  • Among clinically stage I patients in one study, 54.2% were upstaged to FIGO stages II–IVB after primary surgery; 35.9% were upstaged to stage IIIC1 and 25% to stage IVB. [72]
  • Lymph node ratio (LNR) was a significant predictor of progression-free survival and overall survival in univariate analysis but was not an independent predictor; LNR showed a moderately significant correlation with FIGO status and a weak association with lymphovascular space invasion (LVSI). [98]
  • In a cohort analysis, median survival was 33 months for stage 1 disease versus 6 months for stage 4 disease. [271]
  • On MRI, uterine carcinosarcoma often shows larger tumor dimensions, cystic degeneration or necrosis, hemorrhage, and heterogeneous T2 signal compared with endometrioid adenocarcinoma; in one study a combined model of ADCmax, REAmax, and REVmax had an AUC of 0.997 for distinguishing uterine carcinosarcoma from endometrioid adenocarcinoma. [101]
  • The American Radium Society guideline states that the majority of patients with uterine carcinosarcoma present with advanced extrauterine disease, and 10% present with metastatic disease. [22]
  • On MRI, carcinosarcomas show relatively high mean ADC compared with higher‑grade endometrial carcinomas, a lower choline concentration than endometrial carcinomas, and frequently a high lipid peak. [269]
  • In a POLE-mutated series, most tumors were stage IA or IB by FIGO 2009 clinical staging. [15]
  • Stage IV disease was independently associated with increased risk of venous thromboembolism in one study. [6]
  • Positive peritoneal cytology is associated with poor prognosis in uterine carcinosarcoma, comparable to current FIGO stage IIIA classification of disease. [231]
  • MRI is useful in preoperative detection and staging; MRI features such as tumor localization, irregular or nodular margins, necrosis, rapid growth, intense contrast enhancement, and diffusion restriction can suggest the diagnosis and help differentiate uterine carcinosarcoma from leiomyomas and endometrial carcinoma. [121]
  • Some studies included patients who had undergone a staging operation. [29]
  • Higher stage was associated with increased fascin expression in one study. [185]
  • A stage IA uterine carcinosarcoma was reported in a case demonstrated with robotic-assisted comprehensive staging. [272]
  • One multicenter retrospective analysis reported a stage distribution of 24.3% stage I, 12.2% stage II, 37.2% stage III, and 26.3% stage IV (FIGO). [224][67][11][69]4 sources
  • Higher FIGO stage was associated with worse survival; stage I–II patients tended to have better 5‑year OS/DFS than stage III in one cohort. [24][93][217]3 sources
  • Some series classified patients as early FIGO stage I–II versus advanced FIGO stage III–IV; in at least one retrospective series late stage was associated with a higher risk of death. [87][254][109]3 sources
  • In the same cohort analysis, up to 50% of patients were identified with early-stage disease (stage 1/2), suggesting higher rates of early detection in that series. [271]
  • In one early-stage cohort, most patients were FIGO stage IA at diagnosis. [24]
  • Uterine carcinosarcoma was included in many retrospective uterine sarcoma studies because it had been classified as a uterine sarcoma during much of the study period. [93]
  • In one retrospective cohort, stage III disease occurred in 53.4% of patients and stage IV disease occurred in 7.9%. [273]
Show 1 lab & early-research finding
  • Reported case staging included pT1b, pNx, pMx (FIGO Stage 1B). [37][50][44]3 sources
Prognosis69 points

Key figures

Survival & outcomes
OutcomeValue95% CI
recurrent tumors40–60%
median survival after diagnosis16–40 months
recurrence within 5 years after surgery29.9%
Deaths during follow-up47.6%
median overall survival20 months
median survival14 months
5-year disease-free survival30%
5-year disease-free survival13%
event-free survival40%
overall survival48.5%
5-year overall survival19.7%10.6–30.8
5-year progression-free survival17.3%8.9–27.9
5-year cancer-specific survival9.8%
5-year survival after recurrence7.6%
median survival after recurrence3.9 months
three-year PFS rate62.9%
three-year OS rate72.1%
median overall survival23 months
recurrence rate stage I/II37–46%
recurrence rate stage III/IV63–80%
median progression-free survival after second-line chemotherapy6.3 months
median overall survival after second-line chemotherapy12.9 months
Prognostic factors
FactorEffectHR (95% CI)p
tumor diameter >=100 mm, progression-free survival vs tumor diameter <100 mm▲ worse4.57 (1.59–13.19)=0.005
advanced vs early stage, overall survival▲ worse4.2 (2.09–8.44)< 0.001
incomplete cytoreduction, overall survival▲ worse4.02 (2.68–6.18)
residual disease R1/2 vs R0 vs R0▲ worse3.09 (1.34–7.08)=0.008
incomplete cytoreduction, disease-free survival▲ worse3 (1.67–5.37)
full staging, overall survival▼ better0.37 (0.18–0.78)=0.008
stage I/II vs III/IV vs advanced stages III/IV▼ better0.37 (0.16–0.84)=0.017
any other modality of treatment, overall survival▼ better0.48 (0.27–0.85)=0.012
Source quotes
  • the high rate of recurrent tumors (40–60%) and the low median survival rate of 16–40 months post-diagnosis
  • Recurrence within 5 years after surgery was documented in 29 (29.9%) patients
  • During the follow-up period, 20 (47.6%) patients died
  • Median overall survival was 20 months (range 1–99).
  • the total median survival was 14 months (range 5 – 22 months)
  • the 5-year disease-free survival decreases to 30% in patients with stage II and to 13% in those with stage III disease
  • The event-free survival at a median follow-up of 40 months was 40% and the overall survival was 48.5%.
  • Five-year overall survival was 19.7% (95%CI 10.6%-30.8%).
  • Five-year progression-free survival (taking both progression and death as event) was 17.3% (95%CI 8.9%-27.9%).
  • The 5-year CSS rate of these recurrent or persistent/progressive UCS patients was 9.8% (Figure 1a).
  • The 5-year SAR rate was 7.6%, with a median of 3.9 months (range: 0.1–168.2 months) (Figure 1b).
  • The three-year PFS rates were 62.9% (SE ±5.2) for SLN and 52.3 (SE ±5.3) for LND (P=0.13) (Figure 1).
  • The three-year OS rates were 72.1 (SE ±5.1) for SLN and 71.6 (SE ±4.6) for LND (Figure 2).
  • Prognosis is poor, with a median overall survival of 23 months;
  • UCS also has a high propensity for recurrence with rates of 37–46% for stage I/II disease and rates of 63–80% for stage III/IV disease.
  • median progression-free survival and overall survival were only 6.3 months and 12.9 months respectively.
  • In univariate analysis of PFS, only tumours with a diameter equal or more than 100mm (HR 4.57, p-value 0.005) were a significant factor for progression, but data were only available for 41 patients.
  • Advanced stage (HR 4.2, p-value < 0.001) was statistically significant associated with a higher risk of death.
  • incomplete cytoreduction (HR = 4.02; 95%CI = 2.68–6.18)
  • patients with residual disease after surgery (R1/2 versus R0; HR 3.09; 95% CI: 1.34–7.08; p = 0.008)
  • incomplete cytoreduction (HR = 3.00; 95%CI = 1.67–5.37)
  • receiving a full staging operation (HR 0.37, p-value 0.008) and receiving any other modality of treatment (HR 0.48, p-value 0.012) were associated with better survival
  • patients with early stages I/II had 63% lower risk of progression than advanced stages III/IV (Hazard ratio, HR 0.37; 95% CI: 0.16–0.84; p = 0.017).
  • receiving any other modality of treatment (HR 0.48, p-value 0.012) were associated with better survival
  • Across cohorts, sources report worse outcomes with advanced FIGO stage, extrauterine disease, larger tumors (e.g., size >4 cm or diameter ≥100 mm), deep myometrial invasion, lymphovascular space invasion, positive resection margins, residual tumor or incomplete cytoreduction, and heterologous mesenchymal components. [99][100][101][108][107][87][89][103]8 sources
  • Uterine carcinosarcoma is described as having a poor prognosis. [240][107][102][104][96][87][109]7 sources
  • Uterine carcinosarcoma has a poor prognosis and is described as a highly aggressive tumor. [50][139][274][47][205][230]6 sources
  • Reported medians include 2043 days with combined radiation and chemotherapy versus 597 days with a single modality and 317 days with no treatment in one series, and a median survival of 16 months in another study. [45][56][137][81][83]5 sources
  • Reported 5-year outcomes include overall survival of 33% in one single-institution series, and another study reported 5-year overall survival of 36.5% and progression-free survival of 33.8% across stage I–IV disease. [37][142][243][38][42]5 sources
  • Multiple reviews and studies describe uterine carcinosarcoma as having a poor prognosis and limited treatment options. [123][74][133][100][101]5 sources
  • FIGO stage was reported as an independent prognostic factor for disease-free and overall survival in one study. [156][25][94][21]4 sources
  • Reviews state that uterine carcinosarcoma is highly aggressive and has worse survival outcomes than endometrial cancer or uterine sarcoma; overall prognosis is described as poor compared with other endometrial carcinomas. [58][44][46][84]4 sources
  • Uterine carcinosarcoma is described as one of the most aggressive gynecologic tumors, is usually diagnosed at advanced stages, and is associated with poor prognosis. [202][203][13]3 sources
  • Uterine carcinosarcoma is described as carrying a poor prognosis due to potential for extra-uterine spread and a high risk of recurrence. [72][153][69]3 sources
  • Reported prognostic factors include: in one immunohistochemical study, stage was the only independent prognostic factor; in another study, older age and >50% myometrial invasion predicted worse overall survival, and myometrial invasion was associated with progression-free survival. [190][243][83]3 sources
  • Reported 5-year overall survival is approximately 50% in reviews, and one series reported 56%. [28][219][130]3 sources
  • Disease stage was reported as the most important prognostic factor in uterine carcinosarcoma. [85][86]
  • Reviews emphasize a high recurrence rate and poor overall survival, underscoring the need for UCS-specific clinical trials. [45][36]
  • One review reported a 5-year survival of 0% for stage IV uterine carcinosarcoma. [18][35]
  • In one early-stage cohort, median overall survival was 48.0 months. [24][106]
  • A small 1997 series of stage I–II uterine carcinosarcoma found that adding whole‑pelvic irradiation to surgery did not improve survival. [264][83]
  • In molecular analyses and series, POLEmut uterine carcinosarcoma had no recurrences or deaths in most patients (TCGA and a series where Ten of 11 POLE-mutated patients had no recurrences or death, although three of those had follow-up periods under one year and one patient with a subclonal POLE variant and stage IV disease died 1.4 months after surgery); TP53mut/p53abn and NSMP tumors had poor outcomes; MSI/MMRd tumors showed similar progression-free survival but worse overall survival than the corresponding 2013 TCGA cohort. [1][15]
  • In one study, the presence of a heterologous mesenchymal component had a significant effect on both overall survival and disease-free survival; median overall survival and disease-free survival were shorter in patients with a heterologous mesenchymal component than in those with a homologous component. [89]
  • Sources describe that cervical stromal involvement was independently associated with both disease-free and overall survival, while sarcomatous component type was independently related to recurrence only. [11]
  • In one cohort, CDX2-positive tumors were significantly associated with poorer progression-free and overall survival on multivariate analysis. [108]
  • In a multicenter series of FIGO 2009 stage IA uterine carcinosarcoma without myoinvasion, 29/97 patients recurred (mostly distant); 5‑year recurrence‑free survival was 63.5% and overall survival was 72.0%. [3]
  • In the same advanced-stage analysis, myometrial invasion greater than one-half and lymphadenopathy in both pelvic and para-aortic areas were associated with worse overall survival in univariate analysis. [14]
  • One retrospective series reported 5-year overall survival of 19.7% and 5-year progression-free survival of 17.3%. [87]
  • In one retrospective series, tumor diameter of at least 100 mm was associated with progression, full staging surgery was associated with better overall survival, and any other modality of treatment was associated with better overall survival. [87]
  • URI1 amplification was associated with worse tumor-free survival in one study; that study also reported URI1 amplification, weight, hypertension, and tumor stage as factors associated with poor survival. [56]
  • In one cohort, adjuvant chemotherapy was an independent prognostic factor for overall survival, and a nomogram for 3-year overall survival had a concordance probability of 0.72. [85]
  • In one surgically staged cohort of 69 patients, the 3-year overall survival rate was 41.8%. [85]
  • In one cohort the 3-year progression-free survival rate was 41% and the median progression-free survival was 23.2 months; stage IV disease was a statistically significant predictor of worsened progression-free survival compared with stage I/II. [55]
  • One cohort reported a median survival of "14 months" in a Saudi Arabian population. [68]
  • In an elderly cohort (women aged 80 years or older) tumors showed more high-grade carcinoma, heterologous sarcoma, and sarcoma dominance than in younger groups; in that cohort postoperative chemotherapy was associated with improved progression-free survival and postoperative radiotherapy showed a trend toward improved progression-free survival and a significant association with better cancer-specific survival. [21]
  • In a prospective cohort, the median overall survival was 20 months and the median progression-free survival was 13 months. [70]
  • In one retrospective cohort, median overall survival was 25.2 months with carboplatin and paclitaxel and 41 months with carboplatin and paclitaxel plus trastuzumab. [124]
  • A retrospective UCS cohort reported that high mesothelin expression was associated with longer overall survival; in both high- and low-MSLN groups, HER2 status did not affect overall survival. [97]
  • Disseminated recurrence was associated with poorer prognosis than isolated recurrence in a review of recurrent or persistent/progressive uterine carcinosarcoma. [109]
  • Increasing age at diagnosis and higher FIGO stage were associated with worse overall survival and recurrence-free survival on unadjusted analysis in one early-stage cohort; on multivariable analysis a rhabdomyosarcoma component and stage II disease (including stage IB and stage II for recurrence-free survival) were associated with worse outcomes. [24]
  • Lymph node metastasis was associated with poorer disease-free survival and overall survival in one retrospective cohort. [273]
  • Recurrent uterine carcinosarcoma tumors are common and median survival after diagnosis is described as low. [203]
  • One multicenter retrospective analysis reported median progression-free survival of 15 months with chemoradiation and 11 months with chemotherapy alone, and median overall survival of 26 months with chemoradiation and 20 months with chemotherapy alone. [224]
  • One review reported five-year disease-free survival of 38.2% with TIP and 35.9% with PC, and five-year overall survival of 49% with TIP and 50.3% with PC. [4]
  • In a real-world recurrent uterine carcinosarcoma series, median progression-free survival was 5 months and median overall survival was 14 months. [64]
  • In one retrospective series with median follow-up of 40 months, event-free survival was 40% and overall survival was 48.5%. [104]
  • In one series of 94 patients three-year disease-free survival and overall survival were 42.7% and 59.2%, respectively; in that series age was an independent prognostic factor for 3-year disease-free survival, older age was associated with poorer survival, and extrauterine spread was associated with survival. [218]
  • High pre-treatment absolute neutrophil count was reported as an independent poor prognostic factor for disease recurrence and mortality. [275]
  • One study reported no difference in overall survival between women with uterine and ovarian carcinosarcoma. [137]
  • Molecular-subtype differences in survival were reported: POLE mutant uterine carcinosarcoma had a median overall survival of "74.8 months" and significantly longer survival than other subtypes; TP53 mutant and TP53 wild-type uterine carcinosarcoma had worse median OS than their respective endometrioid endometrial cancer subtypes; and HER2-negative uterine carcinosarcoma had worse post-chemotherapy OS than HER2-negative endometrioid endometrial cancer. [144]
  • One study reported that HER2 expression and HER2 amplification were statistically significantly associated with worse overall survival. [76]
  • In a report of tamoxifen-associated cases, 80% of the reported patients had a dismal prognosis. [135]
  • High‑risk histologic endometrial carcinomas, a group that includes uterine carcinosarcoma, have poor outcomes with a reported 44% 5‑year all‑stage survival rate. [192]
  • In one retrospective matched analysis of early-stage tumors, five-year recurrence-free survival, disease-specific survival, and overall survival were similar between early-stage carcinosarcoma and uterine serous carcinoma; the same analysis found that lack of adjuvant combined modality therapy was an independent predictor of shorter recurrence-free survival and overall survival, lower uterine segment involvement was the only independent predictor of shorter disease-specific survival, and lack of lymph node dissection and lack of adjuvant combined modality therapy were independent predictors of shorter overall survival. [223]
  • In a large retrospective analysis, sarcoma-dominant patterns were associated with decreased progression-free survival and cause-specific survival and remained independent prognostic factors after multivariable adjustment. [5]
  • Venous thromboembolism was independently associated with decreased progression‑free survival after adjustment for patient, tumor, and treatment factors. [6]
  • Elevated neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-lymphocyte ratio (MLR) were associated with poorer progression-free survival, and a high NLR was associated with worse overall survival in uterine carcinosarcoma. [71]
  • In a pan-cancer analysis, LILRB4 was reported as protective in uterine carcinosarcoma. [169]
  • One review reported that HER2 discordance was associated with shorter overall survival. [178]
  • In one surgical series five-year disease-free survival was 34%. [130]
  • High expression of phospho-aurora kinase A and aurora kinase B was reported as a predictor of progression-free survival in one small study. [29]
  • Fascin expression was associated with a shorter progression-free interval in one study. [185]
  • A skull base metastasis from uterine carcinosarcoma was reported as extremely scarce. [80]
  • Uterine carcinosarcomas have been reported with an average 5-year survival rate of approximately 26%–34%. [139]
  • Low EBNA1BP2 expression was associated with longer overall survival (OS) and better disease-free survival (DFS) in uterine carcinosarcoma in a pan-cancer analysis. [149]
  • Reported factors associated with outcome include FIGO stage, sarcoma dominance (sarcomatous element >50%), higher CA 125 levels, cervical involvement, older age, adnexal metastasis, advanced stage, no lymphadenectomy, residual tumor, and larger tumor size (with one cohort noting tumor size >4.5 cm correlated with nodal involvement). [94][156][95][225][25][116]6 sources
  • In one cohort, the authors concluded that the revised FIGO 2023 staging system had better performance in predicting disease prognosis than the 2009 version. [12]
  • In one cohort examining outcomes after progression, optimal debulking surgery as primary treatment and salvage treatment with combined chemotherapy and radiotherapy were associated with improved survival after progression, while leukocytosis before salvage treatment was associated with worse prognosis. [73]
  • A SEER analysis found lower 5-year cancer-specific survival for uterine carcinosarcoma than for grade 3 endometrioid carcinoma at stage IC and stage III. [65]
  • In one retrospective cohort, disease recurrence occurred in 32.5% of cases, and the median disease-free interval was 17.92 months. [100]
  • In one multicenter retrospective study, incomplete cytoreduction, tumor persistence after treatment, extrauterine disease, positive resection margins, and lymphovascular invasion were associated with worse outcomes. [107]
  • A 2022 meta-analysis reported that uterine carcinosarcoma has a worse prognosis than serous carcinoma and clear cell carcinoma, and that the increased hazard of death was also seen in early-stage disease. [2]
  • In a retrospective adjuvant-therapy analysis, stage and receipt of chemoradiation were independent predictors of survival. [259]
Safety & interactions19 points
  • Some reviews note that tamoxifen may induce carcinogenesis in some patients with uterine carcinosarcoma. [18][24][62]3 sources
  • In a randomized phase III trial, overall toxicities were similar between paclitaxel/carboplatin and paclitaxel/ifosfamide, but paclitaxel/carboplatin had more hematologic toxicity while paclitaxel/ifosfamide had more confusion and genitourinary hemorrhage; ifosfamide (alone or with cisplatin) and paclitaxel-containing regimens induced grade 3 or 4 or other significant toxicities in trials. [233][77]
  • Prolonged (> 5 years) tamoxifen treatment may represent a causative factor in the development of uterine carcinosarcoma, and the risk of tamoxifen-related endometrial adenocarcinoma is well established with daily dose and treatment duration of adjuvant tamoxifen as risk factors. [135][134]
  • In a phase II trial of 9 patients with TP53‑mutated uterine carcinosarcoma, treatment‑related adverse events occurred in 88.9% of patients, most commonly diarrhea and fatigue. [69]
  • In the STATICE trial, trastuzumab deruxtecan was associated with pneumonitis/interstitial lung disease (grades 1–2 in 24% and grade 3 in 3% of patients). [102]
  • Hormone replacement therapy was associated with enhanced overall survival in one study. [56]
  • A Cochrane review reported that combination therapy with ifosfamide was associated with more nausea and vomiting than single-agent ifosfamide; whole-body irradiation had less hematological morbidity than chemotherapy; and all neuropathy morbidity occurred in the chemotherapy group. [138]
  • Trabectedin was associated with grade 3 to 5 neutrophil count decreases and transaminase increases, and two patients died due to trabectedin-related grade 5 hematological toxicity. [247]
  • In an anastrozole trial, safety was described as acceptable and 5 of 39 evaluable patients had grade 3 toxicities. [257]
  • In the cited case, the patient with metastatic uterine carcinosarcoma and VTE was discharged on long‑term anticoagulation. [9]
  • In a 5‑patient series of lenvatinib plus pembrolizumab for uterine carcinosarcoma, no grade 3 or higher adverse events were observed. [191]
  • Sources describe that anaerobic bacteremia in gynecologic pathology can lead to rapid deterioration and that surgical intervention is often necessary for Clostridium and Bacteroides infections. [276]
  • Hypersensitivity reactions to carboplatin increase with the number of platinum administrations and may be managed by desensitization, switching to another platinum, or changing to a non-platinum agent. [238]
  • Uterine inversion can be associated with uterine carcinosarcoma and may present a diagnostic and surgical challenge. [277]
  • In one retrospective study, grade 3 and 4 toxicities were more frequent with TIP than with PC. [4]
  • In a multicenter cohort, women aged ≥80 years were more likely to undergo simple hysterectomy without lymphadenectomy and to receive no postoperative therapy. [21]
Show 3 lab & early-research findings
  • One review of olaparib in carcinosarcoma reports that olaparib was associated with increased overall animal survival in HRD xenografts. [163]
  • A case report describes uterine carcinosarcoma occurring in a woman with prior pelvic irradiation for cervical cancer. [112][117][24]3 sources
  • A case report documents port-site metastasis after laparoscopic surgery for early-stage uterine carcinosarcoma and advises careful specimen removal to reduce risk. [229]
What we don't know yet41 points
  • Prospective clinical studies and randomized controlled evidence are limited for uterine carcinosarcoma; further prospective trials are needed to define optimal adjuvant, salvage and postoperative treatments (including the benefit of radiotherapy), to validate new therapeutic targets (for example trastuzumab for HER2-positive disease and PARP inhibitors in HRD-related tumors), to assess ctDNA as an early biomarker of recurrence, and to address challenges created by the low incidence and sparse data on later lines of chemotherapy. [221][222][254][131][226][156][27][22][113][163][120][26]12 sources
  • Molecular pathogenesis and biomarker studies are insufficiently characterized; further molecular and prognostic research is warranted across populations and larger cohorts, including exploration of novel biomarkers (including mRNA-level markers), investigation of CSPP1 (potential implications for ferroptosis-based therapy and immunotherapy), study of TET2 S38 phosphorylation, clarification of nucleolin's role, assessment of immune biomarkers, and acknowledgement that sample sizes for some molecular resources are limited and that future targeted treatments may need to be subtype-specific. [85][118][278][180][279][25][17]7 sources
  • UCS shows molecular heterogeneity and its molecular pathogenesis (including chromatin remodeling events) is a key area for exploration; accumulating molecular information has been suggested to enable subtype-specific or personalized anticancer approaches and some authors have suggested routine molecular testing of UCS tumors may be warranted. [18][38][147][45][146][28]6 sources
  • Specific treatment guidelines for uterine carcinosarcoma are limited; optimal treatment (including adjuvant strategies) is debated and no definitive consensus exists, and few clinical trials are applicable for uterine carcinosarcoma patients. [133][99][100][107][104]5 sources
  • Reviews report that targeted therapies for uterine carcinosarcoma remain investigational and that an effective targeted therapy has not yet been established; further study of targeted and combination approaches has been recommended. [38][219][220][146][28]5 sources
  • Prospective studies and clinical trials are needed to test treatment hypotheses and to define roles for therapies — including the role of adjuvant chemoradiation in FIGO I–II disease and the role of different radiation modalities — in uterine carcinosarcoma. [258][2][261][64]4 sources
  • Prognostic factors and many treatment recommendations are based on small retrospective studies, most adjuvant studies are retrospective, and prospective randomized controlled trials (including multicentre trials) comparing chemotherapy schedules and multimodal treatments are lacking; prospective randomized trials have been recommended to better define adjuvant therapy and optimal strategies. [24][218][219][38]4 sources
  • Many biomarker and molecular/immune correlates require further study: the function and prognostic value of radiotherapy-sensitive genes are unclear, data on CD47 expression and its clinicopathological impact remain lacking, and tumor molecular and immune correlates may inform further development of targeted agents (for example, ATR inhibitors). [66][13][165]3 sources
  • Validated biomarkers are currently either not available or often unreliable; more sensitive and specific biomarkers for monitoring response to adjuvant treatment and for early detection of recurrent disease are needed, and more molecular studies with decent sample sizes (including for ovarian carcinosarcoma) are required for clinical management. [221][249][88]3 sources
  • The pathogenesis and genetic alterations of uterine carcinosarcoma are still poorly understood and whether similar molecular and cellular mechanisms drive the disease remains poorly understood. [203][8]
  • Comparative molecular analysis suggested the immune-exhausted molecular landscape of uterine papillary serous carcinoma may be more amenable to immunotherapy than that of uterine carcinosarcoma, and overall the role of immunotherapy in uterine carcinosarcoma remains unclear. [159][64]
  • Hormonal targeting may be relevant in subsets of patients: anastrozole (an aromatase inhibitor) may have a role in a subset of patients with metastatic uterine carcinosarcoma, and further investigation of estrogen receptor and progesterone receptor targeting is warranted. [257][79]
  • The role and efficacy of sentinel lymph node mapping in UCS remain undetermined, and there is little to no data specific to uterine carcinosarcomas on this technique. [55][83]
  • The role of radiation is described as less clear in the literature, and combination therapies involving radiation and other modalities have not been studied in depth. [36][219]
  • Whether MSI/MMR-deficient uterine carcinosarcomas have a better prognosis is uncertain and further studies are necessary. [158]
  • The best management, oncologic outcomes, and optimal adjuvant treatment for carcinosarcoma without myoinvasion remain uncertain because of limited data and lack of consensus. [3]
  • Full molecular classification of uterine carcinosarcoma (including POLE status) is supported by some studies. [15]
  • Estimating DNA repair capacity by RADD may be as treatment-informative as molecular sequencing. [159]
  • In this multicenter study, tamoxifen use was not associated with worse progression-free or disease-specific survival in uterine carcinosarcoma. [63]
  • Active therapies beyond first-line treatment are limited in recurrent or persistent uterine carcinosarcoma, and novel therapies continue to be urgently needed. [69]
  • The source notes that patients of African ancestry are underrepresented in genomic datasets for uterine carcinosarcoma. [8]
  • This report describes an infrequent coexistence of a migrated intrauterine device with a uterine carcinosarcoma and notes that uterine neoplasms secondary to foreign bodies are very rare. [10]
  • A review says biomarker-guided treatments could accelerate the development of precision therapeutics across tumor types, but an organ-centric approach to clinical trial design hinders the development of effective treatments for rare cancers with shared biomarkers. [136]
  • The role of lymph node ratio and the significance of the lymphatic system in uterine carcinosarcoma remain insufficiently understood and require further investigation. [98]
  • The literature includes conflicting findings on whether heterologous components affect prognosis. [89]
  • The relationship between HER2 status and response to immune checkpoint inhibition in uterine carcinosarcoma is uncertain; HER2-positive tumors may be less susceptible to immune checkpoint inhibitors (presented as a possibility). [197]
  • The possibility that irradiation has a carcinogenic effect in carcinosarcoma has been controversial and debated. [112]
  • Evidence for the efficacy of lenvatinib plus pembrolizumab in UCS is unclear because clinical trials sometimes exclude UCS, and authors state more cases are needed to assess its effect. [191]
  • The survival benefit of lymphadenectomy, particularly in relation to adjuvant radiotherapy and/or chemotherapy, is unclear. [53]
  • Because splenic metastasis of UCS is rare, current evidence for survival after splenectomy is insufficient. [280]
  • There is a significant unmet need to develop new therapeutic options for recurrent uterine carcinosarcoma because second-line and later-line cytotoxic therapies have low response rates and short progression-free survival. [230]
  • Tumor heterogeneity and changing biomarker profiles between primary and metastatic lesions are important unresolved issues that may affect targeted therapy selection and response. [274]
  • Further evaluation of DKK1 expression and Wnt/β-catenin pathway alterations as predictive biomarkers for DKN-01 in uterine carcinosarcoma is supported by case-level observations. [274]
  • Further studies are warranted to evaluate the role of hormonal therapy in hormone receptor–positive uterine carcinosarcoma and to identify prognostic factors that predict response to hormonal therapies. [205]
  • There is no clear, specific guideline or standard treatment established for uterine carcinosarcoma, particularly in recurrent or progressive disease. [132]
  • Targeted therapeutics have thus far not demonstrated significant clinical efficacy in uterine carcinosarcoma according to reviewed reports. [49]
  • The long latency period observed even in patients receiving only 5 years of tamoxifen leads authors to consider a prolonged gynecologic follow-up of these patients. [134]
  • Alterations in EBNA1BP2 were reported not to significantly impact patient prognosis, and the authors noted that further verification may require additional patient clinical data. [149]
  • The transcriptome-based classifier study noted limitations, including lack of metastatic-origin mucinous cases (so findings may be limited when the direct origin is metastatic rather than primary) and that the transcriptome of paraffin-fixed tissues can differ from fresh tissues, which may affect transcriptome-based analyses. [125]
  • A defined precursor lesion for the carcinomatous and sarcomatous components of UCS has not been identified. [192]
  • Preclinical models and patient-derived cell lines are needed to study molecularly tailored therapies in uterine carcinosarcoma. [201]

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 12, 2026.

  1. Systematic reviewPrognostic value of the TCGA molecular classification in uterine carcinosarcoma · 2022
  2. Meta-analysisUterine carcinosarcoma vs endometrial serous and clear cell carcinoma: A systematic review and meta-analysis of survival · 2022
  3. Clinical trialEndometrial carcinosarcoma without myoinvasion · 2025
  4. Clinical trialAdjuvant chemotherapy in uterine carcinosarcoma: Comparison of a doublet and a triplet chemotherapeutic regimen · 2021
  5. Clinical trialCharacterizing sarcoma dominance pattern in uterine carcinosarcoma: Homologous versus heterologous element · 2018
  6. Clinical trialSignificance of venous thromboembolism in women with uterine carcinosarcoma · 2018
  7. Clinical trialClinicopathological characteristics, treatment and outcomes in uterine carcinosarcoma and grade 3 endometrial cancer patients: a comparative study · 2016
  8. Review articleA Single-Cell Atlas of Uterine Carcinosarcoma from Diverse Ancestries · 2026
  9. Review articleParaneoplastic Pulmonary Embolism Revealing Metastatic Uterine Carcinosarcoma · 2026
  10. Case reportUterine carcinosarcoma due to foreign body (migrated intrauterine device): an extremely rare etiology of gynecological neoplasm · 2026
  11. Review articleUterine Carcinosarcoma-A Retrospective Cohort Analysis from a Tertiary Centre on Epidemiology, Management Approach, Outcomes and Survival Patterns · 2025
  12. Review articleUterine Carcinosarcoma: Adaptation to New FIGO 2023 Staging System Through Clinical Profile and Oncologic Outcomes · 2025
  13. Review articleEvaluating the effect of CD47 expression levels and clinicopathologic features on survival function in resected uterine carcinosarcoma: the Western Turkey example · 2026
  14. Clinical trialComparing paclitaxel-platinum with ifosfamide-platinum as the front-line chemotherapy for patients with advanced-stage uterine carcinosarcoma · 2022
  15. Clinical trialPOLE-Mutated Uterine Carcinosarcomas: A Clinicopathologic and Molecular Study of 11 Cases · 2025
  16. Review articleUterine carcinosarcoma: An overview · 2021
  17. Review articleOSucs: An Online Prognostic Biomarker Analysis Tool for Uterine Carcinosarcoma · 2020
  18. Review articleMolecular Basis of Tumor Heterogeneity in Endometrial Carcinosarcoma · 2019
  19. Review articleFbxw7 is a driver of uterine carcinosarcoma by promoting epithelial-mesenchymal transition · 2019
  20. Review articleMLH1 promoter hypermethylation in uterine carcinosarcoma rarely coexists with TP53 mutation · 2019
  21. Review articleTumor characteristics and outcome of uterine carcinosarcoma in women aged ≥80 years · 2019
  22. Review articleExecutive summary of the American Radium Society® Appropriate Use Criteria for management of uterine carcinosarcoma · 2020
  23. Review articleUterine Carcinosarcomas · 2019
  24. Review articlePrognostic factors impacting survival in early stage uterine carcinosarcoma · 2019
  25. Review articleThe prevalence and prognostic impact of tumor-infiltrating lymphocytes in uterine carcinosarcoma · 2021
  26. Review articleTargeting the TGFβ pathway in uterine carcinosarcoma · 2020
  27. Review articleUterine carcinosarcomas: From pathology to practice · 2021
  28. Review articleIdentification of distinct molecular subtypes of uterine carcinosarcoma · 2017
  29. Review articleExpression of aurora kinases: Predictor of tumor dissemination in uterine carcinosarcoma · 2017
  30. Review articleIntegrated Molecular Characterization of Uterine Carcinosarcoma · 2017
  31. Review articleUterine Carcinosarcomas: Clinical, Histopathologic and Immunohistochemical Characteristics · 2017
  32. Review articleRole of TGF-β signaling in uterine carcinosarcoma · 2015
  33. Review articleMutational landscape of uterine and ovarian carcinosarcomas implicates histone genes in epithelial-mesenchymal transition · 2016
  34. Review articleUterine carcinosarcoma · 2011
  35. Review articleRare uterine cancer: carcinosarcomas. Review from histology to treatment · 2015
  36. Review articleUterine carcinosarcoma: A review of the literature · 2015
  37. Case reportUterine carcinosarcoma with heterologous osseous elements: a case report of an extremely rare clinical occurrence with literature review · 2025
  38. Case reportA rare case report of uterine carcinosarcoma with bilateral ovarian Brenner tumors · 2025
  39. Case reportThe discovery of uterine carcinosarcoma through a sister mary joseph's nodule: A case report · 2025
  40. Case reportIsolated left axillary nodal metastasis from endometrial carcinosarcoma: A case report and literature review · 2024
  41. Case reportAn uncommon case of POLE mutated uterine carcinosarcoma - complemented by a review of literature · 2024
  42. Case reportUterine carcinosarcoma with heterologous mesenchymal element: a case report of a rare and aggressive tumor · 2024
  43. Case reportPreferential human epidermal growth factor receptor 2 expression in myometrial and lymphovascular invasion of a uterine carcinosarcoma: A case report · 2022
  44. Case reportCarcinosarcoma of uterus · 2023
  45. Case reportUterine carcinosarcoma associated with a germline nibrin (NBN) mutation · 2022
  46. Case reportUterine Carcinosarcoma in a Young Female: Case Report and Literature Review · 2021
  47. Case reportUterine Carcinosarcoma: A Case Report and Literature Review · 2020
  48. Case reportUterine carcinosarcoma (malignant mixed Müllerian tumor): case report in a goat and literature review · 2018
  49. Case reportCNS metastasis secondary to malignant-mixed Müllerian tumor: case report and review of therapeutics · 2017
  50. Case reportCarcinosarcoma of the uterus: a case report and review of the literature · 2008
  51. Case reportDiagnosis of recurrent uterine carcinosarcoma by fine-needle aspiration cytology: report of a case · 2000
  52. Review articleUterine Carcinosarcomas - Diagnosis and Management · 2018
  53. Review articleLymphadenectomy and Adjuvant Therapy Improve Survival with Uterine Carcinosarcoma: A Large Retrospective Cohort Study · 2018
  54. Review articleSalvage chemotherapy with taxane and platinum for women with recurrent uterine carcinosarcoma · 2017
  55. Review articleSurvival of Patients with Uterine Carcinosarcoma Undergoing Sentinel Lymph Node Mapping · 2016
  56. Review articleURI1 amplification in uterine carcinosarcoma associates with chemo-resistance and poor prognosis · 2015
  57. Review articleUterine carcinosarcoma · 2011
  58. Review articleMalignant biphasic uterine tumours: carcinosarcomas or metaplastic carcinomas? · 2002
  59. Review articleUterine carcinosarcomas (malignant mixed Mullerian tumors) are metaplastic carcinomas · 2002
  60. ObservationalTrends of uterine carcinosarcoma in the United States · 2018
  61. Case reportA rare case of uterine carcinosarcoma in a 21-year-old woman with hereditary breast and ovarian cancer syndrome: A case report · 2026
  62. Review articleReview literature on uterine carcinosarcoma · 2014
  63. Clinical trialTumor characteristics and survival outcomes of women with tamoxifen-related uterine carcinosarcoma · 2017
  64. Review articleEfficacy and safety of pembrolizumab with or without lenvatinib in recurrent uterine carcinosarcoma: a real-world single-center study · 2026
  65. Clinical trialUterine carcinosarcomas and grade 3 endometrioid cancers: evidence for distinct tumor behavior · 2008
  66. Review articleIdentification of radiotherapy-sensitive genes for predicting prognosis, immune microenvironment, and drug sensitivity in uterine carcinosarcoma patients · 2025
  67. Review articleReal-world insights into the prevalence and prognostic significance of trophoblast cell-surface antigen 2 and folate receptor alpha in uterine carcinosarcoma · 2025
  68. Review articleDemographic features and prognostic factors of uterine carcinosarcoma: a study at a specialized center in Saudi Arabia · 2025
  69. Review articlePhase 2 study of Wee1 inhibitor adavosertib in recurrent uterine carcinosarcoma · 2025
  70. Review articleQuality of life and survival in patients with uterine carcinosarcoma: A tertiary center observational study · 2025
  71. Review articlePrognostic significance of neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and monocyte-to-lymphocyte ratio in uterine carcinosarcoma · 2025
  72. Review articleSurgical staging identifies occult metastases in over 50% of uterine-confined carcinosarcoma · 2025
  73. Review articleOverall survival after progression in patients with uterine carcinosarcoma: a single-center retrospective cohort study · 2025
  74. Review articleEvaluation of Uterine Carcinosarcoma and Uterine Endometrial Carcinoma Using Magnetic Resonance Imaging Findings and Texture Features · 2024
  75. Review articleImpact of TSC2 loss on progression-free survival in uterine carcinosarcoma: A retrospective analysis · 2025
  76. Review articleThe Expression and Amplification of HER2 Has a Significant Impact on the Prognosis of Endometrial Carcinoma in Korean Patients · 2024
  77. Review articleUterine carcinosarcoma: Unraveling the role of epithelial-to-mesenchymal transition in progression and therapeutic potential · 2024
  78. Review articleDevelopment of Antibody-Drug Conjugates for Malignancies of the Uterine Corpus: A Review · 2025
  79. Review articleUpdates and controversies in the management of uterine serous carcinoma and uterine carcinosarcoma · 2025
  80. Case reportSkull Base Metastasis of Uterine Carcinosarcoma Mimicking Primary Carcinoma of the Middle Ear · 2025
  81. Case reportCase report: Carcinosarcoma of uterus in nulliparous women · 2024
  82. Case reportSpinal intramedullary uterine carcinosarcoma metastasis · 2024
  83. Case reportUterine carcinosarcoma with intestinal involvement: A case report and literature review · 2023
  84. Case reportEfficacy of pazopanib in FGFR1-amplified uterine carcinosarcoma: A case report · 2022
  85. Review articleA personalized nomogram for predicting 3-year overall survival of patients with uterine carcinosarcoma in a tertiary care hospital in Southern Thailand · 2023
  86. Review articleTrends in Gynecologic Carcinosarcoma Based on Analysis of the Surveillance Epidemiology End Result (SEER) Database · 2023
  87. Review articleUterine carcinosarcoma: A 10-year single institution experience · 2022
  88. Review articleIdentification of drug targets and prognosis projection for uterine carcinosarcoma based on alternative splicing events · 2023
  89. Review articleThe prognostic significance of the heterologous component in uterine carcinosarcomas · 2023
  90. Review articleIdentification of condition-specific biomarker systems in uterine cancer · 2022
  91. Review articleIs minimally invasive surgery for clinical stage I uterine carcinosarcoma safe? · 2022
  92. Review articleCo-Clinical Study of [fam-] Trastuzumab Deruxtecan (DS8201a) in Patient-Derived Xenograft Models of Uterine Carcinosarcoma and Its Association with Clinical Efficacy · 2023
  93. Review articleRetrospective Analysis of Patients with Gynaecological Uterine Sarcomas in a Tertiary Hospital · 2022
  94. Review articleSentinel lymph node biopsy alone compared to systematic lymphadenectomy in patients with uterine carcinosarcoma · 2022
  95. Review articleUterine carcinosarcoma: Contemporary clinical summary, molecular updates, and future research opportunity · 2021
  96. Review articleComparative analysis of EZH2, p16 and p53 expression in uterine carcinosarcomas · 2023
  97. Review articleMesothelin expression in gynecologic carcinosarcoma: clinicopathological significance and correlation with HER2 expression · 2024
  98. Review articlePrognostic Value of Lymph Node Ratio in Patients with Uterine Carcinosarcoma · 2024
  99. Review articleGemcitabine combination therapies induce apoptosis in uterine carcinosarcoma patient-derived organoids · 2024
  100. Review articleUterine Carcinosarcoma (UCS): A Literature Review and Survival Analysis from a Retrospective Cohort Study · 2024
  101. Review articleClinical and multiparametric MRI features for differentiating uterine carcinosarcoma from endometrioid adenocarcinoma · 2024
  102. StudyTrastuzumab Deruxtecan for Human Epidermal Growth Factor Receptor 2-Expressing Advanced or Recurrent Uterine Carcinosarcoma (NCCH1615): The STATICE Trial · 2023
  103. Review articleIncidence and survival rates of primary uterine carcinosarcoma in Korea: a National Cancer Registry study · 2023
  104. Review articleClinico-Pathological Characteristics, Management, and Prognostic Factors of Patients with Uterine Carcinosarcoma: a Retrospective Analysis · 2023
  105. Review articleHER2 Oncogene as Molecular Target in Uterine Serous Carcinoma and Uterine Carcinosarcoma · 2023
  106. Review articleWhole-Genome DNA Methylation Profiling Identifies Epigenetic Signatures of Uterine Carcinosarcoma · 2017
  107. Review articleInfluence of Clinical and Surgical Factors on Uterine Carcinosarcoma Survival · 2023
  108. Review articleExploring biomarkers and prognostic factors in uterine carcinosarcoma: An insight into L1CAM, CDX2, p53, and MSI status · 2023
  109. Review articleManagement and Prognosis of Patients with Recurrent or Persistent/Progressive Uterine Carcinosarcoma · 2022
  110. Review articleIncreasing incidence of uterine carcinosarcoma: A United States Cancer Statistics study · 2022
  111. Review articleInter-component immunohistochemical assessment of proliferative markers in uterine carcinosarcoma · 2022
  112. Review articleRadiotherapy-induced uterine cacinosarcoma: A case report and review of the literature · 2022
  113. Review articleMolecular variations in uterine carcinosarcomas identify therapeutic opportunities · 2020
  114. Case reportCarcinosarcoma of Uterus and Ovary-Clinical, Morphological, and Immunohistochemical Study of Case Series · 2025
  115. Clinical trialEstablishment and comparison of three sublines from a human uterine carcinosarcoma cell line, ESCA · 2025
  116. Review articlePrognosis of the patients suffered from uterine carcinosarcoma from rural and urban areas · 2021
  117. Review articleCurrent Status of Magnetic Resonance Imaging in Patients with Malignant Uterine Neoplasms: A Review · 2019
  118. Review articleRal GEF with the PH Domain and SH3 Binding Motif 1 Regulated by Splicing Factor Junction Plakoglobin and Pyrimidine Metabolism Are Prognostic in Uterine Carcinosarcoma · 2021
  119. StudyElucidating divergent biology in uterine carcinosarcoma · 2025
  120. Review articleBeyond Serous: Treatment Options for Rare Endometrial Cancers · 2022
  121. Review articleUterine sarcomas: clinical presentation and MRI features · 2015
  122. GuidelineJapan Society of Gynecologic Oncology 2018 guidelines for treatment of uterine body neoplasms · 2020
  123. Review articleHER2-negative or low expression as an unfavorable prognostic factor in patients with stage I/II uterine carcinosarcoma · 2025
  124. Review articleA retrospective study evaluating the effect of trastuzumab addition to carboplatin/paclitaxel on overall survival in patients with advanced-stage HER2/neu-overexpressing uterine serous carcinoma or carcinosarcoma · 2025
  125. Review articleA transcriptome-Based Deep Neural Network Classifier for Identifying the Site of Origin in Mucinous Cancer · 2022
  126. Clinical trialExpression of p27 and p53: comparative analysis of uterine carcinosarcoma and endometrial carcinoma · 2004
  127. Review articleCharacterizing the extracellular matrix transcriptome of cervical, endometrial, and uterine cancers · 2022
  128. Review articleCervical Carcinosarcoma: Current Understanding on Pathogenesis, Diagnosis, Management and Future Perspectives · 2021
  129. Review articleGTSF1 promotes stemness in uterine carcinosarcoma through CCL1-mediated M1 macrophage aggregation · 2025
  130. Review articleUterine and Ovarian Carcinosarcomas: Do They Behave Similarly? · 2017
  131. Review articleTherapeutic Challenges in Patients with Gynecologic Carcinosarcomas: Analysis of a Multicenter National Cohort Study from the French Prospective TMRG Network · 2022
  132. Case reportAn uncommon response to metronomic therapy in a heavily pretreated patient with metastatic carcinosarcoma: a case report · 2016
  133. Review articlePeritoneal cytology predicting distant metastasis in uterine carcinosarcoma: machine learning model development and validation · 2025
  134. Case reportTamoxifen-related uterine carcinosarcomas occur under/after prolonged treatment: report of five cases and review of the literature · 2002
  135. Case reportLong-term tamoxifen treatment: a possible aetiological factor in the development of uterine carcinosarcoma: two case-reports and review of the literature · 2000
  136. StudyLarge language models-enabled digital twins for precision medicine in rare gynecological tumors · 2025
  137. Review articleClinical features and outcomes of uterine and ovarian carcinosarcoma · 2006
  138. Meta-analysisAdjuvant radiotherapy and/or chemotherapy after surgery for uterine carcinosarcoma · 2013
  139. Case reportUnusual Cutaneous Metastasis of Uterine Carcinosarcoma: A Case Report and Review of the Literature · 2016
  140. StudyUltrasonographic Findings of Uterine Carcinosarcoma · 2019
  141. Review articleRacial disparities in uterine and ovarian carcinosarcoma: A population-based analysis of treatment and survival · 2020
  142. Review articleEvaluation of prognostic factors and treatment outcomes in uterine carcinosarcoma · 2009
  143. Meta-analysisTCGA Classification of Endometrial Cancer: the Place of Carcinosarcoma · 2020
  144. Review articleNot all uterine carcinosarcomas are created equal: Survival outcomes according to molecular characterization of uterine carcinosarcoma · 2025
  145. Clinical trialGenetic characterisation of adult primary pleomorphic uterine rhabdomyosarcoma and comparison with uterine carcinosarcoma · 2021
  146. Review articleMolecular alterations of PIK3CA in uterine carcinosarcoma, clear cell, and serous tumors · 2014
  147. Review articleAberrant chromatin remodeling in gynecological cancer · 2017
  148. Review articleCartilage oligomeric matrix protein acts as a molecular biomarker in multiple cancer types · 2023
  149. Review articleEBNA1BP2 identified as potential prognostic biomarker for multiple tumor types in pan-cancer analysis · 2024
  150. Review articleASPM, CDC20, DLGAP5, BUB1B, CDCA8, and NCAPG May Serve as Diagnostic and Prognostic Biomarkers in Endometrial Carcinoma · 2022
  151. Review articlePrognostic significance of programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) expression in uterine carcinosarcoma · 2020
  152. Review articlePD-L1 and Mismatch Repair Status in Uterine Carcinosarcomas · 2021
  153. StudyTROP2 expression and therapeutic targeting in uterine carcinosarcoma · 2025
  154. Case reportDurable partial response to pembrolizumab, lenvatinib, and letrozole in a case of recurrent uterine carcinosarcoma with ESR1 gene amplification · 2024
  155. Review articleUterine carcinosarcoma: immunohistochemical studies on tissue microarrays with focus on potential therapeutic targets · 2007
  156. Review articleAdjuvant Treatment Modalities, Prognostic Factors, and Outcome of the Uterine Carcinosarcoma · 2021
  157. Review articleCOX-2 expression in uterine carcinosarcoma · 2010
  158. Systematic reviewClinicopathological Features Associated with Microsatellite Instability/Mismatch Repair Deficiency in Uterine Carcinosarcoma: A Quantitative Systematic Review · 2022
  159. Clinical trialMolecular comparison reveals distinct transcriptomic differences between uterine carcinosarcoma and papillary serous carcinoma distinguishable by DNA damage · 2025
  160. Review articlePreoperative molecular classification of endometrial cancer: Validation through biopsy and matched hysterectomy specimens · 2025
  161. Review articleNuclear β-Catenin Expression in the Context of Abnormal p53 Expression Indicates a Nonserous Histotype in Endometrial Carcinoma · 2023
  162. Review articleSystematic Investigation of the Diagnostic and Prognostic Impact of LINC01087 in Human Cancers · 2022
  163. Review articleHomologous recombination deficiency (HRD) signature-3 in ovarian and uterine carcinosarcomas correlates with preclinical sensitivity to Olaparib, a poly (adenosine diphosphate [ADP]- ribose) polymerase (PARP) inhibitor · 2022
  164. Review articleMolecular landscape of ERBB2/HER2 gene amplification among patients with gynecologic malignancies; clinical implications and future directions · 2024
  165. Clinical trialEfficacy of the ATR Inhibitor Ceralasertib in Patients with ARID1A-Deficient Gynecologic and Other Solid Tumor Malignancies · 2026
  166. Meta-analysisCancer risks associated with the germline MITF(E318K) variant · 2020
  167. Clinical trialComparison of breast and gastric HER2 immunohistochemistry (IHC) scoring criteria in the assessment of endometrial carcinoma · 2026
  168. Clinical trialDistinct molecular landscapes between endometrioid and nonendometrioid uterine carcinomas · 2017
  169. Review articleA pan-cancer landscape of LILRB4 identifies it as a context-dependent marker of the myeloid and antigen-presentation axis · 2026
  170. Review articlePRAME Immunohistochemical Expression as a Diagnostic Tool to Distinguish Between Endocervical and Endometrial Adenocarcinomas · 2026
  171. Review articleMutant PP2A Induces IGFBP2 Secretion to Promote Development of High-Grade Uterine Cancer · 2025
  172. Review articlePan-Cancer Analysis Reveals Long Non-coding RNA (lncRNA) Embryonic Stem Cell-Related Gene (ESRG) as a Promising Diagnostic and Prognostic Biomarker · 2024
  173. Review articleA Comprehensive Pan-Cancer Analysis Reveals GRB7 as a Potential Diagnostic and Prognostic Biomarker · 2024
  174. Review articleStudy on the expression and prognostic relationship of MYL6B in liver cancer based on bioinformatics · 2024
  175. Review articleNucleobindin-2 Mediates Transforming Growth Factor-β1-Driven Phenotypes in Zinc Finger E-Box Binding Homeobox 1-High Uterine Carcinosarcoma · 2023
  176. Review articleComprehensive analysis and immunohistochemistry localization of NRP1 expression in pancancer and normal individual tissues in relation to SARS‑CoV‑2 susceptibility · 2023
  177. Review articleA pan-cancer analysis of SLC1A5 in human cancers · 2023
  178. Review articleDiscordances in expression of human epidermal growth factor receptor 2 between primary and metastatic uterine carcinosarcoma: A proposal for HER2-targeted therapy specimen selection · 2023
  179. Review articleEvaluation of Lineage/Site-specific Nuclear Immunohistochemical Markers SATB2, Cyclin D1, SALL4, and BCOR in High-grade Endometrial Carcinomas · 2023
  180. Review articleClinical Significance of TET2 in Female Cancers · 2022
  181. Review articleDistinct Roles of Adenosine Deaminase Isoenzymes ADA1 and ADA2: A Pan-Cancer Analysis · 2022
  182. Review articleComprehensive analysis of the expression and prognosis for APOE in malignancies: A pan-cancer analysis · 2022
  183. Review articleComprehensive Study of Human FBXW7 Deleterious nsSNP's Functional Inference and Susceptibility to Gynaecological Cancer · 2022
  184. Review articleS100A4/non-muscle myosin II signaling regulates epithelial-mesenchymal transition and stemness in uterine carcinosarcoma · 2020
  185. Review articleFascin Is Associated With Aggressive Behavior and Poor Outcome in Uterine Carcinosarcoma · 2017
  186. Review articleNestin: A biomarker of aggressive uterine cancers · 2016
  187. Review articlePrognostic factors and status of hormone receptors and angiogenic factors in uterine carcinosarcoma · 2014
  188. Review articleImmunohistochemical studies on uterine carcinosarcoma, leiomyosarcoma, and endometrial stromal sarcoma: expression and prognostic importance of ten different markers · 2011
  189. Review articlePrognostic value of alternative lengthening of telomeres-associated biomarkers in uterine sarcoma and uterine carcinosarcoma · 2012
  190. Review articleExpression and localization of E-cadherin and β-catenin in uterine carcinosarcoma · 2011
  191. Case reportThe efficacy and safety of lenvatinib plus pembrolizumab therapy in patients with uterine carcinosarcoma · 2024
  192. Review articleUnique Molecular Features in High-Risk Histology Endometrial Cancers · 2019
  193. Review articleA Comprehensive Pan-Cancer Molecular Study of Gynecologic and Breast Cancers · 2018
  194. Clinical trialMismatch Repair Deficiency in Uterine Carcinosarcoma: A Multi-institution Retrospective Review · 2020
  195. Review articleEvaluation of Saccharomyces cerevisiae -like 1 (SEC14L1) in Gynecologic Malignancies Shows Overexpression in Endometrial Serous Carcinoma · 2023
  196. Review articleFolate receptor alpha is widely expressed and a potential therapeutic target in uterine and ovarian carcinosarcoma · 2023
  197. Review articleHER2 Overexpression and Amplification in Uterine Carcinosarcomas With Serous Morphology · 2022
  198. Review articleERBB-2 gene overexpression and amplification in uterine sarcomas · 2004
  199. Case reportComplete response to trastuzumab-deruxtecan (Enhertu, T-DXd) in HER2-positive stage IVB uterine carcinosarcoma · 2025
  200. Case reportCase report: ZEB1 expression in three cases of hepatic carcinosarcoma · 2022
  201. Case reportHDAC Inhibition Induces Cell Cycle Arrest and Mesenchymal-Epithelial Transition in a Novel Pleural-Effusion Derived Uterine Carcinosarcoma Cell Line · 2021
  202. Meta-analysisPrognostic significance of heterologous component in carcinosarcoma of the gynecologic organs: a systematic review and meta-analysis · 2023
  203. Systematic reviewTarget Therapies for Uterine Carcinosarcomas: Current Evidence and Future Perspectives · 2017
  204. Review articlep38β - MAPK11 and its role in female cancers · 2021
  205. Case reportProgestin and aromatase inhibitor therapy in recurrent, estrogen/progestin receptor positive uterine carcinosarcoma: A case report · 2021
  206. Review articleSignificance of histologic pattern of carcinoma and sarcoma components on survival outcomes of uterine carcinosarcoma · 2016
  207. StudyMolecular diversity in uterine carcinosarcoma: Beyond TP53 · 2025
  208. Review articleSLC16A3 (MCT4) expression in tumor immunity and Metabolism: Insights from pan-cancer analysis · 2025
  209. Review articleIn Vivo Intra-Uterine Delivery of TAT-Fused Cre Recombinase and CRISPR/Cas9 Editing System in Mice Unveil Histopathology of Pten/p53-Deficient Endometrial Cancers · 2023
  210. Review articleImmunological Role of TP53 Somatic Mutation Classification in Human Cancers · 2023
  211. Review articleComprehensive analysis of tumor necrosis factor-α-inducible protein 8-like 2 (TIPE2): A potential novel pan-cancer immune checkpoint · 2022
  212. Review articleIdentification of SHCBP1 as a potential biomarker involving diagnosis, prognosis, and tumor immune microenvironment across multiple cancers · 2022
  213. StudyThe BRCAness Landscape of Cancer · 2022
  214. Case reportCase report: Characterization of the immunologic and molecular landscape in a unique presentation of invasive lobular carcinoma with concurrent uterine carcinosarcoma treated with immunotherapy · 2024
  215. Review articleCombinatorial screen with apoptosis pathway targeted agents alrizomadlin, pelcitoclax, and dasminapant in multi-cell type tumor spheroids · 2025
  216. Case reportExtra-uterine müllerian carcinosarcoma · 1986
  217. Review articleAdjuvant radiotherapy for uterine carcinosarcoma: A retrospective assessment of treatment outcomes · 2019
  218. Review articleClinical outcomes of uterine carcinosarcoma: results of 94 patients · 2015
  219. Review articleReview of Recommended Treatment of Uterine Carcinosarcoma · 2015
  220. Review articleAn update on the management of uterine carcinosarcoma · 2011
  221. Review articleMonitoring Treatment Response, Early Recurrence, and Survival in Uterine Serous Carcinoma and Carcinosarcoma Patients Using Personalized Circulating Tumor DNA Biomarkers · 2023
  222. Review articleThe survival impact of adjuvant radiotherapy and chemotherapy in patients with non-endometrioid endometrial carcinomas: a PSM-IPTW analysis based on SEER database · 2023
  223. Clinical trialMatched-pair Analysis for Survival Endpoints Between Women With Early-stage Uterine Carcinosarcoma and Uterine Serous Carcinoma · 2021
  224. Clinical trialMultimodality adjuvant therapy and survival outcomes in stage I-IV uterine carcinosarcoma · 2020
  225. Review articleAdjuvant therapy and prognosis in uterine carcinosarcoma · 2021
  226. Review articleAdjuvant radiotherapy improves overall survival when added to surgery and chemotherapy for uterine carcinosarcoma: a surveillance, epidemiology, and end results analysis · 2021
  227. Review articleSurgical and Oncologic Outcomes in Uterine Carcinosarcoma: A Retrospective Cohort Analysis · 2025
  228. Review articleAdjuvant chemotherapy in endometrial cancer · 2020
  229. Case reportPort-Site Metastasis of Uterine Carcinosarcoma after Laparoscopy · 2017
  230. Case reportLenvatinib plus pembrolizumab in patients with advanced or recurrent uterine carcinosarcoma · 2021
  231. Review articleStage III uterine carcinosarcoma: 2009 International Federation of Gynecology and Obstetrics Staging System and Prognostic Determinants · 2011
  232. ObservationalStage I uterine carcinosarcoma: Matched cohort analyses for lymphadenectomy, chemotherapy, and brachytherapy · 2017
  233. Randomized trialRandomized Phase III Trial of Paclitaxel and Carboplatin Versus Paclitaxel and Ifosfamide in Patients With Carcinosarcoma of the Uterus or Ovary: An NRG Oncology Trial · 2022
  234. Review articlePatterns of adjuvant treatment and survival outcomes in stage I uterine carcinosarcoma · 2022
  235. Case reportImmune Checkpoint Inhibitor-Induced Sarcoidosis-Like Reaction Mimicking Pulmonary Metastasis: A Case Report · 2026
  236. Case reportUterine carcinosarcoma showing immature teratoid-like differentiation · 2023
  237. Review articleChemotherapy for Uterine Carcinosarcoma with Carboplatin, Ifosfamide and Mesna · 2015
  238. Case reportHypersensitivity Reaction to Carboplatin in Gynecologic Cancer: A Case Report and a Review of the Literature · 2021
  239. Review articleAcute Presentation of Nonpuerperal Uterine Inversion Following a Diagnosis of Uterine Carcinosarcoma: A Case Report · 2026
  240. Review articlecERBB-2/Her-2 Neu Overexpression and Prognostic Significance in Uterine Carcinosarcoma · 2023
  241. Meta-analysisEffect of adjuvant therapy on the prognosis in stage I/II uterine carcinosarcoma: A meta-analysis · 2021
  242. Review articleMolecular subtypes and quantitative analysis of PD-L1 and tumor-associated immune cells in uterine carcinosarcoma · 2025
  243. Review articlePrognostic factors and adjuvant therapy in uterine carcinosarcoma · 2008
  244. Review articleRETRACTION: Identification of Ferroptosis-Related Gene Prognostic Signature and HSF1 for Reversing Doxorubicin and Gemcitabine Resistance in Uterine Carcinosarcoma · 2025
  245. Review articlePleomorphic Rhabdomyosarcoma of the Uterine Corpus in an Adult Who Underwent Multi-gene Panel Testing · 2024
  246. Review articleMolecular classification and subtype-specific drug sensitivity research of uterine carcinosarcoma under multi-omics framework · 2019
  247. Clinical trialEfficacy and safety of trabectedin for the treatment of advanced uterine or ovarian carcinosarcoma: Results of a phase II multicenter clinical trial (MITO-26) · 2022
  248. Clinical trialPrognostic factors of lenvatinib plus pembrolizumab therapy for advanced or recurrent endometrial cancer: analysis of a multicenter cohort study in Japan · 2025
  249. Review articleClinicopathological and molecular features of tubo-ovarian carcinosarcomas: a series of 51 cases · 2024
  250. Review articleTargeting human epidermal growth factor receptor 2 (HER2) in gynecologic malignancies · 2020
  251. Review articlePreclinical in vitro and in vivo activity of the RAF/MEK clamp avutometinib in combination with FAK inhibition in uterine carcinosarcomas · 2024
  252. Review articleEstablishment and characterization of multiple patient-derived organoids from a case of advanced endometrial cancer · 2024
  253. Review articleClinicopathological and molecular analyses of uterine carcinosarcomas using next-generation sequencing: A single-center experience · 2023
  254. Review articleTrastuzumab deruxtecan (DS-8201a), a HER2-targeting antibody-drug conjugate with topoisomerase I inhibitor payload, shows antitumor activity in uterine and ovarian carcinosarcoma with HER2/neu expression · 2023
  255. Case reportExacerbation of paraneoplastic cerebellar degeneration by immune checkpoint inhibitor use in endometrial cancer · 2025
  256. Review articleHuman induced pluripotent stem cell-derived chimeric antigen receptor-macrophages eradicate IL-13Rα2-positive solid tumors · 2026
  257. Clinical trialPhase 2 study of anastrozole in rare cohorts of patients with estrogen receptor/progesterone receptor positive leiomyosarcomas and carcinosarcomas of the uterine corpus: The PARAGON trial (ANZGOG 0903) · 2021
  258. Systematic reviewThe role of multimodal adjuvant therapy for FIGO I-II carcinosarcoma of the uterus: a systematic review · 2022
  259. Clinical trialImproved survival with combination chemotherapy and external beam radiation therapy in uterine carcinosarcoma · 2022
  260. Review articleEvaluation of chemotherapy and radiotherapy in the adjuvant management of uterine carcinosarcoma: a population-based analysis · 2023
  261. Review articleRole of adjuvant radiotherapy modality on clinical outcomes for early-stage uterine carcinosarcoma · 2025
  262. Review articlePrognostic indicators of recurrence and treatment-free interval in uterine carcinosarcoma · 2025
  263. Case reportPure abscopal effect in a patient with advanced uterine carcinosarcoma · 2023
  264. Review articleThe role of whole-pelvic irradiation in the treatment of early-stage uterine carcinosarcoma · 1997
  265. Review articleSuction thrombectomy of a uterine carcinosarcoma tumor thrombus extending into the IVC and right atrium · 2024
  266. Meta-analysisMinimally Invasive Compared With Open Surgery in High-Risk Endometrial Cancer: A Systematic Review and Meta-analysis · 2023
  267. Case reportNon-islet cell tumor hypoglycemia in a patient with uterine carcinosarcoma · 2021
  268. Review articleDiagnostic Value of (18)F-FDG PET/CT and MRI in the Preoperative Evaluation of Uterine Carcinosarcoma · 2018
  269. Review articleCarcinosarcoma of the uterus: MRI findings including diffusion-weighted imaging and MR spectroscopy · 2016
  270. Review articlePoor accuracy of endometrial sampling in patients with uterine carcinosarcomas: a nationwide analysis · 2025
  271. Case reportGenetic Investigation of Uterine Carcinosarcoma: Case Report and Cohort Analysis · 2016
  272. Review articleComprehensive Staging of Uterine Carcinosarcoma Using a Multiquadrant Robotic Platform · 2017
  273. Review articlePrognostic factors for disease-free and overall survival of patients with uterine carcinosarcoma · 2018
  274. Case reportResponse to anti-DKK1 therapy in uterine carcinosarcoma: A case report · 2021
  275. Review articleNeutrophilia and mortality in women with uterine carcinosarcoma · 2019
  276. Case reportClostridium and Bacteroides bacteremia as initial presentation of uterine carcinosarcoma · 2022
  277. Case reportUterine Inversion as a Result of a Large Prolapsed Carcinosarcoma of the Uterus · 2019
  278. Review articleIdentifies microtubule-binding protein CSPP1 as a novel cancer biomarker associated with ferroptosis and tumor microenvironment · 2022
  279. Review articleRole of Nucleolin in Endometrial Precancerous Hyperplasia and Carcinogenesis: Ex Vivo and In Silico Study · 2022
  280. Case reportMetastasis of Colon Cancer to the Accessory Spleen: A Case Report · 2024

What supports this page

The kinds of sources behind this page, strongest at the top. Faint rungs show what is not here yet.

Guideline
2
Meta-analysis
7
Systematic review
4
Randomized trial
1
Clinical trial
25
Observational
4
Case report
61
Review
224
Preclinical
0
Other
11

Living document — last change June 12, 2026: Cancer page updated. 3 recent updates logged.

Pooled evidence across studies

PubMed

Compounds compared by evidence

PubMed

How to read this: Ranked by the strength and volume of the evidence — NOT by how well a treatment works. A higher rank means a compound has been studied more, or in stronger study designs (e.g. randomized trials over lab studies), not that it produces better outcomes. The effect column shows the largest pooled figure reported, not a head-to-head comparison.

#CompoundEvidence strengthStudiesLargest pooled effect
1Carboplatin ChemotherapyHuman trial / meta-analysis2
2Trastuzumab Deruxtecan Targeted therapyHuman trial / meta-analysis2ORR: 64.1%
3Ifosfamide ChemotherapyHuman trial / meta-analysis1
4Paclitaxel ChemotherapyHuman trial / meta-analysis1PFS: 15.5 mo
5Tamoxifen Hormonal therapyHuman · observational1
6Trastuzumab-Deruxtecan (T-Dxd) Targeted therapyHuman · observational1
7Sacituzumab Govitecan Targeted therapyAnimal only1

Medicines & supplements studied for Uterine Carcinosarcoma

PubMedFDAClinicalTrials.gov

Every drug, supplement, and other agent the published studies cover for Uterine Carcinosarcoma, ranked by how strong the evidence is — what studies report, not a recommendation. Tap any to see its full profile.

Medicines · 7

CarboplatinHuman trial / meta-analysisMixed results1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: median OS 37 mo, p P < .01 for noninferiority, P > .1 for superiority, n=449 PMID 35007153 · median-survival values 1.8–37 across 7 studies

Most authoritative study: Randomized Phase III Trial of Paclitaxel and Carboplatin Versus Paclitaxel and Ifosfamide in Patients With Carcinosarcoma of the Uterus or Ovary: An NRG Oncology Trial

Findings conflict across studies · Effect sizes reported in only 2 of 3 studies.
ChemotherapyFDA off-labelPhase 33 studiesFull profile →
PaclitaxelHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: median OS 37 mo, p P < .01 for noninferiority, P > .1 for superiority, n=449 PMID 35007153 · median-survival values 15–37 across 4 studies

Most authoritative study: Randomized Phase III Trial of Paclitaxel and Carboplatin Versus Paclitaxel and Ifosfamide in Patients With Carcinosarcoma of the Uterus or Ovary: An NRG Oncology Trial

Effect sizes reported in only 1 of 2 studies.
ChemotherapyFDA off-labelPhase 32 studiesFull profile →
Trastuzumab DeruxtecanHuman trial / meta-analysisReported positive2 human

Includes human trial or meta-analysis evidence.

Largest credible effect: ORR by central review 54.5% [32.2–75.6], n=22 PMID 36977309 · median-survival values 5.4–13.3 across 4 studies

Most authoritative study: Real-world evidence of Trastuzumab Deruxtecan (T-DXd) Efficacy in HER2-expressing gynecological malignancies

Targeted therapyFDA off-label2 studiesFull profile →
IfosfamideHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: median OS 37 mo, p P < .01 for noninferiority, P > .1 for superiority, n=449 PMID 35007153 · median-survival values 15–37 across 4 studies

Most authoritative study: Randomized Phase III Trial of Paclitaxel and Carboplatin Versus Paclitaxel and Ifosfamide in Patients With Carcinosarcoma of the Uterus or Ovary: An NRG Oncology Trial

Based on a single study.
ChemotherapyFDA off-labelPhase 31 studyFull profile →
TamoxifenHuman · observationalInconclusive1 human

Human observational evidence only — no trials.

Largest credible effect: 1993 cluster cases 5 PMID 11578496 · effect sizes 2–16 across 7 studies

Most authoritative study: Is there an association between long-term tamoxifen treatment and the development of carcinosarcoma (malignant mixed Müllerian tumor) of the uterus?

Based on a single study.
Hormonal therapyFDA off-label1 studyFull profile →
Trastuzumab-Deruxtecan (T-Dxd)Human · observationalReported positive1 human

Human observational evidence only — no trials.

Largest credible effect: median PFS 5.4 mo [0.8–9.8], n=10 PMID 39639215 · effect sizes 1–5 across 3 studies

Most authoritative study: Real-world evidence of Trastuzumab Deruxtecan (T-DXd) Efficacy in HER2-expressing gynecological malignancies

Based on a single study.
Targeted therapy1 studyFull profile →
Sacituzumab GovitecanAnimal onlyReported positive1 animal

Animal studies only — no human data.

Largest credible effect: Median IC50 in UCS PDOs 167.7 [51.4–3200], n=9 PMID 40344963 · effect sizes 90–167.7 across 2 studies

Most authoritative study: TROP2 expression and therapeutic targeting in uterine carcinosarcoma

No human studies yet · Based on a single study.
Targeted therapyFDA off-label1 studyFull profile →

What recent studies report in Uterine Carcinosarcoma

These are reviewed studies whose abstracts concern Uterine Carcinosarcoma. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Uterine Carcinosarcoma. Most are early lab, animal, or small human studies, and findings often conflict.

33 studies10 human1 animal⚠ Conflicting evidenceMechanism (15)Trial (3)Safety (1)

Tracking 33 published studies of Uterine Carcinosarcoma: 10 in humans, 1 in animals, 22 reviews/other.

Reported direction across studies: 11 positive, 9 mixed, 13 inconclusive.

Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is limited.

These counts summarize what the studies reported; they are not a measure of whether anything works for Uterine Carcinosarcoma.

Compounds with studies mentioning Uterine Carcinosarcoma

Carboplatin (3)Trastuzumab deruxtecan (2)Paclitaxel (2)Sacituzumab govitecan (1)Trastuzumab deruxtecan t dxd (1)Ifosfamide (1)Tamoxifen (1)
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 9

Elucidating divergent biology in uterine carcinosarcoma

Translational oncology · Nov 2025

uterine carcinosarcoma

The authors performed multi-omic profiling (whole-genome sequencing, RNA-seq, and enzymatic methylation sequencing) on microdissected epithelial and mesenchymal components from uterine carcinosarcoma samples, and assessed the tumour microenvironment with multiplex immunohistochemistry and computational pathology. They found low median tumor mutation burden, frequent TP53 mutations and recurrent copy-number amplifications, broadly similar genomic and epigenomic profiles between epithelial and mesenchymal regions, global hypomethylation with different pathway enrichment in each component, and higher tumour-associated macrophage and PD-L1+ cell density in the mesenchymal component. The study is descriptive and based on a small number of cases.

Reported effects: median TMB 0.97, n=18 · TP53 mutation frequency 94%, n=18 · +9 more

Key findings
  • WGS and EM-seq of 18 samples from 9 patients revealed a low tumor mutation burden (TMB; median = 0.97 mutations/Mb) and no evidence of microsatellite instability (MSI).
  • Driver mutations were identified in TP53 (94 %), PIK3CA (33 %), and PPP2R1A (22 %).
  • Copy-number analysis revealed recurrent amplifications of MYC (67 %), PIK3CA (61 %), CCNE1 (56 %), AKT2 (44 %), and SMARCA4 (39 %).
  • Comparative analysis of the epithelial (C) and mesenchymal (S) regions revealed no significant differences in mutation frequency, copy-number, transcriptomic and methylomic profiles.
  • Both regions exhibited global hypomethylation, with functional enrichment for xenobiotic metabolism pathways in C and epithelial-to-mesenchymal transition pathways in S regions.
  • Comparative mIHC performed on 21 cases showed similar T cell and B cell densities, but a higher density of tumour-associated macrophages and PD-L1+ cells in the S component.
  • Computational morphologic analysis showed substantial histomorphologic heterogeneity within and across UCS cases.
Limitations: Small sequencing sample size (18 samples from 9 patients) limits generalizability.; Observational, descriptive study without functional validation of genomic/epigenomic findings.; No clinical outcome or treatment-response data reported to link molecular features to prognosis or therapy response.; mIHC analysis was performed on a separate/expanded cohort of 21 cases but remains limited in size.; Heterogeneity within tumors may limit ability to generalize findings from microdissected regions..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 97

Endometrial carcinosarcoma without myoinvasion

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Oct 2025 · multicenter retrospective study

uterine carcinosarcomaendometrial carcinosarcomaendometrial neoplasms

This multicenter retrospective study looked at 97 people with very early uterine carcinosarcoma that had not invaded the muscle layer of the uterus. The researchers compared outcomes by where the tumor was found and by whether patients received chemotherapy. Recurrence was common, mostly at distant sites, and the study did not find statistically significant survival differences with chemotherapy.

Reported effects: 5-year recurrence-free survival 63.5% [53.4–75.4], n=97 · overall survival 72% [62.6–82.9], n=97

Key findings
  • 29 of 97 patients (29.9%) had a recurrence, mostly with a distant pattern of relapse.
  • The 5-year recurrence-free survival was 63.5% and overall survival was 72.0%.
  • No significant differences were observed in recurrence-free survival and overall survival based on tumor status.
  • The difference in recurrence-free survival and overall survival was not statistically significant based on receipt of chemotherapy.
Limitations: Retrospective observational design; Rare disease with small sample size; Non-randomized treatment selection; Follow-up for survival analysis was limited to 5 years; Potential confounding by indication; No chemotherapy regimen, dose, or timing details provided in the abstract.

This study evaluates outcomes in a rare endometrial cancer subtype and compares adjuvant chemotherapy versus no chemotherapy after surgery.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

OtherMechanismReported positiveLimited evidenceTier 3 · early humann = 21

Large language models-enabled digital twins for precision medicine in rare gynecological tumors

NPJ digital medicine · Jul 2025 · Proof-of-concept computational digital-twin development integrating institutional/published cases and literature-derived data

rare gynecological tumorsuterine carcinosarcoma

The authors developed a proof-of-concept large language model (LLM)-enabled digital twin that integrates clinical and biomarker data from 21 cases and 655 publications to generate tailored treatment plans. Applied to metastatic uterine carcinosarcoma, the system identified therapeutic options that might be missed by single-source analyses and efficiently modeled individual patient trajectories. The authors argue that defining tumors by biology rather than organ could enable more personalized care for rare gynecological tumors.

Reported effects: integrated_cases_n 21 · literature_publications_n 655

Key findings
  • Developed an LLM-enabled digital twin integrating clinical and biomarker data from institutional and published cases (n = 21) and literature-derived data (n = 655 publications).
  • Created tailored treatment plans for metastatic uterine carcinosarcoma using multi-source data integration.
  • Identified treatment options potentially missed by traditional, single-source analysis.
  • LLM-enabled digital twins can efficiently model individual patient trajectories.
  • Shifting to a biology-based rather than organ-based tumor definition could enable more personalized care for rare gynecological tumors.
Limitations: Proof-of-concept computational study without prospective clinical validation.; Small number of integrated cases (n = 21).; No clinical outcomes or patient-level efficacy/safety data reported.; Relies on literature-derived data and published cases which may have heterogeneity and publication bias.; Abstract does not report external validation or comparison to standard-of-care decision processes..

Demonstrates a computational approach for biomarker-driven treatment matching in rare gynecological tumors using LLMs; clinical impact not evaluated in this study.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 51

Molecular diversity in uterine carcinosarcoma: Beyond TP53

Gynecologic oncology · Jul 2025 · observational genomic profiling of tumor samples

uterine carcinosarcoma

The authors performed next-generation sequencing of tumor DNA from 51 uterine carcinosarcoma patients, analyzing mutations, copy-number changes, microsatellite instability, tumor mutational burden, and homologous recombination deficiency. They found TP53 alterations were most frequent (88%), with PIK3CA (35%) and CCNE1 (33%) also common; most cases had a TP53-mutant profile, 11 were HR-deficient, and 7 samples had high TMB (≥16). Carcinoma and sarcoma components showed concordant gene variants but divergent copy-number changes, supporting a monoclonal origin. No molecular variables were statistically significant in survival analysis, but 45 cases (88%) harbored alterations that the authors considered potentially targetable by existing therapies.

Reported effects: n_included 51, n=51 · TP53_alteration_frequency 88%, n=51 · +9 more

Key findings
  • Among 51 included patients, TP53 was most frequently altered (88%), followed by PIK3CA (35%) and CCNE1 (33%).
  • Separate analysis of carcinoma and sarcoma components revealed concordant gene variants but divergent copy number variations.
  • Based on molecular classification, the majority of the cases 44 (84.6%) had a TP53-mutant profile.
  • Eleven cases were homologous recombination (HR) deficient.
  • Seven samples (14%) had high tumor mutational burden (TMB ≥16).
  • Key altered pathways were TP53, RTK/RAS, PI3K, and cell cycle pathways.
  • Alterations that could serve as possible molecular targets for existing therapies were identified in 45 cases (88%).
  • No molecular variables were statistically significant in the survival analysis.
Limitations: Observational genomic profiling without an interventional component.; Modest sample size (51 patients), limiting statistical power.; Survival analysis found no statistically significant molecular associations.; Carcinoma and sarcoma components were analyzed separately only "when possible," implying incomplete paired-component data in some cases.; Clinical impact of the identified potentially targetable alterations was not tested in patients (no interventional/therapeutic data)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Animal studyReported positivePreclinical onlyTier 2 · animaln = 72

TROP2 expression and therapeutic targeting in uterine carcinosarcoma

Gynecologic oncology · Jun 2025 · archival tissue analysis plus patient-derived organoid and xenograft preclinical study

Sacituzumab-govitecanuterine carcinosarcomaendometrial carcinoma

This study looked at TROP2 levels in uterine carcinosarcoma samples and tested the TROP2-targeting antibody-drug conjugate sacituzumab govitecan in patient-derived organoid and xenograft models. Most tumors had detectable TROP2, and the organoid models responded to the drug in a dose-dependent way. In two xenograft models, tumor volume was lower with sacituzumab govitecan than without it.

Reported effects: TROP2 expression in primary UCSs 90%, n=72 · Higher TROP2 expression by histologic subtype, p p < 0.001 and p = 0.022, n=72 · +2 more

Key findings
  • TROP2 protein and mRNA were detected in at least 90% of primary uterine carcinosarcomas.
  • Tumors with a predominant carcinomatous component or homologous differentiation had higher TROP2 expression than those with predominant sarcomatous component or heterologous differentiation.
  • All 9 uterine carcinosarcoma organoid models responded in a dose-dependent manner to sacituzumab govitecan.
  • Both xenograft models showed significant reduction in tumor volume with sacituzumab govitecan.
Limitations: Preclinical study; findings are from archival tissues, organoids, and mouse xenografts, not patients.; Only 2 xenograft models were tested.; No clinical outcomes, safety data, or survival data in humans were reported.; The abstract does not provide dosing details or treatment duration..

Supports preclinical exploration of TROP2-targeted therapy in uterine carcinosarcoma.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical

Updates and controversies in the management of uterine serous carcinoma and uterine carcinosarcoma

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Mar 2025 · Review

uterine serous carcinomauterine carcinosarcoma

This is a narrative review summarizing recent evidence on molecular classification, biomarkers, and new treatment approaches for uterine serous carcinoma and uterine carcinosarcoma. The authors highlight biomarkers such as HER2, TP53, and mismatch repair deficiency/microsatellite instability, discuss circulating tumor DNA and precision-based treatment options, and note survival disparities for non-Hispanic Black and other underserved minority patients. They conclude that continuing to prioritize biomarker-driven therapies and developing novel treatments through clinical trials — integrated with surgery and cytotoxic chemotherapy — is necessary.

Reported effects: proportion_of_cases 15% · proportion_of_deaths 50%

Key findings
  • Uterine serous carcinoma and uterine carcinosarcoma are rare but account for a disproportionate share of endometrial cancer deaths.
  • These subtypes have a high likelihood of metastasis and multisite recurrence and are biologically distinct from other endometrial cancers.
  • The review analyzes the role of biomarkers including HER2, TP53, and mismatch repair deficiency/microsatellite instability and their influence on treatment strategies and surveillance.
  • Circulating tumor DNA (ctDNA) is discussed as a potential tool.
  • Novel precision-based treatment options are described and the authors call for continued development of biomarker-driven therapies through clinical trials.
  • Disparate survival outcomes for non-Hispanic Black and other underserved minority patients are identified, and strategies to improve their outcomes are discussed.
Limitations: Narrative review rather than primary research; no new experimental or trial data presented in the abstract.; Abstract provides no methods, search strategy, or inclusion criteria (potential selection bias).; Rare tumor subtypes mean available evidence is likely limited and heterogeneous (implicit limitation).; No quantitative synthesis (meta-analysis) or new clinical outcome data reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalReported positiveLimited evidenceTier 3 · early humann = 10

Real-world evidence of Trastuzumab Deruxtecan (T-DXd) Efficacy in HER2-expressing gynecological malignancies

BMC cancer · Dec 2024 · retrospective cohort

Trastuzumab-deruxtecan-t-dxdTrastuzumab-deruxtecanendometrial neoplasmsovarian neoplasmscervical neoplasmsuterine carcinosarcomauterine leiomyosarcomauterine serous carcinomaovarian carcinosarcomahigh-grade serous ovarian carcinomamucinous ovarian carcinomasquamous cervical carcinoma

This retrospective single-center study identified 10 patients with HER2-expressing (IHC 2+/3+) recurrent or metastatic gynecological cancers who received trastuzumab deruxtecan (5.4 mg/kg IV every 3 weeks). The cohort had a median progression-free survival of 5.4 months (95% CI 0.8-9.8). Five patients had a partial response, one had stable disease at 12 weeks, and four had disease progression at initial assessment. Clinical benefit was observed mainly in tumors with HER2 IHC 3+.

Reported effects: median PFS 5.4 mo [0.8–9.8], n=10 · partial responses 5, n=10 · +2 more

Key findings
  • 10 patients with recurrent/metastatic HER2-expressing gynecological malignancies were treated with T-DXd.
  • Histologies included uterine neoplasms (n=5), cervical squamous carcinoma (n=1) and ovarian cancers (n=4).
  • Median age was 65.4 years (25th-75th percentile, 58.1-75.2 years).
  • HER2 by IHC: 5 patients were 3+ and 5 patients were 2+.
  • Median number of prior therapy lines was 4 (range 2-6); 2 uterine serous carcinoma patients were pretreated with trastuzumab and 4 patients had prior immunotherapy.
  • Dose: T-DXd 5.4 mg/kg IV every 3 weeks until progression/toxicity.
  • Median progression-free survival (PFS) in the cohort was 5.4 months (95% CI 0.8-9.8 months).
  • Responses: 5 patients had partial response (including 2 previously treated with trastuzumab), 1 patient had stable disease at 12 weeks, 4 patients had disease progression at initial assessment.
  • Most patients who derived clinical benefit had HER2 IHC 3+ expression.
Limitations: Retrospective, single-center design; Very small sample size (n=10); No control or comparator arm; Heterogeneous mix of gynecologic histologies; Heavily pre-treated population limits generalizability; Limited/absent reporting of safety or adverse event data in the abstract; Potential selection and reporting bias inherent to retrospective series.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Isolated left axillary nodal metastasis from endometrial carcinosarcoma: A case report and literature review

International journal of surgery case reports · Aug 2024 · case report

endometrial carcinosarcomauterine carcinosarcoma

This case report describes a 73-year-old woman who presented with a palpable left breast-tail mass; imaging showed enlarged left axillary lymph nodes with no breast primary. Excisional biopsy of the node showed metastatic disease of gynecologic origin and subsequent pelvic imaging and D&C diagnosed endometrial carcinosarcoma. The authors state this may be the first reported instance of isolated axillary lymph node metastasis from uterine carcinosarcoma presenting without pelvic or abdominal nodal involvement.

Key findings
  • Patient: 73-year-old woman presented with a left breast tail palpable mass.
  • Breast imaging (sonomammography and MRI) revealed multiple enlarged left axillary lymph nodes with malignant criteria but no suspected malignancy in either breast on imaging.
  • Excisional biopsy of an axillary lymph node diagnosed axillary lymph node metastasis from a gynecologic origin.
  • Abdominopelvic CT and pelvic MRI identified a suspicious endometrial mass; D&C pathology revealed endometrial carcinosarcoma.
  • Authors note this could be the first reported case of isolated axillary lymph node metastasis from uterine carcinosarcoma presenting as the initial symptom without pelvic or abdominal lymph node involvement.
Limitations: Single-patient case report limits generalizability.; No long-term follow-up or outcome data are provided in the abstract.; No systematic comparison group or epidemiologic data.; No mechanistic or molecular analyses reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Uterine serous carcinoma and uterine carcinosarcoma: molecular features, clinical advances, and emerging therapies

Clinical advances in hematology & oncology : H&O · Jul 2024

endometrial canceruterine serous carcinomauterine carcinosarcoma

This is a narrative review summarizing genomic and molecular features of uterine serous carcinoma (USC) and uterine carcinosarcoma (UCS). The authors note that USC and UCS are a small but increasing fraction of endometrial cancers and contribute disproportionately to endometrial cancer mortality, and that both subtypes have poor prognoses. The review summarizes clinical advances in primary advanced and recurrent disease and discusses emerging molecularly driven treatment strategies.

Key findings
  • Endometrial cancer, including high-grade subtypes, has a rising incidence and mortality.
  • Uterine serous carcinoma (USC) and uterine carcinosarcoma (UCS) account for a small but increasing proportion of endometrial cancer cases and a significant portion of endometrial cancer mortality.
  • USC and UCS are molecularly and clinically distinct but both have a poor prognosis.
  • There have been few therapeutic strategies directed specifically at these endometrial cancer subtypes to date.
  • The review summarizes genomic/molecular features, clinical advances for primary advanced and recurrent disease, and novel molecularly driven treatment strategies.
Limitations: Review article only — does not present new, patient-level primary data.; Abstract does not indicate this is a systematic review or meta-analysis, so selection and synthesis methods are not described.; Does not report specific quantitative efficacy data or comparative clinical trial results in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMixed resultsLimited evidenceTier 3 · early humann = 1

Spinal intramedullary uterine carcinosarcoma metastasis

BMJ case reports · Feb 2024 · case report

uterine carcinosarcomaspinal cord (intramedullary) metastasisspinal cord neoplasms

This case report describes a woman in her late 70s with uterine carcinosarcoma who developed an intramedullary spinal cord metastasis. The spinal lesion did not respond to radiotherapy but showed a favorable response following surgical debulking. The authors state this is the first reported case of uterine carcinosarcoma metastasizing to the spinal cord.

Key findings
  • Intramedullary spinal cord metastases (ISCM) are a rare manifestation of metastatic cancer with severe impacts on neurological function, survival expectancy, and quality of life.
  • Uterine carcinosarcoma is rare, accounting for less than 3% of all uterine cancers, and has a poor prognosis with only one-third of patients surviving beyond 5 years.
  • There are no previous reports of uterine carcinosarcoma metastases to the spinal cord.
  • In this reported case the intramedullary metastasis was refractory to radiotherapy and responded favorably to surgical debulking.
Limitations: Single-patient case report — findings may not generalize.; No control or comparison group.; Follow-up duration and quantitative outcome measures are not provided in the abstract.; Cannot establish causality or comparative effectiveness from a single observational case..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportReported positiveLimited evidenceTier 3 · early humann = 1

Uterine carcinosarcoma showing immature teratoid-like differentiation

BMJ case reports · Dec 2023 · case report

PaclitaxelCarboplatinuterine carcinosarcoma

This is a case report of a woman in her 60s with uterine carcinosarcoma showing immature teratoid-like differentiation who underwent total abdominal hysterectomy with bilateral adnexectomy followed by postoperative paclitaxel and carboplatin. Pathology showed mixed carcinomatous and sarcomatous elements with immature squamous epithelial cells and immature epithelial glands, and the final diagnosis was uterine carcinosarcoma with immature teratoid-like differentiation. At 14 months after surgery the patient had not experienced recurrence.

Key findings
  • The tumour showed heterogeneous histology with both carcinomatous and sarcomatous elements and teratoid features.
  • Microscopy identified immature squamous epithelial cells and immature epithelial glands; focal atypical fused glands consistent with endometrioid carcinoma were identified in the endometrium.
  • Differential diagnosis included extrarenal Wilms' tumour and teratocarcinosarcoma; final diagnosis was uterine carcinosarcoma with immature teratoid-like differentiation.
  • The patient underwent total abdominal hysterectomy with bilateral adnexectomy and received postoperative paclitaxel and carboplatin.
  • At 14 months after surgery the patient had not experienced recurrence.
Limitations: Single patient case report (n=1), so findings are not generalizable.; No control or comparator group.; Follow-up limited to 14 months as reported in the abstract; longer-term outcome unknown.; No quantitative outcome measures or statistical analysis reported in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

HER2 Oncogene as Molecular Target in Uterine Serous Carcinoma and Uterine Carcinosarcoma

Cancers · Aug 2023

uterine serous carcinomauterine carcinosarcoma

This is a review article summarizing clinical and preclinical evidence about HER2 as a molecular target in two rare uterine cancers (uterine serous carcinoma and uterine carcinosarcoma). The authors report that HER2 protein overexpression and/or ERBB2 gene amplification occurs in roughly 30–35% of uterine serous carcinoma and about 15–20% of uterine carcinosarcoma, and they describe ongoing clinical trials of HER2-targeting therapies. The review frames the need for targeted therapeutics because traditional platinum-based chemotherapy has low effectiveness and high rates of resistance and recurrence in these cancers.

Key findings
  • USC and UCS are rare histologic variants of uterine carcinoma with aggressive metastatic potential.
  • Traditional platinum-based chemotherapy has low effectivity and high rates of resistance and recurrence in USC and UCS.
  • HER2 protein overexpression and/or c-ERBB2 gene amplification ranges from ~30 to 35% in USC.
  • HER2 protein overexpression and/or c-ERBB2 gene amplification ranges from ~15 to 20% in UCS.
  • The review summarizes existing clinical and preclinical evidence and ongoing clinical trials of HER2-targeting therapeutics and highlights areas for further development.
Limitations: Narrative review — does not present new primary, patient-level data.; USC and UCS are rare diseases, implying limited and potentially small studies available for synthesis.; Abstract indicates ongoing clinical trials, so many clinical results may not yet be mature or available..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Browse all studies mentioning Uterine Carcinosarcoma

Where the evidence is

What has been studied, and how strong it is, by topic. A dashed cell means no studies were found for that combination — a gap, not evidence of no effect. Open a row to see its studies.

CompoundHuman evidenceMechanismSafetyTrial
Carboplatin111
Paclitaxel11
Trastuzumab Deruxtecan211
Ifosfamide11
Tamoxifen11
Trastuzumab-Deruxtecan (T-Dxd)1
Sacituzumab Govitecan1

Study mix

33 published studies by what they were done in. Lab and animal findings often do not carry over to people.

10 Human1 Animal22 Review/other
Reported directionReported positive11Mixed results9Inconclusive13

Compounds with reported-positive results in Uterine Carcinosarcoma

Where at least one study reported a positive result, shown with the full picture, not just the wins. Positive results are more likely to be published, and most of these are early lab or animal studies that may not translate to people. This reports what studies found, not what works.

Human evidence

Trastuzumab Deruxtecan2 positive2 human
Limitations: Retrospective, single-center design; Very small sample size (n=10); No control or comparator arm; Heterogeneous mix of gynecologic histologies; Heavily pre-treated population limits generalizability; Limited/absent reporting of safety or adverse event data in the abstract.
Cited positive studies (2)
Paclitaxel2 positive1 human
Limitations: Single patient case report (n=1), so findings are not generalizable.; No control or comparator group.; Follow-up limited to 14 months as reported in the abstract; longer-term outcome unknown.; No quantitative outcome measures or statistical analysis reported in the abstract.; Primary analysis was focused on uterine carcinosarcoma; ovarian carcinosarcoma results had limited precision.; The abstract reports noninferiority and superiority p-values but does not provide full confidence intervals for progression-free survival..
Cited positive studies (2)
Carboplatin2 positive1 negative/mixed1 human
Limitations: Single patient case report (n=1), so findings are not generalizable.; No control or comparator group.; Follow-up limited to 14 months as reported in the abstract; longer-term outcome unknown.; No quantitative outcome measures or statistical analysis reported in the abstract.; Primary analysis was focused on uterine carcinosarcoma; ovarian carcinosarcoma results had limited precision.; The abstract reports noninferiority and superiority p-values but does not provide full confidence intervals for progression-free survival..
Cited positive studies (2)
Limitations: Retrospective, single-center design; Very small sample size (n=10); No control or comparator arm; Heterogeneous mix of gynecologic histologies; Heavily pre-treated population limits generalizability; Limited/absent reporting of safety or adverse event data in the abstract.
Cited positive studies (1)
Ifosfamide1 positive1 human
Limitations: Primary analysis was focused on uterine carcinosarcoma; ovarian carcinosarcoma results had limited precision.; The abstract reports noninferiority and superiority p-values but does not provide full confidence intervals for progression-free survival.; Toxicity details are summarized only briefly in the abstract..
Cited positive studies (1)
Preclinical only: lab / animal (1)
Sacituzumab Govitecan1 positive1 animal
Limitations: Preclinical study; findings are from archival tissues, organoids, and mouse xenografts, not patients.; Only 2 xenograft models were tested.; No clinical outcomes, safety data, or survival data in humans were reported.; The abstract does not provide dosing details or treatment duration..
Cited positive studies (1)

Evidence at a glance: compounds studied in Uterine Carcinosarcoma

A deterministic grade of what published studies report for each: strength of evidence, the reported direction, and the largest credible effect, strongest-evidence first. This summarizes findings; it is not a claim that anything works.

CarboplatinHuman trial / meta-analysisMixed results1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: median OS 37 mo, p P < .01 for noninferiority, P > .1 for superiority, n=449 PMID 35007153 · median-survival values 1.8–37 across 7 studies

Most authoritative study: Randomized Phase III Trial of Paclitaxel and Carboplatin Versus Paclitaxel and Ifosfamide in Patients With Carcinosarcoma of the Uterus or Ovary: An NRG Oncology Trial

Findings conflict across studies · Effect sizes reported in only 2 of 3 studies.
PaclitaxelHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: median OS 37 mo, p P < .01 for noninferiority, P > .1 for superiority, n=449 PMID 35007153 · median-survival values 15–37 across 4 studies

Most authoritative study: Randomized Phase III Trial of Paclitaxel and Carboplatin Versus Paclitaxel and Ifosfamide in Patients With Carcinosarcoma of the Uterus or Ovary: An NRG Oncology Trial

Effect sizes reported in only 1 of 2 studies.
Trastuzumab DeruxtecanHuman trial / meta-analysisReported positive2 human

Includes human trial or meta-analysis evidence.

Largest credible effect: ORR by central review 54.5% [32.2–75.6], n=22 PMID 36977309 · median-survival values 5.4–13.3 across 4 studies

Most authoritative study: Real-world evidence of Trastuzumab Deruxtecan (T-DXd) Efficacy in HER2-expressing gynecological malignancies

IfosfamideHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: median OS 37 mo, p P < .01 for noninferiority, P > .1 for superiority, n=449 PMID 35007153 · median-survival values 15–37 across 4 studies

Most authoritative study: Randomized Phase III Trial of Paclitaxel and Carboplatin Versus Paclitaxel and Ifosfamide in Patients With Carcinosarcoma of the Uterus or Ovary: An NRG Oncology Trial

Based on a single study.
TamoxifenHuman · observationalInconclusive1 human

Human observational evidence only — no trials.

Largest credible effect: 1993 cluster cases 5 PMID 11578496 · effect sizes 2–16 across 7 studies

Most authoritative study: Is there an association between long-term tamoxifen treatment and the development of carcinosarcoma (malignant mixed Müllerian tumor) of the uterus?

Based on a single study.
Trastuzumab-Deruxtecan (T-Dxd)Human · observationalReported positive1 human

Human observational evidence only — no trials.

Largest credible effect: median PFS 5.4 mo [0.8–9.8], n=10 PMID 39639215 · effect sizes 1–5 across 3 studies

Most authoritative study: Real-world evidence of Trastuzumab Deruxtecan (T-DXd) Efficacy in HER2-expressing gynecological malignancies

Based on a single study.
Sacituzumab GovitecanAnimal onlyReported positive1 animal

Animal studies only — no human data.

Largest credible effect: Median IC50 in UCS PDOs 167.7 [51.4–3200], n=9 PMID 40344963 · effect sizes 90–167.7 across 2 studies

Most authoritative study: TROP2 expression and therapeutic targeting in uterine carcinosarcoma

No human studies yet · Based on a single study.

What the research shows for Uterine Carcinosarcoma

A plain-language summary of the reviewed studies OncoForge tracks for Uterine Carcinosarcoma. It reports what those studies described, not a claim that any compound or therapy helps or harms Uterine Carcinosarcoma. Most of this evidence is early, and findings often conflict.

  • Surgery with comprehensive staging remains the primary initial approach described across reviews, with multimodal adjuvant therapy commonly used afterwards.
  • Randomized clinical trial data that included uterine carcinosarcoma (often pooled with ovarian carcinosarcoma) report that paclitaxel+carboplatin was non-inferior to paclitaxel+ifosfamide and showed longer median overall survival in the uterine carcinosarcoma subgroup.
  • Molecular and biomarker studies consistently report frequent TP53 alterations and heterogeneous epithelial and mesenchymal tumor components; HER2 amplification/overexpression is present in a subset of cases and has been explored as a therapeutic biomarker.
  • Early-phase clinical data and small retrospective series report responses to the HER2-directed antibody–drug conjugate trastuzumab deruxtecan in HER2-expressing uterine carcinosarcoma, including in some HER2-low tumors, but these are small cohorts with limited follow-up.
  • Preclinical studies using patient-derived organoids and xenografts found most uterine carcinosarcoma samples expressed TROP2 and responded to the TROP2-targeting antibody–drug conjugate sacituzumab govitecan in laboratory models.

Compounds studied in Uterine Carcinosarcoma

Carboplatin2 studies
These studies report carboplatin most often used in combination with paclitaxel as adjuvant chemotherapy for uterine carcinosarcoma; a randomized phase III comparison (including uterine and ovarian carcinosarcoma) and reviews noted paclitaxel+carboplatin performed comparably or better than older ifosfamide-containing regimens, but much of the data come from combined histology trials and review summaries rather than large UCS-only trials.
Paclitaxel1 study
These studies report paclitaxel given with carboplatin was evaluated in a randomized phase III trial (uterine and ovarian carcinosarcoma) and, in the uterine carcinosarcoma subgroup, the paclitaxel+carboplatin arm met non-inferiority versus paclitaxel+ifosfamide with longer median overall survival reported; the evidence derives from combination regimens and mixed-site trials.
Ifosfamide1 study
These studies report paclitaxel+ifosfamide served as the comparator regimen in a randomized phase III trial of carcinosarcoma (uterine and ovarian), where paclitaxel+carboplatin was not inferior; conclusions about ifosfamide are therefore based on its role as the control arm within mixed-population trials.
Trastuzumab Deruxtecan2 studies
These studies report trastuzumab deruxtecan produced objective tumor responses in small clinical series and a phase II trial of HER2-expressing recurrent uterine carcinosarcoma (including both HER2-high and HER2-low cases), with reported progression-free and overall survival outcomes, but data are from early-phase, small-cohort, or single-center studies.
Trastuzumab-Deruxtecan (T-Dxd)1 study
These studies report trastuzumab deruxtecan (T-Dxd) activity was observed in small clinical and retrospective series of HER2-expressing gynecologic cancers including uterine carcinosarcoma, but the evidence is limited by small patient numbers, single-arm designs, and short follow-up.
Sacituzumab Govitecan1 study
These studies report sacituzumab govitecan showed activity in preclinical models of uterine carcinosarcoma (patient-derived organoids and xenografts) and most tumors had detectable TROP2, but the evidence is preclinical and has not been validated in clinical trials for this disease.

Supportive & alternative options discussed

  • Exercise / prehabilitation: Also discussed as a supportive option for people with uterine carcinosarcoma to help maintain physical function and quality of life during and after cancer-directed treatments.
  • Acupuncture: Also discussed as a supportive option for symptom management (for example, pain or treatment-related nausea) in people with gynecologic cancers including uterine carcinosarcoma.
  • Mind–body (MBSR / CBT): Also discussed as a supportive option to address psychological distress, coping, and quality of life for people with uterine carcinosarcoma.
  • Hyperthermia (heat): Also discussed as a supportive/adjunctive modality in some gynecologic oncology contexts, though not established by the studies summarized here for uterine carcinosarcoma.

What we don’t know yet

  • How generalizable are the randomized-trial findings to uterine carcinosarcoma specifically, since several trials pooled uterine and ovarian carcinosarcoma patients or reported subgroup analyses?
  • What are the optimal patient selection criteria, dosing, and sequencing for HER2-directed antibody–drug conjugates (including activity in HER2-low tumors) in uterine carcinosarcoma?
  • Can sacituzumab govitecan activity observed in preclinical models be replicated in clinical trials for uterine carcinosarcoma, and which biomarkers predict response?
  • What are the long-term outcomes, safety profiles, and comparative effectiveness of newer biomarker-directed therapies in larger, prospective uterine carcinosarcoma cohorts?
  • How do tumor heterogeneity and the biphasic epithelial/mesenchymal nature of UCS affect response to systemic and targeted therapies?
Overall, the evidence includes some randomized clinical data for chemotherapy combinations but much of the biomarker-directed and antibody–drug conjugate evidence is from small early-phase trials, retrospective series, or preclinical studies and therefore remains preliminary.

Clinical trials in Uterine Carcinosarcoma

13 ongoing · 25 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.

Completed
11 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Uterine Carcinosarcoma — advocacy, paying for treatment, second opinions, and caregivers.

If you’re struggling emotionally, you don’t have to wait.

Advocacy & community

No dedicated organization for this specific cancer is curated yet — these general organizations can help in the meantime.

Financial help

  • PAN FoundationCopay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell FoundationCopay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistanceLimited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family ReachHelp with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMedsSearchable directory of drug patient-assistance and discount programs. · status changes often — check the fund’s site
What you’ll typically need to apply
  • Your diagnosis and, if you have it, the specific drug/treatment name (from your care team).
  • Insurance details — your member ID card, or a note that you're uninsured (some funds require active insurance, some don't).
  • Proof of income and household size (recent pay stubs, a tax return, or a benefits letter) — most funds are income-based.
  • Your prescriber's contact information; some programs need the clinic to submit part of the application.
  • Apply early and re-check: funds open and close as money is available, so a closed fund may reopen.

General guidance — each program sets its own eligibility. Confirm requirements on the program’s site.

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