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Ovarian Epithelial Carcinoma

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

Research summary · reviewed
Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

Reviewed Jun 2026 · OncoForge editorial · How we review →

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Evidence at a glanceHuman trial / meta-analysisMixed results⚠ Studies disagree
25 published studies that name Ovarian Epithelial Carcinoma11 human studies approved & graded (trial, observational, or meta-analysis)16 human clinical studies in the Ovarian Epithelial Carcinoma corpus220 source documents in the Ovarian Epithelial Carcinoma corpus

last checked June 12, 2026

Why this grade?

Human trial / meta-analysis — Includes 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.

Guideline / FDA options - context-specific
  • bevacizumab
  • rucaparib
  • carboplatin
  • cisplatin
  • olaparib
  • doxorubicin
  • Gemcitabine
  • Relacorilant
Studied, not standard - investigational
  • primary cytoreductive surgery
  • neoadjuvant chemotherapy
  • PARP inhibitors
  • secondary cytoreductive surgery
  • Tumor Treating Fields
  • paclitaxel plus poldine
  • melphalan
  • endocrine therapy
  • taxane-platinum combination
  • surgery
  • lymphadenectomy
  • ?
  • CA125
  • ifosfamide plus etoposide
  • paclitaxel + epirubicin + cisplatin
  • gamma delta T cells
  • mifepristone
  • taxol
  • cisplatinum-cyclophosphamide
  • lobaplatin
  • paclitaxel
  • aspirin
  • cyclophosphamide and cisplatin
  • liposomal doxorubicin
  • oral metronomic chemotherapy
  • intraperitoneal chemotherapy
  • CYH33
  • anti-PD-1
  • humanized PDX model
  • carboplatin/paclitaxel
  • pegylated liposomal doxorubicin
  • imatinib
  • chemotherapy
  • radiotherapy
  • hormone therapy
  • anastrozole
  • checkpoint inhibitors
  • anlotinib
  • radiation therapy
  • hyperspectral imaging
  • platinum-based chemotherapy
  • targeted therapies
  • heat shock-conditioned OEC lysates
  • dendritic-cell-based immunotherapy
  • PGC1α
  • docetaxel and carboplatin
  • paclitaxel and cisplatin
  • p62/SQSTM1
  • miR-152
  • c-Fos
  • oxamflatin
  • AMHR2-CD
  • REG4
  • miR-106b
  • miR-490-3P
  • RhoC
  • TGF-β1 and VEGF
  • BIBF1120 and SB431542
  • oseltamivir phosphate
  • Snail and Slug shRNA
  • lysophosphatidic acid
  • paclitaxel, cisplatin, gemcitabine, 5-fluorouracil
  • RhoA siRNA and Wnt-5a siRNA
  • TCRγ9δ2(OT3)-Fc
  • resistin
  • RhoC siRNA
  • Lovastatin
  • Nesfatin-1
  • Ghrelin
  • CDR3δ-grafted γ9δ2T cells
  • HE4
  • Lewis y antigen
  • T-oligos
  • luteinizing hormone
  • psammoma bodies
  • EGFR
  • GST epitope fusion proteins
  • OT10 peptide
  • AdipoR1
  • platinum-based systemic chemotherapy
  • MICA
  • PON1
  • Essiac
  • surgical en bloc removal
  • radiotherapy and chemotherapy
  • platinum-based combination chemotherapy
  • platinum-based combination chemotherapy and embolization via the anterior branches of the bilateral internal iliac arteries
  • suramin
  • HMOCC-1
  • HIFU
  • MICA-reactive Vdelta1 gammadelta T cells
  • whole-abdominal radiotherapy
  • cisplatinum
  • genistein
  • adriamycin
  • Pc 4
  • FSH
  • membrane vesicles
  • telomerase determination
  • universal grading system
  • c-fms ribozyme
  • alpha2beta1-integrin
  • LHRH agonists
  • tumor necrosis factor-alpha
  • Lupron-SR
  • Photofrin II
  • Hexametilmelanine
  • abdominopelvic irradiation
  • interleukin 2
  • lymphokine-activated killer cells
  • CA 125
  • adriamycin and cis-platinum
  • melphalan and levamisole
  • paclitaxel liposome + carboplatin
  • short-course hypofractionated radiation therapy
  • 5-fluorouracil
  • cisplatin, etoposide, bleomycin
  • cisplatinum, cytoxan, adriamycin
  • carboplatin and etoposide
  • Oxaliplatin
  • siCXCR4
  • CD44v6-O-MWNTS
  • Niraparib †Rx
  • Tamoxifen
  • Topotecan

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Ovarian Epithelial Carcinoma.

Treatment map: Ovarian Epithelial Carcinoma

Open as a full page →

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.

133
Interventions
0
Standard of care
7
Tested in people
6
Lab / animal
112
Named in lit.
9
Classes
Standard of care (0) Guideline option (8) Tested in people (7) Lab / animal only (6) Named in the literature (112)

Tested in people, by trial phase: Phase III ×1 · Phase II ×2 · phase not reported ×4

Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
—
—
1
—
21
Radiotherapy
—
—
—
—
5
Chemotherapy
—
4
5
2
26
Targeted therapy
—
3
—
1
10
Immunotherapy
—
—
—
—
10
Hormonal therapy
—
—
—
2
5
Repurposed drugs
—
—
—
—
7
Supplements & natural agents
—
—
—
—
1
Other
—
1
1
1
27

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.

Established care — detail (8)
Chemotherapy
carboplatin
FDA-approved for this cancer.
—Guideline option
cisplatin
FDA-approved for this cancer.
—Guideline option
doxorubicin
FDA-approved for this cancer.
—Guideline option
Gemcitabine
FDA-approved for this cancer.
—Guideline option
Targeted therapy
bevacizumab
FDA-approved for this cancer.
—Guideline option
rucaparib
FDA-approved for this cancer.
—Guideline option
olaparib
FDA-approved for this cancer.
—Guideline option
Other
Relacorilant
FDA-approved for this cancer.
—Guideline option
Investigational & adjunct compounds — detail (125)
Phase III trial (1)
Tumor Treating Fields
Phase II trial (2)
ifosfamide plus etoposidepaclitaxel + epirubicin + cisplatin
Tested in people (4)
CA125cisplatinum-cyclophosphamidemelphalanpaclitaxel plus poldine
Named in the literature
primary cytoreductive surgeryneoadjuvant chemotherapyPARP inhibitorssecondary cytoreductive surgeryendocrine therapytaxane-platinum combinationsurgerylymphadenectomy?gamma delta T cellsmifepristonetaxollobaplatinaspirincyclophosphamide and cisplatinoral metronomic chemotherapyintraperitoneal chemotherapyCYH33anti-PD-1humanized PDX modelcarboplatin/paclitaxelpegylated liposomal doxorubicinimatinibchemotherapyradiotherapyhormone therapycheckpoint inhibitorsanlotinibradiation therapyhyperspectral imagingplatinum-based chemotherapytargeted therapiesheat shock-conditioned OEC lysatesdendritic-cell-based immunotherapyPGC1αdocetaxel and carboplatinpaclitaxel and cisplatinp62/SQSTM1miR-152c-FosoxamflatinAMHR2-CDREG4miR-106bmiR-490-3PRhoCTGF-β1 and VEGFBIBF1120 and SB431542oseltamivir phosphateoff-labelSnail and Slug shRNAlysophosphatidic acidpaclitaxel, cisplatin, gemcitabine, 5-fluorouracilRhoA siRNA and Wnt-5a siRNATCRγ9δ2(OT3)-FcresistinRhoC siRNALovastatinoff-labelNesfatin-1GhrelinCDR3δ-grafted γ9δ2T cellsHE4Lewis y antigenT-oligosluteinizing hormonepsammoma bodiesEGFRGST epitope fusion proteinsOT10 peptideAdipoR1platinum-based systemic chemotherapyMICAPON1Essiacsurgical en bloc removalradiotherapy and chemotherapyplatinum-based combination chemotherapyplatinum-based combination chemotherapy and embolization via the anterior branches of the bilateral internal iliac arteriessuraminHMOCC-1HIFUMICA-reactive Vdelta1 gammadelta T cellswhole-abdominal radiotherapycisplatinumgenisteinadriamycinPc 4FSHmembrane vesiclestelomerase determinationuniversal grading systemc-fms ribozymealpha2beta1-integrinLHRH agoniststumor necrosis factor-alphaLupron-SRPhotofrin IIHexametilmelanineabdominopelvic irradiationinterleukin 2lymphokine-activated killer cellsCA 125adriamycin and cis-platinummelphalan and levamisolepaclitaxel liposome + carboplatinshort-course hypofractionated radiation therapy5-fluorouracilcisplatin, etoposide, bleomycincisplatinum, cytoxan, adriamycincarboplatin and etoposideOxaliplatinsiCXCR4CD44v6-O-MWNTS

"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.

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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.

Overview102 points
  • Epithelial ovarian carcinoma studies in these sources describe biomarkers and signaling features linked to malignant potential, invasion, and prognosis. [1][2][3]3 sources
  • Ovarian epithelial carcinoma is described in the sources as a cancer for which advanced-stage chemotherapy regimens and estrogen-receptor studies have been reported. [4][5][6]3 sources
  • Ovarian epithelial carcinoma can present with unusual metastatic sites, including a cystic mediastinal mass, skin metastases, and choroidal metastasis. [7][8][9]3 sources
  • The sources discuss epithelial ovarian cancer (EOC) and epithelial ovarian neoplasms (EON) as related epithelial ovarian tumor categories. [10][11]
  • Epithelial ovarian cancer is described as the most common subtype of ovarian malignancy, accounting for over 95% of ovarian malignancies. [12][13]
  • Standard treatment for epithelial ovarian cancer involves cytoreductive surgery and platinum/taxane chemotherapy. [12][14]
  • PARP inhibitors are described as molecularly targeted treatments for ovarian cancer and as having improved progression-free survival in epithelial ovarian cancer. [14][12]
  • Ovarian epithelial carcinoma is described as the most common ovarian malignancy and as a heterogeneous disease with several histologic subtypes. [15][16]
  • Even with standard ovarian cancer cytoreductive surgery and chemotherapy, one review states that the 5-year survival rate is still lower than 30% due to drug resistance and relapse. [17][18]
  • A review states that the 5-year survival rate for all stages of ovarian cancer has been estimated to be 35–38%. [19][20]
  • One source states that ovarian cancer remains the deadliest gynecological malignancy, and describes high-grade serous carcinomas as usually presenting at advanced stages. [21][22]
  • Epithelial ovarian cancer is described as the fourth leading cause of death for women in the United States and the highest death rate of all gynecological cancer. [23][18]
  • The sources describe a dualistic model of ovarian carcinogenesis with type I and type II tumors. [16][24]
  • Ovarian epithelial carcinoma is the most common ovarian cancer histology, and high-grade serous histology is the most common type. [25]
  • The goal of treatment is to increase overall survival and progression-free survival, without a significant impact on quality of life. [25]
  • Ovarian and tubal cancers are described as lethal gynecological cancers, and more than half of patients are diagnosed at an advanced stage. [26]
  • Epithelial ovarian cancer is a heterogeneous group with eight histologic subtypes according to World Health Organization classification. [27]
  • Ovarian clear cell carcinoma accounts for 3%-10% of epithelial carcinoma. [27]
  • Ovarian epithelial carcinoma is described as the most common ovarian neoplasm type and the most lethal. [28]
  • One review states that ovarian epithelial carcinoma is diagnosed mainly during the perimenopause. [28]
  • One review states that 64% of ovarian cancer cases are diagnosed between ages 41 and 60 years. [28]
  • Ovarian cancer is often diagnosed at advanced stages; one review states that more than 70% of patients are diagnosed at advanced stages due to nonspecific symptoms and a lack of effective early detection methods. [29]
  • One source states that ovarian cancer prognosis is typically poor because it is often diagnosed at late stages, when curative treatment options are limited. [30]
  • The sources describe ovarian clear cell carcinoma as a distinct biological and clinical entity within ovarian cancer. [31]
  • In children and adolescents, epithelial ovarian tumors are described as rare and are said to occur mainly after menarche, primarily in adolescents older than 15 years. [11]
  • Epithelial ovarian cancer encompasses five major histotypes: high-grade serous, low-grade serous, clear cell, endometrioid, and mucinous. [32]
  • The review states that epithelial ovarian cancer is the most lethal form of gynecologic cancer. [32]
  • The review states that epithelial ovarian cancer is a heterogeneous group of diseases with distinct genomic features. [33]
  • The review states that low-grade serous carcinoma has a more indolent nature and milder biological behavior than high-grade serous carcinoma. [34]
  • The Manitoba review states that older patients are often treated similarly to younger patients, but evidence for the best treatment in older patients is limited. [32]
  • The clinical benefit of available treatments is described as limited, and 5-year survival rates for ovarian cancer are reported to remain below 50% after diagnosis. [12]
  • Ovarian cancer is described as one of the most common female cancers worldwide. [35]
  • One review states that ovarian cancer is the number eight cause of cancer-related mortality in women worldwide. [36]
  • One review describes ovarian cancer as the third deadliest gynecological cancer among women. [37]
  • Ovarian cancer is often asymptomatic and is generally diagnosed at an advanced stage. [38]
  • Most tumors initially respond to standard treatments combining surgery and platinum-based chemotherapy. [38]
  • Novel second line treatments and maintenance therapies such as PARP inhibitors and anti-angiogenic antibodies are reported to permit an improvement in survival and patient welfare. [38]
  • Frequent recurrence, subsequent acquired chemoresistance, and widespread dissemination are reported as reasons for poor overall survival. [38]
  • More than 85% of ovarian carcinomas are ovarian epithelial carcinoma. [39]
  • Advanced stage epithelial ovarian cancer is usually incurable. [40]
  • The 2020 review states that overall survival of epithelial ovarian carcinoma has improved significantly during the past several decades with local and systemic chemotherapy, radiation therapies and surgical resection of primary tumors. [39]
  • Ovarian epithelial carcinoma is described as a highly aggressive ovarian tumor and the most frequent ovarian-associated tumor, representing about 85-90% of ovarian tumor diagnoses. [41]
  • One review states that the overall survival at 5 years is 45%, decreasing to 27% in advanced stages of ovarian epithelial carcinoma. [41]
  • Ovarian epithelial cancer is described as the second most common gynecologic malignancy. [42]
  • It is often found in advanced stages and is described as having an insidious onset with no early symptoms. [42]
  • About 75% of epithelial ovarian cancer patients are diagnosed at an advanced stage (III or IV) in one review. [17]
  • Ovarian epithelial carcinoma consists of four histologically distinct subtypes: serous, mucinous, endometrioid, and clear cell. [43]
  • One review states that ovarian epithelial carcinoma has the worst prognosis of all gynecological malignancies. [43]
  • A review states that approximately 60% of ovarian cancers are diagnosed at late stages. [44]
  • A review states that ovarian epithelial carcinoma is the leading cause of deaths from gynecologic malignancy. [45]
  • A review states that epithelial ovarian cancer accounts for about 90% of ovarian cancer. [20]
  • Ovarian epithelial carcinoma is described in the sources as a heterogeneous disease with at least two distinct pathogenesis types, type I and type II, with different molecular profiles. [21]
  • Type I tumors include endometrioid, clear-cell carcinoma, and low-grade serous carcinoma and mostly arise via a defined sequence from endometriosis or borderline serous tumors. [21]
  • Type II carcinomas are usually high-grade serous tumors, and recent evidence suggests that the majority arise from the fimbriated end of the fallopian tube. [21]
  • The causal agents for sporadic ovarian cancers are described as relatively unknown. [23]
  • Patients with ovarian cancer are described as having low 5-year survival and frequent recurrences with rapid metastases to the peritoneal cavity. [46]
  • Ovarian epithelial carcinoma is described as a common malignant ovarian neoplasm with poor five-year survival rate. [47]
  • More than 90% of ovarian cancers are classified as epithelial. [48]
  • Some sources state that ovarian epithelial carcinoma may arise from the ovarian epithelium, while others state that the fallopian tube inner surface epithelium may also be the origin of some ovarian cancers. [48]
  • Ovarian epithelial carcinoma is described in the sources as a lethal gynecologic cancer that is often diagnosed at advanced stages. [49]
  • Ovarian epithelial carcinoma is described as a heterogeneous malignancy with diverse histological phenotypes and genetic and epigenetic aberrations. [50]
  • One review states that ovarian cancer causes the highest rates of mortality among tract malignancies in women and that early-stage diagnosis is inadequate. [51]
  • A review states that ovarian carcinoma is often diagnosed late, after spread into the peritoneal cavity. [52]
  • A review states that lesions derived from the surface epithelium of the ovary account for 80–90% of cases. [52]
  • Type I tumors are described as low-grade serous, mucinous, and endometrioid cancers that commonly arise from genetically stable precursor lesions and have a relatively indolent clinical course. [16]
  • Type II carcinomas are described as originating de novo from the adnexal epithelia and having aggressive biologic behavior. [16]
  • Ovarian carcinomas are the most common form of ovarian cancer, and ovarian epithelial carcinoma includes serous, clear cell, endometrioid, and mucinous histological subtypes. [53]
  • Type I ovarian tumors include low-grade serous, mucinous, endometrioid, malignant Brenner, and clear cell carcinoma, while type II tumors include high-grade serous carcinoma, malignant mixed mesodermal tumors, and undifferentiated carcinoma. [53]
  • Type I tumors typically present as early stage neoplasms that may last more than 20 years, while type II tumors present as late stage, high grade neoplasms that are clinically aggressive and associated with a poor prognosis. [53]
  • Type II tumors are relatively chemosensitive in comparison to type I tumors. [53]
  • Serous tumors are the most common form of ovarian carcinoma and carry the poorest prognosis. [53]
  • Ovarian epithelial carcinoma cells were reported to synthesize and secrete interleukin-10, which the source says probably assists in promoting the development and progression of ovarian carcinoma. [54]
  • Treatment of ovarian epithelial carcinoma was described as often taking place in a metastatic setting because the disease is often not detected until later stages. [55]
  • Brain metastases from ovarian cancer were described as rare in the source. [56]
  • Ovarian epithelial carcinoma is described as the most common form of ovarian cancer in one source. [57]
  • One source states that ovarian carcinoma is one of the most common gynecologic cancers and has the worst prognosis since current therapies are not sufficiently effective at achieving and maintaining remission. [58]
  • One study reported that MICA was expressed on ovarian tumor tissues and that MICA-reactive Vdelta1 gammadelta T cells might serve as a candidate for adoptive cellular therapy of tumors. [59]
  • One study reported that down-regulation of PRA is associated with the development of ovarian epithelial carcinoma. [60]
  • Histopathologic grade of ovarian epithelial carcinoma has generally been found to be of prognostic significance, and histopathologic typing is less valuable in predicting survival but better at predicting tumor responsiveness to chemotherapy. [61]
  • Follicle-stimulating hormone receptor expression was found in 60% of carcinomas in one study of ovarian epithelial tumors. [62]
  • Angiogenesis as assessed by microvessel counts was more intense in stage I invasive ovarian epithelial carcinoma than in stage I low-malignant-potential epithelial carcinoma. [63]
  • Epithelial ovarian carcinoma is described as the leading cause of gynecologic cancer death in one review. [64]
  • Metastatic dissemination of epithelial ovarian carcinoma occurs primarily through exfoliation of cells from the primary tumor, with subsequent implantation, invasion, and growth throughout the organs within the peritoneal cavity. [65]
  • Epithelial ovarian carcinoma is characterized by widespread intra-abdominal metastases mediated primarily by surface shedding of tumor cells and peritoneal implantation. [64]
  • The etiology of epithelial ovarian cancer is probably multifactorial, and genetic, environmental, hormonal, and viral factors appear to be directly or indirectly related to the development of the disease. [66]
  • No screening tests are consistently accurate enough to detect ovarian cancer at an early stage. [66]
  • Ovarian epithelial carcinoma is described in these sources as a cancer in which surgery is used for staging and tumor removal in most cases. [67]
  • CA 125 is described as a marker that may be more useful for monitoring response to treatment and long-term follow-up than for diagnosis. [68]
  • The sources report that ovarian cancer risk was increased in women with a family history of breast, uterine, or ovarian cancer in a mother or sister, and decreased in women who had experienced a livebirth, an induced abortion, or permanent sterilization by tubal ligation. [69]
  • Ovarian mucinous cystadenocarcinoma is described as a rare subtype of ovarian epithelial cancer. [70]
  • Brain metastasis is described as an uncommon but increasing manifestation of ovarian epithelial carcinoma. [71]
  • Cutaneous involvement is reported as uncommon in epithelial ovarian carcinoma metastases. [72]
  • Histopathologic classification of ovarian epithelial carcinoma and its variants may have an increasing role in management. [73]
  • A 1993 review describes a postmenopausal patient with serous papillary cystadenocarcinoma of the ovary associated with large abscess formation and estrogen production. [74]
  • The review states that ovarian cancer accompanied by stromal function is an occasional event, and large abscess association is a rarity. [74]
Show 7 lab & early-research findings
  • Human ovarian epithelial carcinoma has been studied in animal models and surgical series, including stage I disease and heterotransplanted cell lines. [75][76][77]3 sources
  • Ovarian epithelial carcinoma tissues in one study showed overexpression of VEGF, VEGFRs, and activated STAT3 and STAT5. [78]
  • One study found that MMP-2 and MMP-9 were frequently overexpressed in ovarian cancer cells disseminated in the peritoneal cavity. [79]
  • Shed membrane vesicles carrying tumor-associated antigen alpha-Folate Receptor, MMP-9, MMP-2, and uPA were observed in ovarian carcinoma patient fluids and in an ovarian cancer cell line. [80]
  • FSH showed a dose-response effect on ovarian epithelial carcinoma cell lines, and the growth-stimulating effects of FSH could be blocked by simultaneous LH administration. [62]
  • Photodynamic therapy with Pc 4 in OVCAR-3 xenografts produced complete responses in some treated mice, while control tumors continued to grow. [81]
  • Adriamycin and meso-chlorin e6 monoethylene diamine photodynamic therapy acted cooperatively in vitro against OVCAR-3 cells, and HPMA copolymer-bound adriamycin and HPMA copolymer-bound Mce6 also inhibited growth in vitro. [82]
Epidemiology62 points
  • Approximately 75% of ovarian cancers are diagnosed at advanced stages IIIC-IV FIGO, and one review reports that 75% of epithelial ovarian carcinoma cases were diagnosed at advanced stage (stage III/IV). [25][15]
  • The review reports that the 5-year survival rate was 20–39%, and another review reports that survival rates for women with advanced disease range from 20%–30%, while those for women with early stage disease range from 70%–90%. [15][42]
  • The reported annual number of ovarian cancer cases in Colombia is 1,445. [25]
  • In Korea, the proportion of ovarian clear cell carcinoma was 11.6% of epithelial ovarian cancer. [27]
  • In the UKCTOCS trial, 2055 women developed ovarian or tubal cancer among 202,562 analyzed participants at a median follow-up of 16.3 years. [26]
  • One review states that ovarian epithelial carcinoma develops primarily during the perimenopause, and another reports that 64% of ovarian cancer cases are diagnosed between ages 41 and 60 years. [28]
  • In one Taiwan subset study of stage III or IV high-grade serous ovarian cancer, high-grade endometrioid ovarian cancer, primary peritoneal cancer, and fallopian tube cancer, the median age was 60.0 years and 72.1% of patients had FIGO stage III disease. [83]
  • One review states that ovarian malignancies account for less than 1% of all pediatric and adolescent tumors. [11]
  • The pediatric series reported that 8 of 116 ovarian masses were epithelial ovarian neoplasms, and the median age at diagnosis was 17 years. [11]
  • The Manitoba review estimates 3,100 new epithelial ovarian cancer diagnoses and 1,950 deaths in Canada in 2023. [32]
  • The Manitoba review estimates a 5-year overall survival of 44% for epithelial ovarian cancer in Canada. [32]
  • The Manitoba review states that the risk of developing epithelial ovarian cancer increases with age until a plateau of 0.4% per decade starting at age 70. [32]
  • The Manitoba review states that in the United States, the median age at diagnosis is 63 and people over 65 account for 45% of diagnoses and 65% of deaths. [32]
  • The Netherlands LGSC study reports a crude incidence rate of 0.33 to 0.80 per 100,000 person-years and an annual European standardized incidence rate of 0.29 to 0.63 per 100,000 person-years. [34]
  • One review states that ovarian cancer afflicts approximately 20,000 women per year in the United States. [14]
  • One review estimates ovarian cancer incidence at 222,500 cases per year and deaths at about 140,200 per year worldwide. [35]
  • Another review reports an incidence of 314,000 and mortality of 207,000 in 2020. [36]
  • One review states that 80%–90% of ovarian tumors are sporadic and the rest are hereditary. [37]
  • Ovarian cancer was reported as the second leading cause of death among patients with gynecologic tumors worldwide in 2020. [38]
  • Among gynecologic cancers, endometrial carcinoma was described as the most common tumor related to Lynch syndrome, followed by ovarian cancer. [84]
  • The cumulative lifetime risk of ovarian cancer in Lynch syndrome was reported as 6–12%. [84]
  • Ovarian clear cell carcinoma was described as the second reported subtype of ovarian epithelial carcinoma closely related to Lynch syndrome. [84]
  • In 2018, ovarian cancer caused 184,799 deaths and 295,414 new cases were diagnosed worldwide. [39]
  • One review states that ovarian epithelial carcinoma has a mortality of 4.5 deaths per 100,000 inhabitants. [41]
  • One review states that ovarian cancer-related hypercalcemia is rare and that data on its incidence are unavailable. [85]
  • In one review, the reported yearly incidence of malignancy-associated hypercalcemia was 1.46%–2.74%. [85]
  • One source states that ovarian cancer is the second leading cancer in women and the fifth leading cause of cancer-related deaths in women. [22]
  • Higher numbers of lifetime ovulations are described as one risk factor for ovarian cancer, and reactive oxygen species generated by inflammatory cells at sites of ovulation have been suggested to lead to DNA mutations increasing cancer risk. [23]
  • In one study, the lower expressing A allele was associated with a small reduction in risk that did not reach statistical significance. [23]
  • One source states that ovarian cancer is one of the most common causes of death from all cancers among women and the leading cause of death from gynecological malignancies. [47]
  • Another source states that ovarian carcinoma is the fourth most common cause of cancer death among women in the United States and the 12th most common cause of cancer death among women in China. [47]
  • The same source states that mortality is more than 70% within five years. [47]
  • Patients with endometriosis-associated ovarian cancer were younger and more likely to be premenopausal at diagnosis than patients with non-endometriosis-associated ovarian cancer. [86]
  • Patients with endometriosis-associated ovarian cancer had lower preoperative serum CA125 and were more likely to have a normal CA125 level. [86]
  • In the same series, endometriosis-associated ovarian cancer was identified at an earlier stage and showed overrepresentation of clear cell and endometrioid carcinoma. [86]
  • Serum miR-92 was significantly higher in patients with epithelial ovarian carcinoma than in controls in a study of 50 patients and 50 controls, and it showed significant correlations with regional lymph node involvement and clinical stage of the tumour. [87]
  • RhoC mRNA and protein expression was significantly higher in ovarian carcinoma than in benign tumors and normal ovary tissue. [88]
  • One review states that ovarian cancer is the 6th most common cancer among women. [89]
  • A review states that the 5-year survival rate is only 20–30%. [52]
  • The review notes that accurate diagnosis is often not made until the disease has progressed into more advanced stages. [18]
  • Ovarian cancer is described as the leading cause of death among all gynecological cancers in the United States and the sixth leading cause of all cancer deaths among women. [90]
  • One source states that ovarian epithelial carcinoma causes more deaths than any other cancer in women with gynecologic malignancies in the United States. [57]
  • A clear trend of decreasing risk was reported with increasing number of pregnancies, deliveries, use of oral contraceptives, and duration of breast feeding. [66]
  • An increased risk was reported with ovarian dysfunction leading to infertility and exposure to asbestos and talc. [66]
  • The possible increased risk in infertile women who used fertility drugs was described as needing careful examination because of the small number of patients and limited information about infertility type, drugs, dosage, and duration. [66]
  • In the same study, risk was decreased in women who had experienced a livebirth, an induced abortion, or permanent sterilization by tubal ligation. [69]
  • The study inferred that ovarian cancer patients had a genetic predisposition and dysfunctional ovaries. [91]
  • Gonadal dysfunction was suggested as a possible factor that could facilitate pituitary gonadotropin activity and increase the incidence of the disease experimentally. [91]
  • Ovarian mucinous cystadenocarcinoma accounts for 3-5% of ovarian epithelial cancers. [70]
  • Cutaneous involvement is the presenting symptom in 40% of all metastatic ovarian malignancies. [72]
  • Skin metastases from ovarian carcinoma are rarely reported. [8]
  • Malignant ovarian neoplasms derived from ovarian epithelium that produce estrogen are rare among postmenopausal women. [92]
  • Choriocarcinoma within an ovarian carcinoma is exceptionally rare. [73]
  • In SEER data, the incidence of ovarian clear cell carcinoma in epithelial ovarian cancer differed by ethnicity, with 4.8% in whites, 3.1% in blacks, and 11.1% in Asians. [27]
  • In that same Taiwan cohort, 91.2% of patients had high-grade serous histology. [83]
  • In a gynecologic MRI observational study, 43.40% of pelvic masses were ovarian masses. [93]
  • In one cohort of 52 patients with epithelial ovarian cancer, the median age was 56 years, the age range was 34 to 80 years, clinical stage ranged from I to IV with most cases in stage III or IV, and the median preoperative CA125 value was 715.5 IU/ml. [12]
  • In one cohort of 176 primary ovarian clear cell carcinomas, 10 cases had deficient mismatch repair. [84]
  • In one retrospective series of 226 patients with epithelial ovarian cancer, 17 had endometriosis-associated ovarian cancer and 209 had non-endometriosis-associated ovarian cancer. [86]
  • In one case-control study, ovarian epithelial carcinoma risk was increased in single women and in women with a family history of breast, uterine, or ovarian cancer in a mother or sister. [69]
  • In one case-control study, blood group A, never marrying or marrying late in life, more frequent surgery for retroflexion of the uterus, less use of contraceptive appliances, and less daily use of cosmetics were significantly more common among cases than controls. [91]
Show 1 lab & early-research finding
  • The mean ages at diagnosis of ovarian carcinoma and subsequent brain metastases were 58.7 and 62.8 years, respectively, in a 13-case series. [71]
Key biomarkers124 points
  • TP53 was the most frequently mutated gene in two ovarian cancer cohorts described in the sources. [12][14]
  • c-Ets1 was not detected in benign ovarian cystadenoma and was significantly associated with clinical stage, histological grade, clinical outcome, and poor prognosis in epithelial ovarian cancer. [1][2]
  • In patients with germline BRCA1 mutation, the absolute risk of developing epithelial ovarian carcinoma is 39% to 58%, and for BRCA2 it is 13% to 29%. [25]
  • Knowledge of a germline mutation in ovarian neoplasia may provide predictive and prognostic information for selecting targeted therapies and for family counseling. [25]
  • In the endocrine-therapy study, more than 80% of high-grade serous or endometrioid ovarian carcinomas expressed hormone receptors, particularly estrogen receptor alpha, and hormonal receptors were positive in 52 of 53 tumors with available testing. [94]
  • In the endocrine-therapy review, the National Comprehensive Cancer Network guidelines version 3.2012 classified endocrine therapy as “other potentially effective drugs” for recurrent epithelial ovarian cancer. [94]
  • Survivin expression was reported to be associated with PCNA-labeling index, clinical stage, histological grade, clinical outcome, and survival rate in epithelial ovarian carcinoma. [95]
  • Nrf2 and p16 were associated with worse prognosis in univariate analysis, and FIGO stage and Nrf2 remained significant prognostic factors in multivariate analysis. [96]
  • One study found no aromatase activity in two mucinous cystadenocarcinoma specimens or in SK-OV-3 cells, and no aromatase mRNA in three mucinous cystadenocarcinoma specimens, one serous cystadenocarcinoma specimen, or SK-OV-3 cells. [97]
  • One study found a nm23-H2 mutation in 1 of 35 ovarian carcinomas and no nm23 mutation in the benign or low malignant potential tumors studied. [98]
  • In one review, HRD-positive status was defined by deleterious BRCA1/2 mutations and/or LOH positivity. [83]
  • In a 48-patient review, initial CA 125 showed a high correlation with progesterone plasma concentration, and CA 125 and progesterone both decreased during chemotherapy and increased 1 to 4 months before recurrence. [99]
  • The review also stated that progesterone and CA 125 together predicted all recurrences but neither factor alone did. [99]
  • A 2025 review reports that higher chemical complementarity between certain EBV epitopes and IGH CDR3 amino acid sequences was linked to better outcomes in ovarian cancer. [100]
  • In the FIGO stage IA imaging series, the median CA125 level was 65.6 U/ml. [10]
  • In the OCCC machine-learning study, CA125, grade, surgery, T stage, residual tumor volume, N stage, laterality, and tumor size were selected as important variables for the model. [33]
  • The OCCC study reports that CA125 was lower in patients with distant metastasis than in those without distant metastasis. [33]
  • The clear cell carcinoma cytology review states that positive cytology in low-stage cases has prognostic implications and can upstage disease to at least FIGO 1C3. [101]
  • In a large high-grade epithelial ovarian cancer cohort, BRCA1 and BRCA2 mutations were associated with better progression-free survival than BRCA1 and BRCA2 wild-type. [14]
  • In that cohort, AKT2 amplification was associated with shortened progression-free survival. [14]
  • In the same cohort, NOTCH3:MET:PIK3R1:AKT2:PIK3CA alterations were associated with worse progression-free survival, while ATRX:NF2 alterations were associated with better progression-free survival. [14]
  • In the same cohort, MET:NOTCH3:CREBBP:ATR alterations were associated with poor overall survival. [14]
  • CA-125 is reported to have increased serum levels in about 80% of ovarian epithelial cancers. [35]
  • HE4 is described as a serum marker that increases in ovarian cancers and is reported to be as sensitive as CA-125 but more specific in the diagnosis of ovarian tumors. [35]
  • In one study, serum CA-125, HE4, and ROMA were all significantly higher in malignant ovarian tumors than in benign or borderline tumors. [35]
  • In advanced high-grade epithelial ovarian cancer, wb_MTV and wb_TLG were significantly correlated with serum CA125 and HE4 concentrations, and the strongest correlation in that study was between HE4 and wb_MTV40. [102]
  • Loss of ARID1A expression was more frequent in dMMR ovarian clear cell carcinoma than in intact MMR ovarian clear cell carcinoma. [84]
  • The most frequently absent mismatch repair protein in dMMR cases was MSH2/MSH6, followed by MLH1/PMS2, with one case showing isolated loss of MSH6. [84]
  • The 2020 lncRNA study reports that TONSL-AS1 was significantly higher in EOC tissues than in non-tumor tissues, and high TONSL-AS1 level group experienced significantly lower overall survival than the low TONSL-AS1 level group. [39]
  • The review on differential gene expression reports 12 genes were significantly up-regulated in malignant tissues and 13 hub genes showed evident differences in prognosis. [103]
  • Sema4C expression was significantly higher in ovarian epithelial carcinoma tissues than in benign tumors, borderline epithelial tumors, and normal ovarian tissues, and was significantly associated with the clinical and pathological stages of tumors. [104]
  • An immunoprofile defined by HNF1β+/p53+/ARID1A+ was reported to be associated with significantly worse overall survival and progression-free survival in advanced ovarian epithelial carcinoma, and the immunophenotype HNF1β+/p53+/ARID1A+ and clinical stage were reported as significant and independent prognostic factors for overall survival and progression-free survival. [105]
  • The review on PET/CT states that limited evidence suggests PET/CT accuracy in preoperative staging, investigating recurrence, and predicting optimal secondary debulking in epithelial ovarian cancer. [106]
  • CD109 expression was detected in 63 of 120 ovarian epithelial cancer samples in one study. [42]
  • In one review, miR-152 was reported to be significantly downregulated in epithelial ovarian cancer specimens and three ovarian cancer cell lines, and higher miR-152 expression indicated a better overall survival rate in patients with epithelial ovarian cancer. [107]
  • A review states that CA125 is a predictive marker for epithelial ovarian cancer that becomes increasingly sensitive with proximity to diagnosis. [108]
  • A review states that HE4 similarly predicts epithelial ovarian cancer and is used clinically in women with a pelvic mass. [108]
  • A review states that HE4 is more specific than CA125 in women with benign tumors. [108]
  • A review states that both CA125 and HE4 show promise as risk and early detection markers. [108]
  • A review states that LEFTY expression was significantly higher in ovarian clear cell carcinoma than in other histological subtypes of ovarian epithelial carcinoma, and that the expression of both LEFTY1 and LEFTY2 mRNAs was significantly higher in ovarian clear cell carcinoma compared with non-clear-cell ovarian epithelial carcinoma. [43]
  • A review states that LEFTY scores were not associated with overall survival, progression-free survival, clinical stage, or lymph node metastasis in the ovarian clear cell carcinoma cases studied. [43]
  • A review states that miR-106b expression was significantly lower in ovarian carcinomas and borderline tumors than in normal ovarian tissues and benign tumors, and was negatively associated with FIGO stage and differentiation in ovarian carcinoma. [20]
  • MiR-490-3P expression was reported to be significantly lower in ovarian carcinoma and borderline tumors than in benign tumors, and lower in metastatic ovarian carcinoma omentum than in primary ovarian carcinoma, and was negatively associated with differentiation and FIGO staging. [109]
  • Beclin 1 expression was reported to be higher in ovarian borderline tumor and carcinoma than in normal ovary and benign tumor, inversely linked to differentiation, and associated with lower Ki-67 expression and higher cumulative or relapse-free survival rate of ovarian carcinoma. [110]
  • ANXA2 and Lewis y antigen were reported to be significantly higher in ovarian cancer tissues, and their expression patterns were closely correlated. [111]
  • Prohibitin expression showed a trend of gradual loss from benign ovarian tumors to borderline tumors and to carcinomas, and was inversely correlated with cancer grade. [112]
  • RhoC mRNA and protein were reported to be significantly higher in ovarian cancer and correlated with clinicopathological staging. [22]
  • MPO is robustly expressed in a subset of ovarian carcinoma cells. [23]
  • CYR61 expression was significantly higher in ovarian epithelial carcinoma tissue than in benign ovarian tissue in one study, and protein CYR61 levels were associated with lymph node metastases and clinical disease stage. [113]
  • CXCR4 proteins were detected in the cell membrane and cytoplasm of CAOV3 and SKOV3 ovarian cancer cells in one study. [114]
  • The review states that CXCL12 was detected in the ascites of 63 patients in a previous ovarian cancer study. [114]
  • Sources describe PAX8 as highly expressed in ovarian carcinomas and serous effusions; one study reported PAX8 staining in 99% of high-grade serous ovarian carcinomas and 100% of low-grade ovarian carcinomas and serous borderline tumors, and another found PAX8 was stained in none of the breast and almost all ovarian cancer samples. [115]
  • CA-125 is described as the most common marker used in monitoring therapy of this disease, but it is not specific and sensitive enough to be useful as a screening test. [115]
  • RhoA and Wnt-5a expression were positively associated with FIGO stage and degree of differentiation in ovarian carcinoma, and RhoA mRNA expression was significantly positively correlated with Wnt-5a mRNA expression in ovarian carcinoma. [48]
  • The sources describe RhoC as a biomarker for differentiation and progression of ovarian carcinoma. [88]
  • The sources describe serum miR-92 as a possible new tumor biomarker for diagnosis and assessment of prognosis in epithelial ovarian carcinoma. [87]
  • hTERT protein expression was reported in ovarian cystadenocarcinoma, borderline tumor and cystadenoma as 71.4%, 59.1% and 0%, respectively, and the review concludes that hTERT is not an independent biomarker to differentiate borderline tumor from malignant tumor. [89]
  • The review suggests using hTERT immunohistochemistry together with serum CA-125 in difficult situations where histology does not distinguish malignant from borderline ovarian tumor. [89]
  • Sox2 expression was reported to increase from benign and borderline tumors to malignant ovarian tumors and to have positive correlations with FIGO stage or pathological stage in serous and mucinous cystadenocarcinoma samples. [116]
  • Nuclear survivin expression was reported to be associated with clinical stage, histologic grade, proliferating cell nuclear antigen labeling index, and clinical outcome in ovarian epithelial carcinoma patients. [117]
  • Prohibitin was reported to be significantly up-regulated by LH in ovarian epithelial tumor cells. [118]
  • A review reports that AdipoR1 and AdipoR2 expression was assessed in ovarian epithelial carcinoma specimens. [119]
  • A sulfatide study reported higher sulfatides in ovarian cancer tissue than in normal ovary tissue. [18]
  • CA 125, Cyfra 21-1, IL-7, IL-8, IL-10, IL-2R, TNF-R2, HE4, and tTG were elevated in ovarian cancer patients compared with benign cases in the serum biomarker study. [53]
  • Soluble EGFR was lower in ovarian cancer patients in comparison to benign cases. [53]
  • The CEM carcinoma group had higher serum CA 72-4, while the serous carcinoma group had higher serum CA 125 and SMRP. [53]
  • IGFBP-1 and SMRP were described as subtype-specific biomarkers in this study. [53]
  • MPO was higher in CEM carcinomas, and IP-10 was lower in CEM carcinomas compared with serous carcinomas. [53]
  • Ascitic IL-10 levels in ovarian carcinoma were significantly correlated with disease stage but not cytological grade. [54]
  • Altered mRNA expression of ST3Gal I, ST3Gal III, ST3Gal IV, ST3Gal VI, and ST6Gal I was reported in malignant ovarian cancers. [120]
  • In one study, ST3Gal III, ST3Gal IV, and ST3Gal VI mRNA expressions were decreased, while ST3Gal I and ST6Gal I mRNA expressions were increased, in ovarian cancer tissues compared with normal controls. [120]
  • HMOCC-1 positivity was reported in 83.2% of ovarian carcinomas. [58]
  • VEGF expression was significantly higher in ovarian carcinomas than in benign and normal ovarian tissues, and VEGFR expression was in agreement with VEGF expression in ovarian carcinoma tissues. [78]
  • In ovarian carcinoma cells, VEGF, VEGFR1, and VEGFR2 were significantly correlated with P-STAT3 and P-STAT5, but not with P-STAT1 and P-STAT6. [78]
  • MICA was expressed on ovarian tumor tissues in one study. [59]
  • In one study, expression of both MMP-2 and MMP-9 was noted in cancer cells in peritoneal fluid of all cases studied. [79]
  • In OVCAR-3 and Caov-3, the PRB/PRAB mRNA ratio was strongly stimulated by 17-estradiol in a time- and dose-dependent manner. [60]
  • The new universal grading system was reported to function as a prognostic indicator and to correlate with clinical stage, histologic subtype, operative completeness, para-aortic lymph node metastasis, and Bax expression. [121]
  • FSHR mRNA expression was detected in ovarian epithelial inclusions, cystadenomas, borderline tumors, and carcinomas, with lower positivity in carcinomas than in the other lesions studied. [62]
  • Microvessel counts were significantly higher in stage I invasive epithelial ovarian carcinoma than in stage I low-malignant-potential epithelial ovarian carcinoma, and angiogenesis as assessed by microvessel counts might assist in differentiating these entities. [63]
  • Histopathologic grade has generally been found to be of prognostic significance in ovarian epithelial carcinoma. [61]
  • Histopathologic typing is less valuable in predicting survival but better at predicting tumor responsiveness to chemotherapy. [61]
  • The role of gonadotropins in ovarian epithelial cancer development is still controversial. [62]
  • Telomerase activity was reported to be significantly higher in ovarian epithelial carcinoma than in normal counterparts. [122]
  • EGFR positivity was reported in 61% of primary ovarian epithelial carcinoma specimens in one study. [123]
  • PR positivity was reported in 29% of primary ovarian epithelial carcinoma specimens in one study. [123]
  • ER positivity was reported in 57% of primary ovarian epithelial carcinoma specimens in one study. [123]
  • In eight of eight biopsy samples of human epithelial ovarian cancers, mRNA for LHRH was detected, and six of these specimens expressed mRNA for the LHRH receptor. [124]
  • A bFGF-like protein was present in seven ovarian epithelial neoplasms and in primary culture of dispersed ovarian cancer cells. [125]
  • DNA ploidy did not predict tumor recurrence or survival rates in one study of 59 patients with invasive epithelial ovarian carcinoma. [126]
  • Normal ovarian epithelium expressed urinary-type plasminogen activator receptor but little or no urinary-type plasminogen activator, whereas epithelial ovarian carcinomas frequently expressed urinary-type plasminogen activator together with its receptor. [127]
  • Ovarian carcinoma-associated plasminogen activators and metalloproteinases were reported to catalyze hydrolysis of basement membrane components. [128]
  • Serum CA 125 was elevated above 35 U/ml in 75.4% of cases at diagnosis and in 48.8% of cases in follow-up in one report, and CA 125 positivity was reported more often in advanced stage disease and recurrences than in early disease. [68]
  • One report found a positive association between CA 125 levels and pathological response at second-look laparotomy in 86.7% of cases. [68]
  • Some untreated ovarian epithelial cancers were estrogen receptor rich by cytosol binding criteria. [5]
  • In one advanced-disease series, receptor-rich and receptor-poor groups did not differ significantly in survival or time to first progression. [5]
  • The sources report high-affinity estrogen binding consistent with receptor, occasional heterogeneity between tumor sites, and progestin-specific binding in some specimens. [5]
  • A monoclonal antibody against estrogen receptor shifted estradiol binding peaks in ovarian adenocarcinoma cytosols and nuclear fractions. [6]
  • In one case of estrogen-producing epithelial ovarian cancer, serum estradiol was elevated before treatment and decreased to normal postmenopausal levels after surgery. [92]
  • Immunohistochemical studies in one estrogen-producing tumor showed that the enzymes required to produce estrogen were present in the tumor. [92]
  • LncRNA SNHG22 has been studied as playing an oncogenic role in ovarian epithelial carcinoma and has been reported to affect chemoresistance by sponging miR-2467. [129]
  • Expression of the NUCB2/NESF-1 protein has been linked to tumor development and metastasis in cancers. [130]
  • In one cohort, 21 of 52 patients had deleterious BRCA mutations. [12]
  • Signature 3 was the most common mutational signature in one ovarian cancer cohort and was associated with failure to repair DNA double-strand breaks by homologous recombination. [12]
  • Mismatch repair deficiency in ovarian clear cell carcinoma was associated with younger age in one cohort. [84]
  • In that cohort, intratumoral stromal inflammation and plasma cell infiltration were significantly associated with mismatch repair status, and diffuse intratumoral stromal inflammation correlated significantly with deficient mismatch repair in multivariate analysis. [84]
  • DNA index provided statistically significant prognostic information on outcome in a small cohort of patients with advanced ovarian carcinoma without macroscopic residual disease after primary operation. [131]
Show 17 lab & early-research findings
  • One study found progesterone receptor expression in all ovarian epithelial carcinoma cell lines tested. [132]
  • One study reported overexpression of PTPN6 transcripts and proteins in 7 of 8 ovarian epithelial carcinoma cell lines and increased PTPN6 transcript expression in 10 of 11 invasive ovarian epithelial cancer tissues. [133]
  • A 2025 review reports significant upregulation of CSNK1D and KLK6 in BRCA1-deficient ovarian cancer cell lines compared with control ones, and concludes that CSNK1D and KLK6 expression levels could be promising biomarkers for BRCA1-deficient ovarian cancer. [134]
  • One review reports that c-Fos was overexpressed in ovarian epithelial carcinoma and was correlated with clinicopathological characteristics. [17]
  • A review states that REG4 mRNA and protein expression levels were increased in ovarian cancer cell lines and that higher expression was seen in some more invasive lines. [19]
  • HE4 is described as an overexpressed serum marker in ovarian cancer patients and as a biological marker of ovarian cancer. [51]
  • Lewis y antigen is reported to be overexpressed in more than 75% of ovarian epithelial neoplasms to some degree and high levels are associated with poor prognosis. [51]
  • NRF2 protein was found to be overexpressed in ovarian epithelial carcinoma. [135]
  • A DNA methylation study assessed 1,505 CpG sites associated with 808 genes in 15 ovarian cell lines and 27 primary tumors, found 489 CpG sites associated with 337 genes that varied significantly between ovarian cancer-derived cell lines and primary ovarian cancer tumors at an FDR less than 1%, and reported 90 CpG sites associated with 68 genes that differed between at least one pair of tumor histologies at an FDR less than 1%. [90]
  • The tissue level of IL-10 in ovarian carcinoma was significantly higher than in benign ovarian tumour and normal controls, and IL-10 expression was detectable in cell lysate and supernatant from ovarian carcinoma cell lines. [54]
  • In one study, PRA was 0 in malignant ovarian tissues, while PRB remained detectable, and PRB mRNA was detected in all cell lines examined and ovarian cancer tissues. [60]
  • Shed membrane vesicles carrying alpha-Folate Receptor were identified in ascites and serum of an ovarian carcinoma patient, and vesicles from an ovarian cancer cell line contained MMP-9, MMP-2, and uPA. [80]
  • FSH may be a growth-promoting factor in ovarian epithelial cell proliferation, and LH may block the growth-stimulating effects of FSH. [62]
  • c-fms mRNA and protein expression were reported in ovarian epithelial carcinoma cell lines and in 7 of 9 ovarian neoplasms studied. [136]
  • High levels of urinary-type plasminogen activator were detected in 15 of 19 ascites samples, and ovarian carcinoma cell lines secreted urinary-type plasminogen activator, whereas normal ovarian epithelial cells did not secrete detectable plasminogen activator. [127]
  • Gonadotropin-releasing hormone and its messenger ribonucleic acid were detected in some ovarian carcinoma specimens and the SK-OV3 cell line, raising the possibility of an autocrine regulatory role in ovarian carcinoma growth. [137]
  • In the reported case, CA125 decreased from 537.2 U/mL to 18.8 U/mL after short-course hypofractionated radiation therapy combined with camrelizumab. [70]
Standard management60 points
  • For patients with high-grade or metastatic epithelial ovarian carcinoma, the source suggests primary complete cytoreductive surgery followed by adjuvant therapy as the initial treatment of choice. [25][36]
  • One source describes cytoreductive surgery followed by platinum-based systemic chemotherapy as an effective treatment for advanced ovarian epithelial carcinoma. [29][138]
  • Sources describe HRD testing as guideline-recommended at initial diagnosis for newly diagnosed advanced high-grade ovarian cancer, and describe PARP inhibitors as suggested maintenance options in selected stage III/IV patients, including some with HRD-positive disease. [29][83]
  • Current treatment regimens for advanced ovarian cancer are described as inadequate, and there is increased interest in novel biomarkers and molecular therapeutics. [139][16]
  • Neoadjuvant chemotherapy followed by interval cytoreductive surgery is suggested when complete cytoreduction with primary surgery is unlikely because of unresectable metastatic disease, imaging/laparoscopic/laparotomy criteria for irresectability, poor functional status, or comorbidities. [25]
  • Hyperthermic intraperitoneal chemotherapy is described as controversial as an alternative in advanced or metastatic epithelial ovarian carcinoma. [25]
  • Standard epithelial ovarian cancer treatment includes surgical resection of all visible tumors and systemic chemotherapy, depending on stage and risk factors. [140]
  • In clinically early-stage epithelial ovarian cancer, pelvic and para-aortic lymphadenectomy is part of surgical staging and was considered the standard surgical staging method in the referenced consensus recommendations. [140]
  • Advanced epithelial ovarian carcinoma is described as chemosensitive to platinum plus paclitaxel combination chemotherapy. [141]
  • The OVAR17 trial evaluated optimal initial treatment duration of bevacizumab in combination with standard chemotherapy in FIGO stage IIB-IV epithelial ovarian, fallopian tube, or peritoneal carcinoma. [142]
  • Central pathology review at enrolment was concluded to be an integral part of future clinical studies of ovarian carcinomas. [142]
  • One study of advanced ovarian epithelial carcinoma used immediate or delayed cytoreduction surgery followed by cisplatinum and cyclophosphamide chemotherapy every 28 days for a maximum of 8 courses, with cisplatinum 45 mg/m2 for 2 consecutive days and cyclophosphamide 900 mg/m2 on day 2. [143]
  • For children and adolescents, low-risk early-stage epithelial ovarian neoplasms are treated with surgery alone, high-risk early-stage disease should receive three to six cycles of cisplatin- or carboplatin-based chemotherapy after surgery, and stage III and IV disease is recommended to receive six to eight cycles of chemotherapy. [11]
  • In children and adolescents, surgery may be performed upfront or following neoadjuvant chemotherapy, and some protocols also incorporate bevacizumab as part of chemotherapy and for post-chemotherapy maintenance. [11]
  • For adult patients with germline or somatic BRCA1 or BRCA2 mutations, PARP inhibitors are recommended as maintenance therapy. [11]
  • Sources describe epithelial ovarian cancer as typically treated with six to nine cycles of platinum/taxane chemotherapy either before or after surgical debulking. [32]
  • The results support the common recommendation to perform primary debulking surgery in patients eligible for primary surgery. [34]
  • Sources describe cytotoxic chemotherapy and surgical debulking as the standard of care for primary treatment of epithelial ovarian cancer. [14]
  • In one cohort, all patients underwent standard cytoreductive surgery followed by adjuvant carboplatin/paclitaxel chemotherapy, and cytoreductive surgery outcomes were categorized as R0, R1, and R2. [12]
  • For advanced-stage ovarian cancer, one review states that the standard therapy is complete cytoreductive surgery of all visible tumors and six cycles of chemotherapy, and that complete resection of all macroscopic disease is the strongest independent variable in predicting overall survival. [36]
  • Sources describe primary laparotomy as important for determining the extent of tumor spread and as an opportunity for maximum treatment. [35]
  • Standard treatment was described as surgery combined with platinum-based chemotherapy, and maintenance therapies such as PARP inhibitors and anti-angiogenic antibodies were described as newer treatment approaches. [38]
  • In one phase 1 trial of recurrent or persistent epithelial ovarian, fallopian tube, or primary peritoneal carcinoma, modulated electro-hyperthermia was combined with weekly paclitaxel or weekly cisplatin. [144]
  • The 2020 review states that primary cytoreductive surgery and adjuvant chemotherapy targeting residual disease are used after initial regression of intraperitoneal dissemination. [145]
  • The 2020 review states that local and systemic chemotherapy, radiation therapies, and surgical resection of primary tumors have been used in epithelial ovarian carcinoma. [39]
  • The 2020 nomogram study included patients who reached clinical complete remission after initial or intermediate cytoreductive surgery and standard adjuvant platinum-based chemotherapy. [15]
  • PET/CT consensus is lacking in epithelial ovarian cancer; it is most commonly used to investigate suspected recurrence or progression, and management after PET/CT changed in about one-third of cases, with the greatest impact when assessing suitability for focal radiotherapy or secondary surgical debulking in recurrent disease. [106]
  • Among cases with recent conventional imaging available, clinical conclusions after PET/CT were the same in about three-quarters of cases. [106]
  • Immune checkpoint blockers against CTLA-4 or PD-1/PD-L1 are described as among the most promising immunotherapies against cancer, but only 15% of ovarian epithelial carcinoma patients are responders to immune checkpoint blocker treatment. [41]
  • Ovarian cancer-related hypercalcemia should be evaluated for etiology and severity before therapy planning; laboratory measurements of PTH and 1,25(OH)2D and scintigraphy scans of the parathyroid gland are useful in differential diagnosis, and anti-hypercalcemic infusion is described as helpful while treatment of the primary disease is more essential. [85]
  • One review states that platinum-based chemotherapy such as cisplatin is described as the most effective treatment for OECa. [43]
  • Women at high risk for epithelial ovarian cancer undergo bilateral salpingo-oophorectomy at hysterectomy, while bilateral salpingectomy with ovarian retention may be an alternative for women who wish to retain ovarian function, although its efficacy remains to be demonstrated. [108]
  • In the MPO study, patients with FIGO stage Ic to IV received platinum-based chemotherapy. [23]
  • The review of recurrent platinum-resistant ovarian carcinoma studied CT-guided permanent iodine-125 seed implantation combined with gemcitabine chemotherapy. [146]
  • The source says bevacizumab is mentioned as an antiangiogenesis therapy that may be beneficial against ovarian epithelial carcinoma, especially in obese patients. [47]
  • In the neck lymphatic metastasis series, patients underwent cytoreductive surgery as initial exploration and platinum-containing chemotherapy after surgery, and optimal debulking surgery was defined as residual tumor with a volume of less than 1 cm. [49]
  • Patients in the series were assessed with physical examination, CT of the abdomen and pelvis, chest x-rays, and CA-125 testing. [49]
  • No markers with high sensitivity and specificity are currently available to facilitate clinical diagnosis, staging, and monitoring for therapeutic interventions. [51]
  • Patients in the cited tissue study had not received chemotherapy before surgery, and all patients underwent lymphadenctomy during the operation. [51]
  • Current prognostic factors do not allow reliable prediction of response to chemotherapy and survival for individual ovarian cancer patients, and the cited study provides a rationale for evaluating drugs that target EGFR, E-cadherin, and MMP-9 pathways. [147]
  • For solitary cerebral metastases from ovarian epithelial carcinoma, the source describes surgical en bloc removal followed by postoperative radiotherapy and chemotherapy, and states that multimodal treatment by surgery, radiation and chemotherapy is the best choice of treatment. [56]
  • The source notes that individualized combinatorial therapy based on proteomic mapping of phosphorylation end points may require evaluation of the patient's metastatic tissue. [55]
  • One source describes primary cytoreductive surgery followed by adjuvant platinum-based combination chemotherapy as the control approach in advanced ovarian epithelial carcinoma. [148]
  • One source describes neoadjuvant platinum-based combination chemotherapy and embolization via the anterior branches of the bilateral internal iliac arteries as an alternative treatment for patients with advanced ovarian epithelial carcinoma when the chance of optimal cytoreductive surgery is low. [148]
  • One study evaluated cytoreductive surgery followed by high-dose, platin-based chemotherapy in stage II-IV epithelial ovarian carcinoma, and another evaluated consolidation with single-dose, whole-abdominopelvic radiotherapy after complete remission. [149]
  • Both grade and type should be specified in the surgical pathology report for any ovarian carcinoma, and histopathologic typing may help suggest chemotherapeutic agents to be used. [61]
  • Photodynamic therapy with Pc 4 was described as warranting clinical trials in the source study. [81]
  • One review states that ovarian carcinoma patients in the cited grading study were treated with surgery and cisplatin-based chemotherapy. [150]
  • Second-look surgery remained a hallmark for assessing disease status at the completion of adjuvant chemotherapy, but its continued use in advanced ovarian cancer was described as depending on appropriately trained surgeons and access to consolidation and salvage therapy, preferably in prospective trials. [151]
  • In one surgical series of presumed stage I-II invasive ovarian epithelial carcinoma, patients received cis-platinum, doxorubicin, and/or cyclophosphamide after surgical staging. [77]
  • One review described surgical staging and adjuvant therapy, with second-look laparotomy, as part of definitive management for stage I ovarian epithelial carcinoma. [76]
  • One review states that surgery is necessary in almost all cases for staging accuracy and surgical treatment, and that chemotherapy becomes a primary treatment even in early stages. [67]
  • The same review states that the best benefit in overall survival was obtained in stages III and IV when surgery, polychemotherapy including CDDP, and irradiation were combined. [67]
  • One advanced ovarian cancer study used monthly adriamycin and cis-platinum for nine courses. [4]
  • A pilot study used melphalan with levamisole in stage III, stage IV, or recurrent epithelial ovarian cancer to determine a tolerable dosage schedule, possible adverse effects, and a general estimate of response rate and duration. [152]
  • The review states that treatment for ovarian mucinous cancer is similar to that for more common ovarian serous cancer, but ovarian mucinous cystadenocarcinoma is resistant to platinum-based chemotherapy compared with other types of ovarian epithelial cancer. [70]
  • The review states that the current treatment plan mainly refers to ovarian serous cancer, but the treatment effect is poor, and large-scale prospective studies on treatment are rare with an urgent need for new treatment methods. [70]
  • For epithelial ovarian cancer diagnosed during the second trimester of pregnancy, chemotherapy with preservation of the fetus could be considered and should be discussed. [153]
  • The Belgian registry study reported that completeness of staging surgery, lymphadenectomy with at least 20 pelvic or para-aortic nodes removed, and timely start of chemotherapy after surgery were below benchmark targets, with poorer indicator results in lower-volume hospitals for lymphadenectomy, staging, timely start of chemotherapy, and genetic testing. [154]
  • All patients in one retrospective series underwent primary surgical cytoreduction, and some received adjuvant chemotherapy or additional radiotherapy. [155]
Treatments & compounds studied146 treatments

Chemotherapy

  • neoadjuvant chemotherapy: Neoadjuvant chemotherapy followed by interval cytoreductive surgery is described for cases in which complete primary cytoreduction is unlikely. [25][27]
  • paclitaxel plus poldine · 9 findings
    • Paclitaxel was studied in combination with lobaplatin in a phase I trial and was also used with modulated electro-hyperthermia in recurrent or persistent epithelial ovarian, fallopian tube, or primary peritoneal carcinoma. [29][144][153][9][11]5 sources
    • Paclitaxel was used in cited clinical reports, including a postoperative carboplatin plus paclitaxel regimen and Taxol treatment in a recurrent case. [37][11][153][9]4 sources
    • Paclitaxel plus poldine was studied in advanced ovarian epithelial carcinoma, with the report describing the combination as effective and less toxic than intravenous chemotherapy alone. [156]
    • Paclitaxel, epirubicin, and cisplatin were studied as a first-line three-drug regimen in advanced ovarian epithelial carcinoma and were described as highly active by objective response rate. [157]
    • Paclitaxel was studied with modulated electro-hyperthermia in a phase 1 trial, with no dose-limiting toxicity in the paclitaxel arm and no severe treatment-emergent adverse events reported. [144]
    • Paclitaxel, cisplatin, gemcitabine, and 5-fluorouracil were listed as chemotherapeutic agents used in vitro in one ovarian carcinoma study. [46]
    • Paclitaxel was used after surgery in one pregnancy-associated case and with radiotherapy in a patient with choroidal metastases. [153][9]
    • Paclitaxel and cisplatin were used in a stage IIIC serous adenocarcinoma case report. [85]
    • Paclitaxel liposome plus carboplatin, 5-Fu plus CF plus oxaliplatin, capecitabine plus oxaliplatin, bevacizumab plus FOLFOX4, S-1, and bevacizumab plus oxaliplatin plus raltitrexed were given as multiline chemotherapy in one reported case. [70]
  • melphalan: Melphalan was studied in advanced or recurrent stage III and IV ovarian epithelial carcinoma, with a reported complete and partial response rate of 29.2% and no enhancement from adding fluorouracil or dactinomycin. [158]
  • taxane-platinum combination: Taxane-platinum combination chemotherapy was the most commonly used postoperative regimen in the clear cell ovarian cancer cohort. [27]
  • ifosfamide plus etoposide: Ifosfamide plus daily oral etoposide was studied in previously treated relapsed ovarian epithelial carcinoma, with modest response and no obvious advantage over single agents. [141]
  • taxol · 3 findings
    • Taxol at low nanomolar concentrations inhibited growth of KF 28 cells and reduced Ang-1 and VEGF expression in one study. [159]
    • Taxol inhibited growth of some ovarian epithelial carcinoma cell lines in vitro. [132][144][159][9]4 sources
    • Taxol was restarted after resection of recurrent disease in one patient. [9]
  • cisplatinum-cyclophosphamide: A cisplatinum-cyclophosphamide regimen in advanced ovarian epithelial carcinoma produced objective responses in 35 of 50 evaluable patients, including 17 pathological complete remissions, with median survival of 29 months and median time to progression of 25 months. [143]
  • lobaplatin: Lobaplatin combined with paclitaxel was studied in a phase I dose-escalation trial in platinum-sensitive recurrent ovarian epithelial carcinoma, with a maximum tolerated dose of 30 mg/m2 and reported response and survival outcomes. [29]
  • carboplatin · 5 findings
    • A pregnancy-associated case received two courses of carboplatin during pregnancy followed by postoperative carboplatin plus paclitaxel; a pediatric series reported chemotherapy use in malignant epithelial ovarian neoplasms but the regimen was not specified in the cited text. [11][153][9]3 sources
    • Carboplatin and paclitaxel are described as the standard platinum-taxane chemotherapy combination used before or after surgical debulking. [32]
    • Carboplatin was used in cited clinical reports, including during pregnancy and in a postoperative carboplatin plus paclitaxel regimen, and one case report noted recurrence that failed to respond to carboplatin therapy. [37][23][153][9]4 sources
    • Carboplatin was later tried for recurrent disease in one patient, with progression noted. [9]
    • Carboplatin and etoposide were given after surgical drainage in one reported case, with clinical improvement noted. [74]
  • liposomal doxorubicin: Liposomal doxorubicin was used as second-line chemotherapy in one pediatric series and was also combined with bevacizumab in salvage chemotherapy in another report. [11]
  • oral metronomic chemotherapy: Oral metronomic chemotherapy was used with palliative intent in one pediatric series. [11]
  • pegylated liposomal doxorubicin: Pegylated liposomal doxorubicin, gemcitabine, and topotecan are listed as later-line chemotherapy options. [32]
  • chemotherapy: Chemotherapy was administered in 65.4% of patients in the LGSC review and increased over time. [34]
  • cisplatin · 3 findings
    • Cisplatin is named in reviews as part of polychemotherapy associated with improved overall survival and was also used in several clinical and preclinical studies. [67][144][160][43][138][73][153][9]8 sources
    • Cisplatin was studied with modulated electro-hyperthermia in the same phase 1 trial, where one confirmed partial response and two CA125 responses were observed. [144][160][43][67]4 sources
    • Cisplatin, etoposide, and bleomycin were used as a chemotherapy regimen after a mixed ovarian tumor was recognized histopathologically. [73]
  • platinum-based chemotherapy · 2 findings
    • One study suggested intensive therapy for high-risk stage I disease, including platinum-based chemotherapy, and another nomogram study included patients who achieved complete remission after cytoreductive surgery and chemotherapy. [76][15][23]3 sources
    • Platinum-based chemotherapy was part of standard adjuvant treatment in the recurrence nomogram study and was also given to all FIGO stage Ic to IV patients in one ovarian carcinoma study. [15][23]
  • platinum-based systemic chemotherapy: Platinum-based systemic chemotherapy was described as an effective treatment in a review, with reported complete response and 5-year survival figures. [138]
  • platinum-based combination chemotherapy: Platinum-based combination chemotherapy was used in advanced ovarian epithelial carcinoma in one comparative study, but the individual drugs were not specified. [148]
  • cisplatinum: Cisplatinum-based chemotherapy was used in a small retrospective series, and five of six treated patients had a complete response. [155]
  • doxorubicin: Doxorubicin and ifosphamide were part of chemotherapy regimens in the same retrospective series. [155]
  • adriamycin: Adriamycin and meso-chlorin e6 monoethylene diamine were studied in photodynamic therapy combinations in OVCAR-3 cells, with reports of synergy, additivity, and one antagonistic dose combination. [82][161]
  • Hexametilmelanine: Hexametilmelanine and epirubicin are named in a review as part of polychemotherapy associated with improved overall survival in ovarian cancer. [67]
  • adriamycin and cis-platinum: Adriamycin plus cis-platinum produced a pathologically proven response rate of 52.2%, with median survival of 22 months overall in one advanced ovarian cancer study. [4]
  • melphalan and levamisole: Melphalan and levamisole were studied in a pilot trial, with complete responses in some patients and no serious toxicity reported. [152]
  • 5-fluorouracil: 5-fluorouracil, oxaliplatin, and capecitabine are mentioned as gastrointestinal cancer drugs considered as another option. [70]
  • Gemcitabine: The source describes gemcitabine as a pyrimidine antagonist often used for ovarian cancer patients with platinum-resistance. [162]
  • Oxaliplatin: The source reports oxaliplatin was evaluated using the CD44v6-O-MWNTS delivery system in ovarian cancer models. [162]
Show 3 lab & early-research entries
  • cyclophosphamide and cisplatin: Cyclophosphamide and cisplatin were used in one pediatric case series patient. [11]
  • docetaxel and carboplatin: Docetaxel and carboplatin were given after surgery in one hypercalcemia case report. [85]
  • cisplatinum, cytoxan, adriamycin: Cisplatinum, Cytoxan, and Adriamycin were used as initial chemotherapy in one patient with clear cell ovarian carcinoma. [9]

Targeted therapy

  • bevacizumab · 3 findings
    • Sources describe bevacizumab-containing regimens as suggested first-line adjuvant therapy for selected high-risk stage III/IV disease and as options in recurrent platinum-sensitive or platinum-resistant settings; the provided sources do not establish mixed outcome findings across studies. [25][11][163][47][70]
      ⚠ Contradicting evidence: Sources include both reports of benefit or potential benefit and a randomized trial showing no improvement when bevacizumab was added to weekly paclitaxel. (the more authoritative source is [163]).
      5 sources
    • Bevacizumab was studied in recurrent measurable sex cord-stromal tumors and in a randomized phase 2 trial with weekly paclitaxel, where adding bevacizumab did not improve clinical outcomes. [163]
    • The review states that bevacizumab may be beneficial for recurrent or progressive ovarian mucinous cancer. [70]
  • PARP inhibitors: Sources describe tumor-based sequencing as identifying alterations aligned with targeted treatment in some patients, and describe BRCA1/2 mutations as associated with longer progression-free survival; they also describe PARP inhibitors as suggested maintenance options in selected BRCA1/2-positive recurrent stage III/IV epithelial ovarian cancer. [25][14][12]3 sources
  • rucaparib: Rucaparib meta-analysis data reported a pooled objective response rate of 0.331 and grade 3 or higher adverse events in 61% of patients. [164]
  • CYH33: CYH33, a PI3K inhibitor, showed tumor inhibitory activity in ovarian clear cell carcinoma models, with one humanized PDX result not reaching statistical significance. [31]
  • imatinib: Imatinib was reported in recurrent ovarian granulosa cell tumors, with case-level reports of remission or stabilization. [163]
  • anlotinib: Anlotinib monotherapy or anlotinib combined with chemotherapy was reported in a retrospective study of platinum-resistant recurrent ovarian cancer, with an objective response rate of 17.14% and a disease control rate of 60.00%. [165]
  • targeted therapies: Targeted therapies, surgeries, chemotherapy, radiation therapy, or combinations of these were reported in the included epithelial ovarian cancer patients in one review. [39]
  • olaparib: Olaparib maintenance monotherapy was reported to improve progression-free survival versus placebo in platinum-sensitive BRCA1/2-mutated recurrent ovarian cancer, and real-world cohorts described discontinuation and hematologic toxicity during treatment. [166]
  • p62/SQSTM1: p62/SQSTM1 inhibition and ZZ-domain deletion were studied in cisplatin-treated SKOV3/DDP cells and were associated with reduced viability or NF-κB activity. [167]
  • BIBF1120 and SB431542: BIBF1120 and SB431542 were used as VEGFR and TGF-β1R inhibitors, respectively, in the cited study. [22]
  • EGFR: A review reported that drugs targeting EGFR, E-cadherin, and MMP-9 pathways may be promising in ovarian cancer treatment. [147]
  • siCXCR4: The source reports small interfering RNA targeting CXCR4 (siCXCR4) was designed and used with the CD44v6-O-MWNTS delivery system in ovarian cancer experiments. [162]
Show 1 lab & early-research entry
  • PGC1α: PGC1α was studied as a cisplatin-resistance-related target, and its inhibition reduced mitochondrial biogenesis and increased apoptosis in cisplatin-resistant cells. [160]

Immunotherapy

  • anti-PD-1: Anti-PD-1 therapy and CYH33 plus anti-PD-1 were evaluated in humanized PDX mice in an ovarian clear cell carcinoma study. [31]
  • checkpoint inhibitors: Checkpoint inhibitors in ovarian cancer have shown limited success, with single-agent objective response rates around 10% to 15% in clinical trials. [12]
Show 8 lab & early-research entries
  • gamma delta T cells: Expanded gamma delta T cells showed in vitro cytotoxicity against ovarian epithelial carcinoma cell lines and were studied as a candidate for future adoptive immunotherapy. [168]
  • dendritic-cell-based immunotherapy: Autologous dendritic-cell-based immunotherapy using ovarian epithelial cancer cell lysates was reported to induce T-cell activation and effector responses against ovarian epithelial carcinoma cells in vitro. [41]
  • AMHR2-CD: AMHR2-CD vaccination in mouse models produced T-cell responses and tumor growth control with a benign autoimmune phenotype. [44]
  • TCRγ9δ2(OT3)-Fc: TCRγ9δ2(OT3)-Fc showed binding to multiple carcinoma cell lines, mediated ADCC in vitro, and inhibited tumor growth and enhanced survival in ovarian carcinoma xenograft models. [169]
  • CDR3δ-grafted γ9δ2T cells: CDR3δ-grafted γ9δ2T cells were reported to produce cytokines, exhibit cytotoxicity in vitro, and show antitumor effects in nude mice, and were described as candidates for clinical tumor immunotherapy. [170]
  • GST epitope fusion proteins: GST epitope fusion proteins were reported to promote gamma delta T-cell cytokine secretion, proliferation, and cytotoxicity in vitro and to suppress tumor growth in nude mice. [171]
  • OT10 peptide: A Vdelta2 CDR3 sequence derived from tumor-infiltrating lymphocytes bound specifically to the ovarian tumor cell line SKOV3, and a deltaI97 substitution altered iso-butylamine responsiveness. [172]
  • interleukin 2: Interleukin-2-stimulated lymphokine-activated killer cell activity was compared between control and patient-derived cells, with ascitic cells showing similar activity to controls against two cell lines. [173]

Hormonal therapy

  • endocrine therapy: Endocrine therapy in advanced high-grade ovarian cancer was reported as feasible and well tolerated, with limited objective responses in a multicenter retrospective study. [94]
  • hormone therapy: Hormone therapy for progressive and recurrent malignant ovarian sex cord-stromal tumors had an overall response rate of 71% in a systematic review of 31 patients. [163]
  • anastrozole: Anastrozole produced a partial response in 2.6% of patients and stabilization in 76.3% in a phase 2 trial. [163]
  • LHRH agonists: Exogenous LHRH agonists were reported to have antiproliferative activity in epithelial ovarian cancer, probably mediated through LHRH receptors. [124]
Show 2 lab & early-research entries
  • mifepristone: Mifepristone was reported to cause dose- and time-dependent growth inhibition in ovarian epithelial carcinoma cell lines in vitro. [132]
  • Lupron-SR: Lupron-SR, a gonadotropin-releasing hormone agonist, produced latent and transient inhibition of OVCAR-3 tumor growth in nude mice. [174][75]

Radiotherapy

  • radiotherapy · 2 findings
    • Radiotherapy is described as having an unclear role in malignant ovarian sex cord-stromal tumors and being reserved for inoperable disease, residual lesions after surgery, or chemotherapy resistance. [163]
    • Radiotherapy was used with debulking and taxol chemotherapy in one patient with choroidal metastases. [9]
  • radiation therapy: Radiation therapy is described as being used at different stages of cancer treatment, including as primary treatment, with other treatments, before surgery, or after surgery. [37]
  • whole-abdominal radiotherapy: Single-dose whole-abdominopelvic radiotherapy after negative second-look laparotomy was associated with reported 5-year and 10-year survival figures, with no severe postradiation complications in one study. [149]
  • abdominopelvic irradiation: Abdominopelvic irradiation was reported to potentially sterilize minimal-volume persistent ovarian carcinoma after chemotherapy, while bulky disease remained disease-free in none of the patients in one small series. [175]
Show 1 lab & early-research entry
  • short-course hypofractionated radiation therapy: Short-course hypofractionated radiation therapy was administered to metastatic lymph nodes in the reported case. [70]

Repurposed drugs

  • aspirin: Aspirin was associated with lower ovarian cancer risk in some long-term frequent-use analyses, but not in analyses of ever frequent use overall. [30]
  • resistin: Resistin increased VEGF mRNA expression in HO-8910 cells in a time-dependent manner. [47]
  • genistein: Genistein was used experimentally to block tyrosine phosphorylation in ovarian carcinoma cell studies. [3]
Show 4 lab & early-research entries
  • oxamflatin: Oxamflatin, an HDAC inhibitor, induced morphological changes and decreased cell viability and DNA synthesis in ovarian cancer cell lines. [45]
  • oseltamivir phosphate: Oseltamivir phosphate was studied as an inhibitor of Neu1 signaling in A2780 ovarian carcinoma cells and xenografts. [46]
  • Lovastatin: Lovastatin induced apoptosis and suppressed proliferation, migration, invasion, and lamellipodia formation in OVCAR3 cells. [88]
  • suramin: Suramin was reported to have limited growth-inhibitory activity in most ovarian carcinoma cell lines and to stimulate growth in one ER-positive line. [176]

Supplements & natural agents

Show 1 lab & early-research entry
  • Essiac: Essiac was reported to have antioxidant, immunomodulatory, and neoplastic cell-specific cytotoxic activity in vitro against ovarian epithelial carcinoma cells. [177]

Procedures & devices

  • primary cytoreductive surgery: Primary cytoreductive surgery is described as first-line surgery intended to achieve complete resection, with adjuvant platinum-plus-taxane chemotherapy often given afterward. [25]
  • secondary cytoreductive surgery: Secondary cytoreductive surgery is described for persistent or recurrent disease after primary surgery and chemotherapy in platinum-sensitive or platinum-resistant settings. [25]
  • Tumor Treating Fields: Tumor Treating Fields with paclitaxel did not significantly improve overall survival in the intent-to-treat population, although an exploratory post-hoc subgroup analysis reported a median overall survival of 16 months in pegylated liposomal doxorubicin-naive patients. [178]
  • surgery · 2 findings
    • Surgery was performed in most patients in the LGSC review, and debulking surgery was the most common approach. [34]
    • In the ovarian clear cell carcinoma cohort, all patients underwent surgery and optimal surgery was achieved in 89.3%. [27][34]
  • lymphadenectomy: Lymphadenectomy was associated with longer operation time, higher blood loss, more perioperative adverse events, and a higher adjuvant chemotherapy rate, while survival differences were not significant in the cited study. [140]
  • intraperitoneal chemotherapy: Intraperitoneal chemotherapy was associated with decreased intraperitoneal recurrence and a lower risk of recurrence after 2 years compared with intravenous chemotherapy in one cohort. [179]
  • humanized PDX model: The humanized PDX model was established using CD34+ stem cells from fresh umbilical cord blood. [31]
  • psammoma bodies: Psammoma bodies were associated with better long-term survival in serous carcinomas in one study. [24]
  • cisplatin: Hyperthermic intraperitoneal chemoperfusion with cisplatin or cisplatin plus doxorubicin was used after peritonectomy in patients with peritoneal carcinomatosis from ovarian primary, with reported major complications and operative mortality. [138]
  • surgical en bloc removal: Surgical en bloc removal was used in a reported series of solitary cerebral metastases from ovarian epithelial carcinoma. [56]
  • platinum-based combination chemotherapy and embolization via the anterior branches of the bilateral internal iliac arteries: Neoadjuvant platinum-based combination chemotherapy plus embolization via the anterior branches of the bilateral internal iliac arteries was associated with higher optimal debulking rates, less blood loss, shorter operative time, and no significant overall survival difference versus control in one study. [148]
  • HIFU: HIFU was described as a potential treatment modality for ovarian cancer in an animal-model paper. [57]
  • MICA-reactive Vdelta1 gammadelta T cells: MICA-reactive Vdelta1 gammadelta T cells were described as a candidate for adoptive cellular therapy of tumors. [59]
  • membrane vesicles: Shed membrane vesicles containing alpha-Folate Receptor, MMP-9, MMP-2, and uPA were described in ovarian carcinoma. [80]
  • universal grading system: A universal grading system for invasive ovarian carcinomas was reported to be simple, reproducible, and useful across histologic types and clinical stages. [150]
  • c-fms ribozyme: A hammerhead ribozyme targeting c-fms mRNA reduced growth potential and decreased c-fms expression in TYK-nu cells, and was described as a promising tool for blocking the M-CSF autocrine loop. [136]
  • lymphokine-activated killer cells: Autologous mononuclear cells were reported not to be effective LAK sources except perhaps for ascitic mononuclear cells. [173]
Show 6 lab & early-research entries
  • hyperspectral imaging: The study assessed the feasibility of near-infrared hyperspectral imaging for epithelial ovarian cancer detection in ex vivo tissue samples. [36]
  • heat shock-conditioned OEC lysates: Heat shock-conditioned ovarian epithelial cancer lysates were reported to induce dendritic-cell maturation markers in vitro. [41]
  • Snail and Slug shRNA: Snail and Slug shRNA knockdown was used in A2780 ovarian carcinoma cells in one preclinical study. [46]
  • MICA: MICA was described as a promising imaging target, and monoclonal antibody 10C6 was proposed for early tumor diagnosis in mice bearing MICA-positive human ovarian epithelial carcinoma. [180]
  • Photofrin II: Photodynamic therapy with Photofrin II and 630 nm laser light completely ablated treated OVCAR-3 tumors in nude mice. [181]
  • CD44v6-O-MWNTS: The source reports CD44v6 single-chain antibody-modified oxidized multi-walled carbon nanotubes (CD44v6-O-MWNTS) were used to co-deliver gemcitabine and siRNA, internalize into cancer cells, and were reported to inhibit ovarian cancer growth in vitro and in vivo. [162]

Other

  • ?: Histologic grade 2/3 was associated with poorer disease-free survival in the lymphadenectomy study. [140]
  • CA125: Annual screening compliance in the UKCTOCS trial was reported for multimodal and ultrasound screening groups. [26]
  • ?: The Taiwan HRD study reported an overall HRD prevalence of 52.9%, tumor BRCA mutations of 14.7%, and BRCA wild-type LOH-positive status of 38.2%. [83]
  • ?: The LGSC review describes a growing evidence base for endocrine, molecularly targeted, and anti-angiogenic treatment modalities in front-line and recurrent settings. [34]
  • ?: The review states that ovarian cancer often develops resistance to standard chemotherapeutic regimens. [37]
  • TGF-β1 and VEGF: TGF-β1 and VEGF promoted proliferation, migration, invasion, and lamellipodia formation in ovarian cancer cell models, while VEGFR or TGF-β1R inhibitors suppressed these phenotypes. [22][47]
  • Nesfatin-1: Nesfatin-1 inhibited proliferation and growth of HO-8910 cells by G1 phase arrest in the cited study. [182]
  • Ghrelin: Ghrelin inhibited proliferation and growth of HO-8910 cells by G1 phase arrest in the cited study. [183]
  • HE4: HE4 and Lewis y antigen were studied as tissue and culture markers in ovarian cancer, with higher expression in malignant than benign or normal tissues. [51][52]
  • Lewis y antigen: Lewis y antigen and TGF-β1 expression were studied in ovarian tissues and were reported to be positively correlated in ovarian cancer tissues. [51][52]
  • luteinizing hormone: Luteinizing hormone was reported to up-regulate prohibitin in ovarian epithelial tumor cells. [118]
  • AdipoR1: Adiponectin receptor expression was studied in ovarian epithelial carcinoma specimens, but no prognostic correlations were reported. [119]
  • PON1: The rs854560 T allele and rs662 A allele of PON1, as well as the combined variant genotype, were associated with reduced ovarian cancer risk in a case-control study. [184]
  • radiotherapy and chemotherapy: Postoperative radiotherapy and chemotherapy were given after surgery in a reported series of solitary cerebral metastases from ovarian epithelial carcinoma. [56]
  • HMOCC-1: HMOCC-1 inhibited attachment of RMG-I cells to cultured human mesothelial cells in a concentration-dependent manner. [58]
  • telomerase determination: Telomerase determination was suggested as a possible diagnostic approach for ovarian carcinoma, with a need for accurate quantification. [122]
  • CA 125: CA 125 is described as a marker that may be more useful for monitoring response to treatment and long-term follow-up than for diagnosis. [68]
Show 14 lab & early-research entries
  • miR-152: miR-152 mimic transfection inhibited proliferation and migration in ovarian cancer cell lines. [107]
  • c-Fos: c-Fos overexpression increased proliferation and colony formation, while c-Fos interference reduced them in ovarian cancer cell models. [17]
  • REG4: REG4 overexpression or recombinant REG4 increased growth, migration, invasion, and reduced apoptosis in ovarian cancer cell models. [19]
  • miR-106b: MiR-106b transfection slowed growth, induced cell-cycle arrest and apoptosis, and reduced migration and invasion in ovarian carcinoma cell lines. [20]
  • miR-490-3P: MiR-490-3P overexpression suppressed tumor development in vivo in the source study. [109]
  • RhoC: RhoC overexpression increased proliferation, migration, invasion, and lamellipodia formation, while RhoC knockdown weakened these phenotypes in ovarian cancer cell models. [22]
  • lysophosphatidic acid: Lysophosphatidic acid, CXCL12, and pertussis toxin were studied in ovarian cancer cell lines for effects on proliferation, migration, invasion, and signaling. [114]
  • RhoA siRNA and Wnt-5a siRNA: RhoA siRNA and Wnt-5a siRNA reduced growth and migration and induced G1 arrest and apoptosis in OVCAR3 cells. [48]
  • RhoC siRNA: RhoC siRNA transfection was associated with reduced growth, G1 arrest, and apoptosis in OVCAR3 cells. [88]
  • T-oligos: T-oligos showed cytotoxic activity in some ovarian epithelial carcinoma cell lines, activated apoptotic pathways, and had additive or greater-than-additive activity with histone deacetylase drugs in clinical testing. [139]
  • Pc 4: Pc 4 photodynamic therapy in OVCAR-3 xenografts produced complete responses in some mice, with responses varying by dose. [81]
  • FSH: FSH and LH were studied as gonadotropins in ovarian epithelial tumors, with FSH showing growth-stimulating activity in vitro and LH blocking that effect. [62]
  • alpha2beta1-integrin: Blocking antibodies to alpha2 and beta1 integrin subunits inhibited ovarian carcinoma cell adhesion and migration on type I collagen in vitro, and the DGEA peptide was reported to block adhesion to collagen. [185]
  • tumor necrosis factor-alpha: Tumor necrosis factor-alpha induced dose- and time-dependent inhibition of Caov-3 cell proliferation in vitro. [186]
Staging & risk18 points
  • Several cohorts enrolled or reported predominantly advanced disease, including patients with stage III or IV disease, stage IIIC-IV disease, or stage II-IV disease. [83][187][149]3 sources
  • One guideline refers to advanced disease as FIGO stages IIIC-IV, and one review defines early-stage disease as FIGO stages I–IIA and advanced-stage disease as FIGO stages IIB–IVB. [25][34]
  • FIGO stage I is limited to one or both ovaries, stage II to the uterus and pelvic structures, stage III to extension to the small bowel or omentum, and stage IV to distant metastases to the liver or outside the peritoneal cavity. [23]
  • In the pediatric series, two of seven malignant epithelial ovarian neoplasms were stage Ia, two were stage II, two were stage IIIc, and one was stage IV, and the series used the FIGO 2014 classification system. [11]
  • In the lymphadenectomy study, surgical staging upstaged 28 patients in the lymphadenectomy group and 6 patients in the non-lymphadenectomy group. [140]
  • Positive cytology upstages clear cell ovarian cancer to at least FIGO 1C3. [101]
  • In the neck lymphatic metastasis series, retroperitoneal pelvic and para-aortic lymph node metastasis was classified as FIGO stage IIIc, and neck lymph node metastasis was classified as FIGO stage IV. [49]
  • In one series, patients with endometriosis-associated ovarian cancer were identified at stage I more often than patients with non-endometriosis-associated ovarian cancer. [86]
  • The review states that ovarian epithelial carcinoma is often diagnosed late after spread into the peritoneal cavity. [52]
  • In the Lewis y and TGF-β1 review, Lewis y was present in 95.24% of stage III–IV ovarian cancer specimens and 84.62% of stage I–II specimens, and TGF-β1 was detected in 85.71% of stage III–IV specimens and 74.36% of stage I–II specimens. [52]
  • The same review reported stronger Lewis y expression intensity in stage III–IV than in stage I–II ovarian cancer. [52]
  • The 2020 nomogram study used FIGO stage and reported stage I to IV as recurrence-related factors, and advanced stage was an independent risk factor for recurrence. [15]
  • Sema4C expression in ovarian cancer tissues was significantly associated with clinical and pathological stages of tumors. [104]
  • One study classified ovarian epithelial carcinoma using FIGO stage I to IV, and another cohort ranged from stage I to IV. [98][143][12]3 sources
  • In one endocrine-therapy cohort, most patients had FIGO stage IIIC or IV disease, and FIGO stage IIIC at initial diagnosis was the most common stage in one Korean olaparib cohort. [94][166]
  • In the clear cell ovarian cancer cohort, stage I disease was present in 194 of 303 staged patients, stage II in 34, stage III in 66, and stage IV in 11. [27]
  • In the MRI observational study, all malignant neoplasms were in or above FIGO stage II at the time of imaging. [93]
Show 1 lab & early-research finding
  • Reported cases included one ovarian mucinous cystadenocarcinoma with FIGO stage IVB disease, one endometrioid adenocarcinoma of the ovary with stage Ic(a), one FIGO stage III endometrioid carcinoma of the ovary, and one stage 1aII clear cell adenocarcinoma of the ovary. [70][92][153][9]4 sources
Prognosis102 points
  • A review states that invasion and metastasis are the main factors influencing prognosis, and that the 5-year survival rate is only 20–30%. [29][52]
  • Sources describe type II tumors/carcinomas as having aggressive biologic behavior and contributing to poor prognosis. [24][16]
  • c-Ets1 expression was significantly associated with poor prognosis in epithelial ovarian cancer. [1][2]
  • After clinical remission following standard treatment for advanced or metastatic epithelial ovarian carcinoma, 70% of women are reported to have recurrent disease within the first two years of follow-up. [25]
  • In the clear cell ovarian cancer cohort, median overall survival was not reached in stage I, 112.4 months in stage II, 48.7 months in stage III, and 18.3 months in stage IV. [27]
  • In the clear cell ovarian cancer cohort, 5-year relapse-free survival was 68% for stage I and II combined and 5-year overall survival was 91% for stage I and II combined. [27]
  • In the lymphadenectomy study, the median disease-free survival was comparable between groups and the adjusted hazard ratio for lymphadenectomy was 0.667. [140]
  • In the lymphadenectomy study, 5-year overall survival was 97.7% with lymphadenectomy and 97.2% without lymphadenectomy. [140]
  • FIGO stage was associated with worse disease-free survival and overall survival in one retrospective cohort of ovarian carcinomas. [96]
  • Survivin expression was reported to be significantly associated with survival rate in epithelial ovarian carcinoma. [95]
  • The review platform study reported that 83.2% of original diagnoses were confirmed and 2.5% were finally confirmed as major discrepancies after case discussion. [142]
  • In one advanced ovarian epithelial carcinoma study, patients with minimal residual disease before chemotherapy had higher median survival than those without minimal residual disease, and patients with good performance status before treatment had higher median survival than those with poorer performance status. [143]
  • After a median follow-up of 60 months in one study, 15 of 53 patients were alive and 14 of those were disease-free. [143]
  • In the 48-patient CA 125 and progesterone review, the prognostic value for 5-year survival was somewhat higher for progesterone than CA 125. [99]
  • In the pediatric series, the three-year progression-free survival rate was 37.5% and the three-year overall survival rate was 70%. [11]
  • In the pediatric series, three-year event-free survival was 25% when treatment abandonment was counted as an event. [11]
  • The pediatric review states that normalization of CA-125 after the first cycle of chemotherapy is associated with improved survival in early-stage ovarian cancer. [11]
  • The pediatric series reported that one patient with stage Ia borderline serous cystadenocarcinoma remained alive at 79 months after surgery. [11]
  • The Manitoba review states that overall survival decreased with advancing age. [32]
  • In patients aged 70 to 79, surgery alone had the best survival in the Manitoba cohort. [32]
  • In patients aged 80 to 89, surgery alone had the best survival in the Manitoba cohort. [32]
  • In one cohort, the median progression-free survival was 20 months for high-grade serous ovarian cancer and undefined for endometrioid epithelial ovarian cancer, with no statistically significant difference in progression-free survival between the two histotypes. [12]
  • One review states that if ovarian cancer is diagnosed and treated in time, the 5-year survival rate can go up to 95% when the cancer has not metastasized outside the ovary. [37]
  • The same review states that without proper detection and treatment, the 5-year survival rate is estimated to be around 25%. [37]
  • The review on advanced-stage disease states that complete resection of all macroscopic disease is the strongest independent variable in predicting overall survival. [36]
  • In one PET/CT study, HE4 performed better than CA125 to predict metabolic tumor burden before primary treatment. [102]
  • In one review, ovarian cancer was described as having a poor prognosis because it is often diagnosed at an advanced stage. [38]
  • In the ovarian clear cell carcinoma cohort, no significant differences in overall survival or disease-free survival were found between dMMR and intact MMR patients. [84]
  • In the phase 1 modulated electro-hyperthermia trial, progression was observed in all patients. [144]
  • The 2021 survival review reports that approximately 25% of patients with epithelial ovarian cancer survive more than 5 years and 15% survive more than 10 years. [40]
  • In the nomogram study, advanced stage, histological grade, histological type, lymph node metastasis, and pretreatment CA125 level were independent risk factors for recurrence. [15]
  • The 2021 survival review reports that serous subtype had significantly lower ovarian cancer-specific survival and overall survival than the other three histological subtypes. [40]
  • The same review reports that endometrioid, mucinous, and clear cell subtypes had better ovarian cancer-specific survival than serous subtype in multivariate analysis. [40]
  • The review on immunophenotypic profiles reported that the HNF1β+/p53+/ARID1A+ immunophenotype was associated with significantly worse overall survival and progression-free survival. [105]
  • In the Korean olaparib cohort, median progression-free survival from the start of olaparib maintenance therapy was 14.6 months. [166]
  • In the Korean olaparib cohort, median overall survival was not reached and 24-month overall survival was 82.1%. [166]
  • The 2019 review states that the 5-year survival rate was 42.5% in CD109-positive patients and 64.8% in CD109-negative patients. [42]
  • The same review reports that CD109 expression was associated with overall survival but not recurrence-free survival, and that CD109 expression was not an independent prognostic factor for overall survival or recurrence-free survival in multivariate analysis. [42]
  • One review states that ovarian cancer-related hypercalcemia usually indicates a poor prognosis. [85]
  • One review states that the risk of fatal ovarian cancer increased by 52% for each 0.1 mmol/L increase in total serum calcium levels. [85]
  • One review states that CD109 expression is useful for predicting the chemotherapeutic effect in patients with ovarian epithelial cancer, especially serous carcinoma. [42]
  • A review states that advanced-stage ovarian clear cell carcinoma outcomes are generally unfavorable despite slow growth. [43]
  • A review states that the 5-year overall survival rate for ovarian cancer is slightly over 45% after current standard of care, with most patients having recurrence. [44]
  • A review states that the average cumulative risk of epithelial ovarian cancer by age 70 years is 39% for BRCA1 mutation carriers and 11% for BRCA2 mutation carriers. [108]
  • A review states that risk-reducing salpingo-oophorectomy reduced future risk of epithelial ovarian cancer by more than 80% in women with BRCA1 or BRCA2 mutations. [108]
  • A review states that in women with a significant family history, risk-reducing salpingo-oophorectomy reduces risk of epithelial ovarian cancer by at least 69%. [108]
  • A review states that prior use of menopausal hormone therapy for over 2 years was the only statistically significant risk factor in one WHI analysis, with hazard ratio 1.50. [108]
  • A review states that no tubal ligation had an estimated hazard ratio of 1.24 for epithelial ovarian cancer risk in one WHI analysis, but this was not statistically significant. [108]
  • A review states that modest family history conferred a 19% increase in epithelial ovarian cancer risk in one WHI analysis, but this was not statistically significant. [108]
  • A review states that LEFTY scores were not associated with overall survival, progression-free survival, clinical stage, or lymph node metastasis in the ovarian clear cell carcinoma cases studied. [43]
  • A review states that high LEFTY scores in ovarian clear cell carcinoma were associated with lower Ki-67 labeling indices. [43]
  • Age and FIGO staging were independent prognostic factors for overall and relapse-free ovarian carcinomas in the cited study, whereas Beclin 1 expression was not. [110]
  • Beclin 1 expression might be employed to indicate worse prognosis of ovarian carcinomas, although it was not an independent factor in the cited study. [110]
  • MiR-490-3P expression was negatively associated with FIGO staging. [109]
  • In one study, the GG genotype was more frequent in FIGO I early stage carcinoma than in FIGO II to IV later stage disease, and it was more frequent in patients lacking lymph node involvement than in patients with lymph node involvement. [23]
  • One source states that poor five-year survival is less than 30%, and another source states that mortality is more than 70% within five years. [47]
  • In the neck lymphatic metastasis series, patients with NLNM identified at initial surgery survived longer than patients with NLNM identified at cancer recurrence, and within Group A, survival was longer when the tumor was confined to the pelvic cavity than when it had extended into the abdominal cavity at initial surgery. [49]
  • In the Cox model from the neck lymphatic metastasis series, NLNM identified at cancer recurrence was associated with a higher hazard of death than NLNM identified at initial surgery, non-serous histology was associated with a higher hazard of death than serous histology, and brain metastasis was associated with a higher hazard of death. [49]
  • In the neck lymphatic metastasis series, the median survival period after brain metastasis was 4.4 months. [49]
  • High Lewis y levels are reported to be associated with poor prognosis. [51]
  • Low-grade serous and mucinous carcinomas commonly manifest with early-stage disease and a resultant excellent prognosis. [16]
  • Nuclear survivin expression was reported as a strong, independent prognostic marker for poor clinical outcomes in epithelial ovarian carcinoma. [117]
  • The sources state that type I tumors have a relatively indolent clinical course and overall good prognosis. [16]
  • Type II tumors are associated with a poor prognosis. [53]
  • Serous tumors carry the poorest prognosis among ovarian carcinoma subtypes. [53]
  • In the peritoneal carcinomatosis series, the overall 3-year survival was 61.4% and median survival was 41 months. [138]
  • In the reported series of 11 patients with solitary cerebral metastasis from ovarian epithelial carcinoma, mean survival was 28 months, and the cause of death in that series was recurrence of the systemic disease in all cases. [56]
  • In one study of advanced ovarian epithelial carcinoma, median overall survival was 26.00 months in the intervention group and 25.00 months in the control group, and the overall survival rates were not significantly different between the two groups. [148]
  • The median disease-free interval was 18.20 months in the intervention group and 14.20 months in the control group in one study. [148]
  • One source states that the median survival could not be improved significantly by neoadjuvant platinum-based combination chemotherapy and embolization. [148]
  • In one study, survival was significantly better in patients with less than or equal to 2 cm residual disease at the completion of the original operation. [149]
  • One study reported favorable long-term survival after consolidation with single-dose whole-abdominal radiotherapy in patients with a negative second-look laparotomy. [149]
  • Tumor grade correlated with survival in both early and advanced stage disease in a series of invasive ovarian carcinomas, and tumor grade was significant by multivariate analysis in stage I/II disease and in stage III/IV disease. [150]
  • EGFR positivity was associated with shorter progression-free period and shorter overall survival in one study. [123]
  • PR and ER status were not related to patient survival in one study. [123]
  • Among 27 patients with advanced ovarian carcinoma without macroscopic residual disease after primary operation, 11 of 16 with a DNA index more than 1.3 died of tumor, compared with 2 of 11 with a DNA index less than 1.3. [131]
  • After a median follow-up of 120 months, 14 patients were alive without evidence of disease and 13 had died of progressive disease. [131]
  • Menopausal status was of borderline significance for predicting survival. [131]
  • When age and stage were controlled for, only estimated blood loss and residual tumor predicted poor outcome. [126]
  • Age, histologic grade, and residual volume were reported to stratify patients into high- and low-risk categories for recurrence after negative second-look surgery. [151]
  • In one series of presumed stage I-II invasive ovarian epithelial carcinoma, cumulative 5-year actuarial survival was 73% ± 6%. [77]
  • In that series, 5-year actuarial survival was 75% ± 12% for stage I disease and 71% ± 8% for stage II disease. [77]
  • In the stage I review, 11% of patients had treatment failures detected at second-look laparotomy and 9% later had recurrences after being declared free of disease. [76]
  • In the stage I review, 8 of 9 deaths were associated with Broders grade 3 or 4 and/or stage IC. [76]
  • Five-year actuarial survival and disease-free survival were higher in patients surgically staged by a gynecologic oncologist than in those operated on by a nononcologist. [77]
  • In the same comparison, 5-year actuarial survival was 83% ± 7% versus 59% ± 11%, and disease-free survival was 76% ± 8% versus 39% ± 11%. [77]
  • Residual tumor mass is described as a factor that decisively influences survival. [67]
  • In one small series, three of ten patients with minimal disease were disease-free at 30+, 72+, and 78+ months after abdominopelvic irradiation, and a fourth patient was disease-free at 24+ months after a third laparotomy. [175]
  • The review states that the prognosis of ovarian mucinous cancer patients is poor, and the median overall survival of stage III/IV ovarian mucinous cancer patients is less than 15 months. [70]
  • The review states that cutaneous metastases have a median survival time of four months, and intervals longer than 40 months between diagnosis of ovarian carcinoma and cutaneous symptoms have a better prognosis. [72]
  • One patient with choroidal metastases had a sustained clinical remission for three years after debulking, radiotherapy, and Taxol chemotherapy. [9]
  • One pregnancy-associated case remained in complete remission at 18 months of follow-up after surgery and chemotherapy. [153]
  • In the clear cell ovarian cancer cohort, median relapse-free survival was 138.5 months in stage I, 33.4 months in stage II, 19.3 months in stage III, and 9.7 months in stage IV. [27]
  • In the Manitoba cohort, advanced stage, treatment modality, and advanced age were associated with worse survival. [32]
  • In the Netherlands LGSC cohort, the average 5-year relative survival was 61%. [34]
  • In the Netherlands LGSC cohort, stage I and stage II disease had 5-year relative survival of 89% and 87%, respectively. [34]
  • In the Netherlands LGSC cohort, stage III disease had worse relative survival than stage I or stage II disease, and stage IV disease had worse relative survival than stage I, stage II, and stage III disease. [34]
  • In the Danish cohort, days alive and out of hospital did not differ significantly between age cohorts after debulking surgery. [187]
  • In the long-term survivor cohort, the most common cause of death was primary ovarian cancer. [40]
  • Advanced stage, malignant ascites, residual tumor at completion of operation, increased estimated blood loss, increased hospitalization days, and increased operating room hours were predictors of death in one cohort. [126]
Show 2 lab & early-research findings
  • MMP-2 overexpression in tumor cells was significantly associated with poor prognosis in epithelial ovarian carcinoma, with a pooled hazard ratio of 1.42. [188]
  • In one report, no difference in 2-year survival was associated with in vitro LAK response among stage III patients. [173]
Safety & interactions28 points
  • Grade 1/2 device-related skin adverse events occurred in 83.6% of patients receiving Tumor Treating Fields therapy. [178]
  • In the UKCTOCS trial, both screening tests were associated with minor complications with low complication rates, screening itself did not cause anxiety unless more intense repeat testing was required after abnormal screens, and unnecessary surgery occurred after false-positive screening results in both screening groups. [26]
  • In the endocrine-therapy study, two patients switched to another type of hormone treatment for toxicity reasons, and 4.9% of patients had grade 1/2 arthralgia. [94]
  • In the melphalan study, overall toxicity was quite high and 16 toxicity deaths were recorded in the regimens that included fluorouracil and dactinomycin. [158]
  • In the paclitaxel plus poldine study, two patients stopped halfway due to anaphylactic shock. [156]
  • In one cisplatinum-cyclophosphamide study, toxicity was moderate with a particularly low incidence of nephrotoxicity and no case of serious long-lasting neuropathy. [143]
  • In the lobaplatin-paclitaxel phase I study, 75.0% of patients experienced grade 3 or higher treatment-emergent adverse events; grade 3 to 4 neutropenia occurred in all 12 patients and grade 3 to 4 thrombocytopenia occurred in 5 of 12 patients; no treatment-related deaths or irreversible discontinuations due to adverse events were reported. [29]
  • The hyperspectral imaging review notes that fluorescent agents used for immunofluorescence can produce mild adverse effects such as gastrointestinal disorder, nausea, vomiting, effusion, loss of appetite, diarrhea, and abdominal pain. [36]
  • In the phase 1 modulated electro-hyperthermia trial, no dose-limiting toxicity occurred in the 12 evaluable patients, no severe treatment-emergent adverse event occurred in the paclitaxel arm, and in the cisplatin arm four grade 3 treatment-emergent adverse events were reported: anemia, nausea, neutropenia, and thrombocytopenia. [144]
  • The spheroid review states that non-adherent spheroids become refractory to chemotherapy. [145]
  • The 2020 nomogram study reports that patients with ER-positive expression in tumor tissue had shorter recurrence-free interval than those with negative expression, but the authors note inconsistent conclusions across studies. [15]
  • One review states that continuously high serum calcium levels can cause severe neurologic and renal complications in patients with cancer, and that antihypercalcemic therapy, including saline hydration and calciuresis, may be effective. [85]
  • The p62/SQSTM1 review states that cisplatin-resistant SKOV3/DDP cells were less sensitive to cisplatin treatment. [167]
  • A review states that bilateral salpingo-oophorectomy below age 65 may be avoided because of its potential association with cardiovascular disease, hip fracture, dementia, and Parkinson’s disease. [108]
  • A review states that adding bilateral salpingectomy with ovarian retention to hysterectomy in women without BRCA1/2 mutations showed no negative effects on ovarian function or perioperative complications. [108]
  • In the iodine-125 seed plus gemcitabine study, the common side effects were mild gastrointestinal reactions. [146]
  • No severe postradiation complications were encountered in one study of single-dose whole-abdominal radiotherapy, and mild complications were seen in three patients. [149]
  • Bowel obstruction occurred in 5 of 15 patients after abdominopelvic irradiation in one series, and all episodes were associated with recurrent tumor. [175]
  • The review states that prior bevacizumab and other anti-vascular endothelial growth factor treatments can predispose to cutaneous metastases via acquired resistance and subsequent angiogenesis. [72]
  • Ovarian skin metastases can mimic herpes zoster lesions and present with painful inflammatory skin changes. [8]
  • In one pregnancy-associated case, chemotherapy was given while preserving the fetus and the child had normal development at 18 months. [153]
  • In the rucaparib meta-analysis, 98.7% of patients experienced treatment-emergent adverse events. [164]
  • The Manitoba review states that older patients often have comorbidities, polypharmacy, or decreased functional status, and in the Manitoba cohort, 21.1% of all patients had a chemotherapy dose reduction, 13.2% had dose interruption, 22.7% of patients who received chemotherapy completed no more than two cycles, and 59% of patients over 70 did not receive chemotherapy at any point in their disease course. [32]
  • In the anlotinib retrospective study, two patients discontinued treatment because of intolerable adverse events, and no grade 4 to 5 adverse events were reported. [165]
  • In the Korean olaparib cohort, 64 adverse events were observed, including hematologic and non-hematologic events; the most common hematologic adverse event was anemia, the most common non-hematologic adverse event was nausea or vomiting, and dose reduction was performed in 41% of cases. [166]
Show 3 lab & early-research findings
  • The 2020 lncRNA study reports that overexpression of miR-490-3p reduced the effects of TONSL-AS1 overexpression. [39]
  • A review states that vaccination with AMHR2-CD was accompanied by a rather benign autoimmune phenotype in mouse models. [44]
  • The reported case did not experience fatigue, bone marrow suppression, or impaired liver and kidney function during treatment. [70]
What we don't know yet69 points
  • There is controversy about the potential use of hyperthermic intraperitoneal chemotherapy as an alternative in advanced or metastatic epithelial ovarian carcinoma, and the guideline notes uncertainty about the choice of intraperitoneal chemotherapy drug, dose, dwell time, ideal temperature, and perfusion duration. [25]
  • The TRUST trial is expected to provide additional information in 2024. [25]
  • The UKCTOCS review concludes that population screening for ovarian and tubal cancer in average-risk women using these strategies should not be undertaken, and that decreased incidence of stage III/IV cancers during multimodal screening did not translate to mortality reduction. [26]
  • The efficacy of endocrine therapy remains debatable. [94]
  • Further study focusing on ovarian clear cell carcinoma is required because of its distinct biology and increasing incidence. [27]
  • It remains controversial whether ovarian epithelial carcinoma possesses steroidogenic enzymes. [97]
  • The relevance of qualitative changes in nm23 genes to ovarian carcinoma progression was being investigated. [98]
  • The prevalence data for HRD are available from selected countries. [83]
  • Investigating mechanisms underlying immune-cold to immune-hot transitions and tumor immunotyping may provide insights for designing cancer therapies. [31]
  • The results justify a more detailed study of the role of EBV and the anti-EBV immune response in ovarian cancer. [100]
  • OCCC rarity complicates patient recruitment for clinical trials. [31]
  • Data on childhood epithelial ovarian neoplasms are scarce and sporadic. [11]
  • There are no well-validated predictors of candidacy for aggressive standard-of-care treatment in the geriatric population. [32]
  • Randomized controlled trials and large retrospective series are scarce because low-grade serous carcinoma is rare. [34]
  • The duration of chemotherapy is controversial. [163]
  • The role of radiotherapy in malignant ovarian sex cord-stromal tumors is unclear. [163]
  • There is a continued need for new therapies, identification of patients who would benefit most from these therapies, and development of optimal therapeutic strategies. [12]
  • Clinical use of checkpoint inhibitors in ovarian cancer has shown limited success. [12]
  • The clinical benefit of tumor-based next-generation sequencing in ovarian cancer is largely unknown beyond detection of somatic BRCA1 and BRCA2 mutations. [14]
  • Low days alive and out of hospital after surgery was associated with poor performance status, primary debulking surgery, extensive surgery, and long duration of surgery. [187]
  • Studies on hyperspectral imaging for epithelial ovarian cancer detection are limited. [36]
  • Further studies on tumor markers and their sensitivity and specificity in diagnosing malignant ovarian masses need to be performed. [35]
  • There is currently no conventional guideline, unified treatment plan, or method for prognostic evaluation for gynecologic small-cell neuroendocrine carcinoma. [189]
  • The usefulness and safety of modulated electro-hyperthermia combined with chemotherapy in ovarian cancer were described as lacking evidence before the phase 1 trial. [144]
  • Genetic risk factors and pathways involved in prognosis are not yet completely understood, and determining genetic markers with diagnostic and prognostic values would pave the way for efficient management of cancer. [103]
  • There is no widely accepted tool or model predicting recurrence risk of EOC patients. [15]
  • Key regulators and their functions may present relevant targets for novel therapeutics to reduce treatment resistance and recurrence of ovarian cancer. [145]
  • Greater impact is seen when considering localized therapy in recurrent epithelial ovarian cancer, beyond which clinical presentation and conventional imaging may suffice. [106]
  • Only a minority of ovarian epithelial carcinoma patients respond to immune checkpoint blockade, so complementary treatments are needed. [41]
  • Further studies are needed to determine the relative efficacy and safety of olaparib capsules and tablets. [166]
  • The underlying mechanism between TGF-β1 and Lewis y remains unknown. [17]
  • The efficacy of bilateral salpingectomy with ovarian retention remains to be demonstrated. [108]
  • The significance of LEFTY expression in tumor tissues remains to be clarified. [43]
  • Targeted immunity against non-ovarian-specific tumor-associated antigens has provided modest therapeutic results, and more effective ways to control the disease are needed because of the high recurrence rate and low five-year survival rate. [44]
  • Ovarian cancer screening remains difficult, and understanding links between premalignant conditions such as endometriosis and endometriomas and type I cancers may offer possibilities for prevention and early intervention. [21]
  • The mechanism of ovarian cancer metastasis promoted by LPA requires further investigation. [114]
  • The causal agents for sporadic ovarian cancers are relatively unknown. [23]
  • The molecular mechanism of PAX8 in the carcinogenesis of ovarian epithelial carcinomas remains unclear and requires further analysis. [115]
  • The role of Wnt-5a in ovarian carcinoma remains undetermined in one review. [48]
  • The role of nesfatin-1 in ovarian epithelial carcinoma remains unknown outside the reported cell-line study. [182]
  • The role of ghrelin in ovarian epithelial carcinoma remained unknown before the reported cell-line study. [183]
  • The role of RhoC in ovarian epithelial carcinoma should be considered for further study as a biomarker and target therapy. [88]
  • No markers with high sensitivity and specificity are currently available for clinical diagnosis, staging, and monitoring of therapeutic interventions, and several issues remain to be established for HE4 and Lewis y, including glycosylation status, structure, association with occurrence, development, invasion, migration, resistance, and underlying mechanisms. [51]
  • Abnormalities in the TGF-β signaling pathway can interfere with signal transduction, and dysfunction of this pathway is closely correlated with ovarian cancer progression. [52]
  • The exact role of FSH and LH in ovarian epithelial carcinoma development has not yet been characterized. [118]
  • The etiology and prognostic significance of ovarian serous carcinomas with excessive psammoma bodies remain obscure. [24]
  • Better knowledge of hereditary ovarian cancer syndromes and associated cytogenetic abnormalities has led to increased interest in novel biomarkers and molecular therapeutics. [16]
  • The evidence for elevation of sulfatides in ovarian cancer was based on a colorimetric assay that might have cross-reacted with other lipids. [18]
  • The origins and functional roles of circulating biomarkers in ovarian epithelial tumorigenesis remain to be pinpointed, and further investigation of the observed serum biomarker differences would be justified. [53]
  • The PON1 study reported weak evidence for gene-environment interaction with smoking and no evidence for interaction with obesity. [184]
  • The principles governing gamma delta T-cell specificity and diversity remain unclear due to lack of detailed structural analysis, and more detailed structural analysis is needed to elucidate the key structural basis of gamma delta TCR specificity for tumors. [190]
  • Extending proteomic findings to the bedside will require optimized protocols and reference standards. [55]
  • Altered sialyltransferase expression may be important in malignant ovarian cancers, but the clinical-pathologic parameters studied did not correlate with any given sialyltransferase mRNA expression. [120]
  • The role of HMOCC-1 in treatment remains potential rather than established. [58]
  • HIFU has the potential to serve as a treatment for ovarian cancer, based on an animal-model paper. [57]
  • The value of consolidation therapy in advanced epithelial ovarian carcinoma patients was described as controversial, and a collaborative, prospective, randomized multiarm study is indicated to resolve the controversy about consolidation therapy. [149]
  • The role of hematogenous metastasis in the intraperitoneal dissemination of ovarian cancer remains unclear. [64]
  • It is still obscure whether LHRH produced locally has a stimulatory, inhibitory, or no impact on the proliferation of ovarian cancer cells. [124]
  • The expression of bFGF may vary as a function of histologic grade, but this was not established in the study. [125]
  • There is uncertainty about whether autologous mononuclear cells are effective LAK sources, except perhaps for ascitic mononuclear cells. [173]
  • The role of external radiotherapy was described as having a very good series in response when used to the total pelvis or total abdomen. [67]
  • The optimal treatment for cutaneous ovarian metastases remains unknown. [72]
  • Large-scale prospective studies on treatment are rare, and there is an urgent need for new treatment methods. [70]
  • The literature in these sources describes rare presentations and case-based management rather than established general conclusions. [7]
  • Observational studies reported lower ovarian cancer risk among frequent aspirin users, and most studies relied on a single assessment of aspirin use, which may have led to misclassification. [30]
  • The value of ovarian cancer surveillance in Lynch syndrome was described as controversial, and further studies were said to be needed to examine MMR germline mutations and MLH1 promoter hypermethylation in the cohort. [84]
  • Further research is needed to confirm the relationship between CD109, TGF-β1, and chemoresistance in ovarian epithelial cancer, and more research is needed to determine the association of CD109 with neoplastic cell growth in ovary tissue. [42]
  • Additional studies are needed to better define how resistin, VEGF, and ovarian cancer interactions are initiated and regulated and to determine whether similar effects play a role in vivo. [47]
  • It is unclear to what extent ovarian cancer cell lines accurately model the disease with respect to molecular characteristics, including DNA methylation status, and the proposed cell of origin of ovarian carcinoma is currently under debate. [90]
Biology & pathways91 points
  • Homologous recombination repair is a major pathway for repair of double-strand DNA breaks, and signature 3 is associated with failure to repair DNA double-strand breaks by homologous recombination. [83][12]
  • VEGF secreted by ovarian carcinoma cells may activate STAT pathway via VEGFRs in ovarian carcinoma cells, and Taxol exposure may inhibit the initiating event in angiogenesis, namely, vascular regression. [78][159]
  • Enhanced proteolytic capability of ovarian carcinoma cells relative to normal ovarian epithelium was suggested as a biochemical mechanism for invasion and spread, and increased cell surface proteolysis mediated by urinary-type plasminogen activator bound to its receptor may contribute to metastatic behavior in ovarian carcinoma. [128][127]
  • Sources describe a hormonal role in ovarian carcinogenesis, with a rationale for endocrine therapy in these cancers. [94]
  • OCCC is associated with endometriosis and a putative precursor lesion, and PIK3CA and ARID1A mutations have been noted at high frequency, while BRCA mutation and TP53 mutation are commonly found at low frequency compared with high-grade serous carcinoma. [27]
  • Mutation of nm23 genes and the K-ras gene may affect carcinogenesis or progression of ovarian carcinoma by modulating nm23 gene expression. [98]
  • Changes in tyrosine phosphorylation control proteins may play a role in ovarian cancer development. [133]
  • Aspirin is a non-selective, irreversible inhibitor of cyclooxygenase enzymes and may act through COX-independent pathways including WNT/β-catenin, NF-κB, mTOR, and AMPK. [30]
  • Immune checkpoint blockade therapies have demonstrated clinical benefit, but most immune-cold solid tumors are not responsive to these treatments. [31]
  • Hormonal stimulation of the ovary and repeated disruption and repair of the ovarian surface epithelium during ovulation are proposed hypotheses for epithelial ovarian tumor development. [11]
  • Epithelial ovarian cancers have distinct genomic features, and ovarian clear cell carcinoma is distinguished by the presence of transparent cytoplasm. [33]
  • Sources describe a distinct immune microenvironment in ovarian cancer and suggest that immune escape is more likely in high-grade serous ovarian cancer, which may affect immunotherapy response. [12]
  • FIGO staging defines ovarian cancer stages according to tumor extension, lymph node spread, and distant spread. [36]
  • Base excision repair removes small, non-helix-distorting base lesions from the genome and repairs damaged DNA throughout the cell cycle, and oxidative damage induced by ionizing radiation is commonly corrected by the BER pathway. [37]
  • Lynch syndrome is caused predominantly by germline mutations in one of four DNA mismatch repair genes, including MLH1, MSH2, MSH6, and PMS2. [84]
  • ARID1A abnormalities or loss of protein expression were described as key and early molecular events in the progression of ovarian clear cell carcinoma, PIK3CA or PTEN alterations appear to be required for this process, and inactivation of the ARID1A subunit is observed in approximately half of cases. [84]
  • TONSL-AS1 may sponge miR-490-3p to upregulate CDK1. [39]
  • Sources describe ovarian CSC-enriched spheroid-forming cells with a quiescent phenotype and suppression of focal adhesion and cell cycle-related genes. [145]
  • Ovarian epithelial carcinoma evades the immune response through expression of the PD-1/PD-L1 complex, and infiltration of effector T cells into the tumor site is associated with better prognosis and prolonged survival. [41]
  • The presence of Treg cells in the tumor site and in ascites correlates with poor prognosis, and low CD8+ T cell infiltration increases the probability of dying from ovarian epithelial carcinoma. [41]
  • CD109 is described as a glycosylphosphatidylinositol-linked cell surface glycoprotein and a component of the transforming growth factor beta 1 receptor system, and one review states that CD109 degrades the TGF-β1 receptor and blocks TGF-β1 signaling, thereby preventing tumor suppression. [42]
  • Cisplatin stimulated PGC1α expression and upregulation of mitochondrial biogenesis through PGC1α in ovarian cancer cells. [160]
  • p62 can activate the NF-κB pathway by regulating the ubiquitination of RIP1. [167]
  • FUT1 was a transcriptional target of TGF-β1 through the MAPK pathway in ovarian cancer cells. [17]
  • REG4 has been reported to be a potent activator of the EGFR/Akt/AP-1 signaling pathway. [19]
  • miR-106b directly targets RhoC by binding its 3'UTR. [20]
  • Ovarian epithelial cancers, particularly serous cancers and their precursors with serous differentiation, are likely to be derived from the fallopian tube instead of ovarian surface epithelia. [112]
  • Ovarian carcinomas can undergo epithelial-mesenchymal transition-related changes involving loss of E-cadherin expression in later stage tumors, and EGFR activation can promote disruption of adherens junctions through induction of MMP-9. [46]
  • LPA may promote ovarian cancer invasion and metastasis by regulating genes involved in angiogenesis and metastasis, and the CXCL12-CXCR4 axis can promote tumor growth, angiogenesis, invasion and migration. [114]
  • Resistin induced VEGF expression and production in ovarian epithelial carcinoma cells through the PI3K/Akt pathway and Sp1. [47]
  • The 8q24.3 region was indicated as the most significant region in an integrative analysis of copy number and gene expression in ovarian clear cell adenocarcinoma, and the 8q24.3 gain contained PTK2 and was suggested as a potential therapeutic target in a subset of ovarian clear cell adenocarcinomas. [191]
  • Lovastatin exposure in OVCAR3 cells was associated with reduced proliferation, migration, invasion, and lamellipodia formation, along with lower RhoC and several downstream proteins. [88]
  • Ovarian epithelial carcinoma spread into the peritoneal cavity is an early event in tumorigenesis, and remodeling of the extracellular matrix and subsequent cell surface interactions enable transformation by promoting chromosomal instability and stimulating signal transduction cascades. [50]
  • Lewis y and TGF-β1 expression were positively correlated in ovarian cancer, with a linear correlation between the expression intensity of Lewis y and TGF-β1. [52]
  • Gonadotrophins and estrogen induced ROS production in ovarian epithelial carcinoma and also enhanced NRF2 expression. [135]
  • TP53, K-ras/BRAF, CTNNB1, and PIK3CA mutations are characteristic of high- or low-grade serous, endometrioid, and clear cell carcinomas, respectively. [16]
  • Psammoma bodies may be associated with increased apoptotic tumor cell death related to normal TP53 function. [24]
  • Genes for sulfatide biosynthesis, especially UGT8 and Gal3ST1, were higher in ovarian carcinoma cells than in normal stromal tissue, ST turnover genes were not different between ovarian carcinoma cells and normal stromal tissue, ceramide synthase 4 was higher and other ceramide synthases were decreased in ovarian cancer cells except CerS3, and the mRNAs for SPT3 and DES2 were elevated in ovarian cancer cells. [18]
  • The sonic hedgehog pathway was upregulated in Sertoli-Leydig tumor compared with serous ovarian epithelial carcinoma. [13]
  • Strong MAA staining was seen in the ovarian epithelial carcinoma part, while the stromal part was negative. [120]
  • MICA may play an important role in immune responses against epithelial tumours and function as a stimulating factor for the growth of Vdelta1 gammadelta T cells. [59]
  • PRA down-regulation is associated with the development of ovarian epithelial carcinoma. [60]
  • Angiogenesis was more intense in stage I invasive epithelial ovarian carcinoma than in stage I low-malignant-potential epithelial ovarian carcinoma. [63]
  • Co-expression of M-CSF and c-fms was reported in ovarian epithelial carcinoma, suggesting an autocrine loop, and the c-fms transcript level correlated strongly with high-grade histology, advanced clinical presentations and poor outcome. [136]
  • MMP-2 is reported as the predominant gelatinolytic MMP secreted by primary ovarian cancer cells derived from both ovarian tumors and ascites fluid, and primary ovarian cancer cells catalyze proMMP-2 activation; MT1-MMP-catalyzed activation of proMMP-2 may play a physiologic role in intraperitoneal invasion of ovarian carcinoma cells. [65]
  • Interaction of MMP-2 with the ovarian carcinoma cell surface resulted in a 2.5- to 5-fold increase in invasiveness. [65]
  • Ovarian carcinoma cells showed preferential adhesion to interstitial type I collagen, and antibodies against alpha2 and beta1 subunits inhibited adhesion to type I collagen by 56% and 95%, respectively. [64]
  • Caov-3 ovarian carcinoma cells reduce the bioactivity of TNF-alpha by a novel yet unknown mechanism. [186]
  • No specific gonadotropin-releasing hormone receptors were found in the tumor samples tested in one nude-mouse study, and the latency and transience of the gonadotropin-releasing hormone agonist effect in that model suggested an indirect mechanism of action. [174]
  • The possible indirect mechanisms mentioned include altered circulating steroids, gonadotropins, cell-cycle regulatory events, or other undefined actions related to gonadotropin-releasing hormone agonist administration. [174]
  • The sources suggest an immunosuppressive effect directly related to tumor burden. [173]
  • The sources describe estrogen receptor binding in ovarian epithelial carcinoma and note that diethylstilbestrol inhibited the antibody-shifted estradiol binding peak. [6]
  • Radiotherapy may affect the tumor immune microenvironment, release tumor-associated antigens and immune-stimulating factors, and transform immune "cold tumors" into "hot tumors", and the abscopal effect of radiotherapy is rare in clinical cases. [70]
  • Epithelial ovarian cancer could produce estradiol by itself through potential interactions between cancer cells and stromal cells. [92]
  • MMP-2 and MMP-9 were overexpressed in ovarian cancer cells disseminated in the peritoneal cavity, c-Ets1 controls the expression of some genes involved in extracellular matrix remodeling, and ovarian cancer cells can shed membrane vesicles that contain matrix-degrading proteinases and may mediate invasion and spread. [79][1][80]3 sources
  • Ovarian epithelial carcinoma may lack aromatase, although one study reported aromatase enzymatic activity in three epithelial ovarian carcinoma cell lines and confirmed estrogen synthesis in conditioned medium. [97][192]
    ⚠ Contradicting evidence: One source suggests lack of aromatase, while another reports aromatase activity in some epithelial ovarian carcinoma cell lines. (the more authoritative source is [97]).
  • bFGF might be one of the growth factors regulating ovarian cancer cell proliferation through an autocrine mechanism, and human epithelial ovarian cancers might have a local system based on LHRH to regulate cell proliferation. [125][124]
  • Mifepristone caused dose- and time-dependent growth inhibition of ovarian epithelial carcinoma cell lines in vitro, downregulated progesterone receptor expression, and blocked cells in G0/G1 phase with fewer cells in S phase. [132]
  • Ovarian tumor cell proliferation in vitro was inhibited by testosterone and androstenedione, but not cortisol, by a mechanism independent of steroid receptors. [28]
  • Lobaplatin forms bifunctional platinum–DNA adducts and inter-/intra-strand crosslinks, leading to replication stress, cell-cycle arrest, and apoptosis, and paclitaxel stabilizes microtubules and induces mitotic arrest. [29]
  • The PI3K signaling pathway promotes cell proliferation, growth, tumorigenesis, and motility. [31]
  • Heat shock treatment increased surface calreticulin and released HMGB1 in ovarian epithelial cancer cell lines, except that A2780 did not show significant changes in calreticulin exposure, and heat shock-conditioned ovarian epithelial cancer lysates induced maturation and activation markers on dendritic cells. [41]
  • Sources describe LEFTY as a TGF-β superfamily member that reduced cell proliferation and decreased pSmad2 expression in OCCCa cells. [43]
  • MiR-490-3P directly targeted CDK1 and was reported to promote G1/S or G2/M arrest and apoptosis while reducing cell proliferation, migration, and invasion in the source study, and overexpression reduced CDK1, Bcl-xL, MMP2/9, CCND1, and SMARCD1 expression and induced P53 expression. [109]
  • Beclin 1 is described as an autophagy-related protein involved in autophagy, differentiation, anti-apoptosis, and cancer suppression. [110]
  • RhoC promotes reorganization of the actin cytoskeleton, regulates cell shape and attachment, coordinates cell motility and actomyosin contractility, and overexpression was associated with cell invasion and metastasis of ovarian cancer. [22]
  • RhoC knockdown resulted in low growth, G1 arrest, apoptotic induction, and decreased Akt, stat-3, bcl-xL, and survivin expression with increased Bax and Caspase-3 expression. [22]
  • MPO-generated oxidants could impact tumor cell growth and survival. [23]
  • RhoA and Wnt-5a may be associated with ovarian carcinogenesis and apoptosis inhibition. [48]
  • RhoC is described as a small G protein involved in tumor mobility, invasion, and metastasis, and RhoC knockdown in OVCAR3 cells was associated with low growth, G1 arrest, and apoptotic induction. [88]
  • Nesfatin-1 inhibited proliferation and growth of HO-8910 cells by G1 phase arrest and enhanced apoptosis. [182]
  • Ghrelin and GHSR1a are expressed in ovarian epithelial carcinoma in vivo and in vitro, and ghrelin inhibited proliferation and growth of HO-8910 cells by G1 phase arrest and enhanced apoptosis and autophagy. [183]
  • TGF-β may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal ovarian epithelial cells, whereas most malignant ovarian cell lines are resistant to TGF-β, and TGF-β production may represent a significant tumor escape mechanism from host immunosurveillance and may increase angiogenesis and enhance interaction between cancer cells and extracellular matrix. [52]
  • Survivin is a member of the inhibitor of apoptosis protein family. [117]
  • T-oligos mimic DNA damage responses in cells and induce cytotoxic effects in certain tumor cell lines. [139]
  • Ovarian tumors and cell lines showed distinct clustering in a DNA methylation study, and serous and endometrioid tumors formed distinct clusters with one exception. [90]
  • Ovarian epithelial tumorigenesis involves unchecked proliferation, immune evasion, angiogenesis, stroma formation, tumor cell invasion and migration, and implantation and growth within distant tissues. [53]
  • Type I tumors were reported to more often have BRAF, KRAS, PTEN, and CTNNB1 mutations, while TP53 mutations were common in type II carcinomas, and AKT2, HLA-G, apolipoprotein E, p53, MIB1, and bcl-2 are overexpressed in type II tumors compared with type I tumors. [53]
  • Adrenomedullin was detected in ovarian epithelial carcinoma tissue, and bFGF induced its expression in the CAOV(3) cell line through the JNK-AP-1 pathway. [193]
  • ULBP4 was reported to induce proliferation and cytotoxic activation of human ovarian epithelial carcinoma-derived Vdelta2(+) T cells in vitro. [194]
  • Synthesized ovarian epithelial carcinoma-derived CDR3delta peptides could bind specifically to tumor cell lines and tissues, and CDR3delta appears to have a determinant role in antigen binding. [190]
  • Essiac showed significant antioxidant activity, immunomodulatory effects, and neoplastic cell-specific cytotoxicity in vitro, and the source also reported significant inhibition of several CYP450 enzymes and dose-dependent inhibition of clot fibrinolysis by Essiac. [177]
  • Cultured epithelial ovarian carcinoma cell lines expressed EGFR in 5 of 5 lines, and one of five lines expressed ER. [176]
  • EGF caused proliferation in two ovarian carcinoma cell lines, beta-estradiol caused proliferation in one ER-positive line, and suramin had limited effectiveness in inhibiting growth in four of five cell lines and increased growth of one ER-positive ovarian carcinoma cell line in a dose-dependent manner. [176]
  • In a mouse xenograft model, infiltration of alpha-SMA positive stroma cells into the spheroid was associated with functional vascularization and tumor growth. [195]
  • Ezrin was overexpressed in ovarian carcinoma, with the highest values in metastases, and interleukin-1alpha and epidermal growth factor increased tyrosine phosphorylation, ezrin translocation, and cell growth in SKOV3 cells. [3]
  • Carbon dioxide exposure increased SKOV-3 cell growth in vitro, and the effect was reported to be independent of the carbon dioxide-related decrease in culture media pH. [196]
  • FSH stimulated ovarian epithelial carcinoma cell growth in vitro, and LH blocked the growth-stimulating effects of FSH. [62]
  • Ovarian carcinoma cells adhered preferentially to type I collagen, and this adhesion was inhibited by blocking antibodies to alpha2 and beta1 integrin subunits; type I collagen also promoted ovarian carcinoma cell migration in a concentration-dependent, saturable manner, and culturing ovarian carcinoma cells on type I collagen gels led to a significant increase in conversion of the matrix metalloproteinase 2 zymogen to the 66-kD form. [185]
  • Adhesion to an extracellular matrix comprised primarily of interstitial collagen increased plasminogen activator activity in 5 of 5 cell lines. [64]
  • Murine ovaries exposed to 7,12-dimethylbenz(a)anthracene in beeswax developed one epithelial carcinoma among 35 animals. [197]

Sources

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

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  83. Review articlePrevalence of homologous recombination deficiency in ovarian, primary peritoneal, and/or fallopian tube cancer: results from HALO-Taiwan subset · 2026
  84. Review articleMismatch repair deficiency is associated with specific morphologic features and frequent loss of ARID1A expression in ovarian clear cell carcinoma · 2021
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  86. Review articleClinical analysis of ovarian epithelial carcinoma with coexisting pelvic endometriosis · 2013
  87. Review articleSerum microRNA-92 expression in patients with ovarian epithelial carcinoma · 2013
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  89. Review articleHuman telomerase reverse transcriptase expression in ovarian tumors · 2012
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  92. Case reportOvarian epithelial carcinoma with estrogen-producing stroma · 2007
  93. Review articleEvaluation of Gynecological Mass Lesions Using Magnetic Resonance Imaging: An Observational Study · 2026
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  95. Clinical trialExpression of survivin is associated with malignant potential in epithelial ovarian carcinoma · 2002
  96. Clinical trialPrognostic and predictive values of Nrf2, Keap1, p16 and E-cadherin expression in ovarian epithelial carcinoma · 2015
  97. Clinical trialLack of evidence for aromatase expression in human ovarian epithelial carcinoma · 1994
  98. Clinical trialMutation of the nm23 gene, loss of heterozygosity at the nm23 locus and K-ras mutation in ovarian carcinoma: correlation with tumour progression and nm23 gene expression · 1995
  99. Clinical trialRelationship between CA 125 and progesterone production in women with ovarian carcinoma · 1990
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  101. Review articleThe diagnostic accuracy and prognostic implication of pelvic and peritoneal fluid cytology specimens in ovarian clear cell carcinoma · 2024
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  104. Review articleSemaphorin-4C is upregulated in epithelial ovarian cancer · 2020
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  107. Review articleMicroRNA-152 inhibits ovarian cancer cell proliferation and migration and may infer improved outcomes in ovarian cancer through targeting FOXP1 · 2018
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  109. StudyMicroRNA-490-3P targets CDK1 and inhibits ovarian epithelial carcinoma tumorigenesis and progression · 2015
  110. Review articleAberrant Beclin 1 expression is closely linked to carcinogenesis, differentiation, progression, and prognosis of ovarian epithelial carcinoma · 2014
  111. Review articleThe expression of annexin II and Lewis y antigen in ovarian epithelial tumors and the correlation between them · 2015
  112. Review articleInhibitory role of prohibitin in human ovarian epithelial cancer · 2014
  113. Review articleCysteine-rich, angiogenic inducer, 61 expression in patients with ovarian epithelial carcinoma · 2014
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  115. Review articlePAX8 is a novel marker for differentiating between various types of tumor, particularly ovarian epithelial carcinomas · 2013
  116. Review articleExpression of Sox2 in human ovarian epithelial carcinoma · 2011
  117. Review articleNuclear survivin is associated with malignant potential in epithelial ovarian carcinoma · 2011
  118. Review articleProhibitin as a novel target protein of luteinizing hormone in ovarian epithelial carcinogenesis · 2011
  119. Review articleAdiponectin receptor expression in human malignant tissues · 2010
  120. Review articleAltered mRNA expressions of sialyltransferases in ovarian cancers · 2005
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  122. Review articleTelomerase activity in the female reproductive tract and neoplasms · 1998
  123. Review articleEGFR and steroid receptors in ovarian carcinoma: comparison with prognostic parameters and outcome of patients · 1997
  124. Review articleExpression of the messenger RNAs for luteinizing hormone-releasing hormone (LHRH) and its receptor in human ovarian epithelial carcinoma · 1995
  125. Review articleBasic fibroblast growth factor and ovarian cancer · 1995
  126. Review articleClinicopathologic variables, operative characteristics, and DNA ploidy in predicting outcome in ovarian epithelial carcinoma · 1995
  127. Review articleCoordinate expression of urinary-type plasminogen activator and its receptor accompanies malignant transformation of the ovarian surface epithelium · 1994
  128. Review articleSecretion of extracellular matrix-degrading proteinases is increased in epithelial ovarian carcinoma · 1994
  129. Review articleSmall nucleolar RNA host gene 22 (SNHG22) promotes the progression of esophageal squamous cell carcinoma by miR-429/SESN3 axis · 2020
  130. Review articleNucleobindin-2/Nesfatin-1-A New Cancer Related Molecule? · 2021
  131. Review articleDNA index by flow cytometric analysis: an additional prognostic factor in advanced ovarian carcinoma without residual disease after primary operation · 1996
  132. Clinical trialResponse of human ovarian carcinoma cell lines to antiprogestin mifepristone · 1996
  133. Clinical trialOverexpression of the protein tyrosine phosphatase, nonreceptor type 6 (PTPN6), in human epithelial ovarian cancer · 1995
  134. Review articleIdentification of CSNK1D and KLK6 as two common upregulated genes present in BRCA1 mutated triple-negative breast cancer and ovarian epithelial carcinoma · 2025
  135. Review articleNRF2 is overexpressed in ovarian epithelial carcinoma and is regulated by gonadotrophin and sex-steroid hormones · 2012
  136. Review articleModulation of c-fms proto-oncogene in an ovarian carcinoma cell line by a hammerhead ribozyme · 1997
  137. Review articlePresence of gonadotropin-releasing hormone and its messenger ribonucleic acid in human ovarian epithelial carcinoma · 1993
  138. Review articlePeritoneal carcinomatosis from ovarian epithelial primary: combined aggressive treatment · 2009
  139. Review articleT-oligos inhibit growth and induce apoptosis in human ovarian cancer cells · 2011
  140. Clinical trialLymphadenectomy in clinically early epithelial ovarian cancer and survival analysis (LILAC): a Gynecologic Oncology Research Investigators Collaboration (GORILLA-3002) retrospective study · 2024
  141. Clinical trialPhase II study of ifosfamide plus daily oral etoposide in previously treated ovarian cancer: a Hoosier Oncology Group (HOG) study · 2004
  142. Clinical trialBetter resource utilisation and quality of care for ovarian cancer patients using internet-based pathology review · 2017
  143. Clinical trialA cisplatinum-cyclophosphamide regimen in advanced ovarian cancer: reporting 5-year results · 1993
  144. Review articleModulated electro-hyperthermia with weekly paclitaxel or cisplatin in patients with recurrent or persistent epithelial ovarian, fallopian tube or primary peritoneal carcinoma: The KGOG 3030 trial · 2021
  145. Review articleIntegrative analysis of transcription factors and microRNAs in ovarian cancer cell spheroids · 2020
  146. Review articleEfficacy of permanent iodine-125 seed implants and gemcitabine chemotherapy in patients with platinum- resistant recurrent ovarian carcinoma · 2014
  147. Review articleImmunohistochemical expression of epidermal growth factor receptor, E-cadherin, and matrix metalloproteinase-9 in ovarian epithelial cancer and relation to patient deaths · 2010
  148. Review articleNeoadjuvant intraarterial chemotherapy and embolization in treatment of advanced ovarian epithelial carcinoma · 2004
  149. Review articleWhole-abdomen, single-dose consolidation radiotherapy in patients with pathologically confirmed complete remission of advanced ovarian epithelial carcinoma: a long-term survival analysis · 2004
  150. Review articleToward the development of a universal grading system for ovarian epithelial carcinoma: testing of a proposed system in a series of 461 patients with uniform treatment and follow-up · 1998
  151. Review articleSecond-look surgery in the management of epithelial ovarian carcinoma · 1994
  152. Review articleChemotherapy of advanced ovarian epithelial carcinoma with melphalan and levamisole: a pilot study of the Gynecologic Oncology Group · 1981
  153. Case reportPreservation of pregnancy in a patient with a stage IIIB ovarian epithelial carcinoma diagnosed at 22 weeks of gestation and treated with initial chemotherapy: case report and literature review · 2004
  154. Review articleQuality of surgery and treatment and its association with hospital volume: A population-based study in more than 5000 Belgian ovarian cancer patients · 2024
  155. Review articleThe role of chemotherapy in malignant mixed mullerian tumors of the female genital tract · 2001
  156. Randomized trialChemotherapeutic effects of different paclitaxel plus poldine combination methods for treatment of ovarian carcinoma · 2011
  157. Clinical trialEscalating doses of paclitaxel and epirubicin in combination with cisplatin in advanced ovarian epithelial carcinoma: a phase I-II study · 2003
  158. Randomized trialTreatment of women with disseminated or recurrent advanced ovarian cancer with melphalan alone in combination with 5-fluorouracil and dactinomycin or with the combination of cytoxan, 5-fluorouracil and dactinomycin · 1980
  159. Review articleEvaluation of the antiangiogenic effect of Taxol in a human epithelial ovarian carcinoma cell line · 2004
  160. Review articlePGC1α promotes cisplatin resistance in human ovarian carcinoma cells through upregulation of mitochondrial biogenesis · 2018
  161. Review articleIsobolographic assessment of the interaction between adriamycin and photodynamic therapy with meso-chlorin e6 monoethylene diamine in human epithelial ovarian carcinoma (OVCAR-3) in vitro · 1995
  162. Review articleCD44v6-O-MWNTS-Loaded Gemcitabine and CXCR4 siRNA Improves the Anti-tumor Effectiveness of Ovarian Cancer · 2021
  163. Review articleCurrent status of treatment for malignant ovarian sex cord-stromal tumors · 2024
  164. Meta-analysisEfficacy and safety of rucaparib in patients with recurrent high-grade ovarian carcinoma: A systematic review and meta-analysis · 2024
  165. Review articleEffectiveness and safety of mono-anlotinib mono therapy or in combination with chemotherapy in platinum-resistant recurrent ovarian cancer: a single-center retrospective study · 2023
  166. Review articleReal-World Experience of Olaparib Maintenance in High-Grade Serous Recurrent Ovarian Cancer Patients with BRCA1/2 Mutation: A Korean Multicenter Study · 2019
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  169. Review articleA novel antibody-like TCRγδ-Ig fusion protein exhibits antitumor activity against human ovarian carcinoma · 2013
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  173. Review articleEffector function of lymphokine-activated killer cells and cytotoxic T lymphocytes in ovarian epithelial carcinoma · 1990
  174. Review articleGnRH agonist therapy in human ovarian epithelial carcinoma (OVCAR-3) heterotransplanted in the nude mouse is characterized by latency and transience · 1994
  175. Review articleAbdominopelvic irradiation for persistent advanced ovarian carcinoma · 1989
  176. Review articleEstrogen receptor-positive human epithelial ovarian carcinoma cells respond to the antitumor drug suramin with increased proliferation: possible insight into ER and epidermal growth factor signaling interactions in ovarian cancer · 2004
  177. Review articleIn vitro analysis of the herbal compound Essiac · 2007
  178. Randomized trialTumor Treating Fields therapy in platinum-resistant ovarian cancer: Results of the ENGOT-ov50/GOG-3029/INNOVATE-3 pivotal phase 3 randomized study · 2025
  179. Review articleDescription of first recurrence in advanced stage high grade serous ovarian cancer receiving intraperitoneal versus intravenous systemic treatment · 2025
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  181. Review articlePhotodynamic therapy of human ovarian epithelial carcinoma, OVCAR-3, heterotransplanted in the nude mouse · 1992
  182. StudyNesfatin-1 inhibits ovarian epithelial carcinoma cell proliferation in vitro · 2013
  183. Review articleGhrelin inhibits ovarian epithelial carcinoma cell proliferation in vitro · 2013
  184. Review articleGenetic polymorphisms in the Paraoxonase 1 gene and risk of ovarian epithelial carcinoma · 2008
  185. Review articleMetastatic dissemination of human ovarian epithelial carcinoma is promoted by alpha2beta1-integrin-mediated interaction with type I collagen · 1998
  186. Review articleReduction of tumor necrosis factor-alpha bioactivity by a human ovarian epithelial cancer cell line in vitro · 1995
  187. Review articleDays alive and out of hospital after surgical treatment of epithelial ovarian cancer: A Danish nationwide cohort study · 2023
  188. Meta-analysisPrognostic value of MMP-2 for patients with ovarian epithelial carcinoma: a systematic review and meta-analysis · 2017
  189. Review articlePrevalence, Associated Factors, and Survival Outcomes of Small-Cell Neuroendocrine Carcinoma of the Gynecologic Tract: A Large Population-Based Analysis · 2022
  190. Review articleGammadelta T cells recognize tumor cells via CDR3delta region · 2007
  191. Review articleIntegrative analysis of copy number alteration and gene expression profiling in ovarian clear cell adenocarcinoma · 2013
  192. Review articleAromatization of testosterone by epithelial tumor cells cultured from patients with ovarian carcinoma · 1988
  193. Review articleBasic fibroblast growth factor upregulates adrenomedullin expression in ovarian epithelial carcinoma cells via JNK-AP-1 pathway · 2009
  194. Review articleThe NKG2D ligand ULBP4 binds to TCRgamma9/delta2 and induces cytotoxicity to tumor cells through both TCRgammadelta and NKG2D · 2009
  195. Review articleThe role of angiogenesis, vascular maturation, regression and stroma infiltration in dormancy and growth of implanted MLS ovarian carcinoma spheroids · 2004
  196. Review articleEffect of carbon dioxide on human ovarian carcinoma cell growth · 2001
  197. Review articleChemical induction of ovarian epithelial carcinoma in mice · 1984

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
4
Systematic review
0
Randomized trial
5
Clinical trial
16
Observational
0
Case report
15
Review
167
Preclinical
0
Other
11

Living document — last change June 12, 2026: Cancer page updated. 8 recent updates logged.

Pooled evidence across studies

PubMed
  • 5-year 5-year relative survival after primary debulking by residual disease (subgroup): 73% · (regimen unspecified)
    2 studies · 100% agree · consistent36734363

Numbers pooled deterministically across 22 published studies that passed our figure-accuracy checks — a quick synthesis, not a formal meta-analysis. Updated 8/16/2026.

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
1Relacorilant OtherHuman trial / meta-analysis1—
2Anastrozole Hormonal therapyInsufficient evidence1—
3Bevacizumab Targeted therapyInsufficient evidence1—
4Carboplatin ChemotherapyInsufficient evidence1—
5Cisplatin ChemotherapyInsufficient evidence1—
6Gemcitabine ChemotherapyInsufficient evidence1—
7Liposomal Doxorubicin ChemotherapyInsufficient evidence1—
8Niraparib †Rx Targeted therapyInsufficient evidence1—
9Olaparib Targeted therapyInsufficient evidence1—
10Paclitaxel ChemotherapyInsufficient evidence1—
11Rucaparib Targeted therapyInsufficient evidence1—
12Tamoxifen Hormonal therapyInsufficient evidence1—
13Topotecan OtherInsufficient evidence1—

Ranked across 13 compounds with published studies for this cancer. Updated 8/16/2026.

Medicines & supplements studied for Ovarian Epithelial Carcinoma

PubMedFDAClinicalTrials.gov

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

Medicines · 13

BevacizumabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: Overall response rate (ORR) 69.05%, p both P < 0.05, n=84 PMID 35720032 · response rates 69.05–97.62 across 5 studies

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

Effect sizes reported in only 1 of 2 studies · Includes a retracted study.
Targeted therapyFDA approved2 studiesFull profile →
OlaparibHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: Overall response rate (ORR) 69.05%, p both P < 0.05, n=84 PMID 35720032 · response rates 69.05–97.62 across 5 studies

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

Effect sizes reported in only 1 of 2 studies · Includes a retracted study.
Targeted therapyFDA approved2 studiesFull profile →
RelacorilantHuman trial / meta-analysisMixed results1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: PFS HR 0.66, p P = .038, n=178 PMID 37364223 · hazard ratios 0.36–0.67 across 3 studies

Most authoritative study: Relacorilant + Nab-Paclitaxel in Patients With Recurrent, Platinum-Resistant Ovarian Cancer: A Three-Arm, Randomized, Controlled, Open-Label Phase II Study

Based on a single study.
OtherFDA approvedPhase 21 studyFull profile →
AnastrozoleInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Hormonal therapyFDA off-label1 studyFull profile →
CarboplatinInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA approved1 studyFull profile →
CisplatinInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA approved1 studyFull profile →
GemcitabineInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA approved1 studyFull profile →
Liposomal DoxorubicinInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Chemotherapy1 studyFull profile →
Niraparib †RxInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Targeted therapy1 studyFull profile →
PaclitaxelInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
RucaparibInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Targeted therapyFDA approved1 studyFull profile →
TamoxifenInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Hormonal therapyFDA off-label1 studyFull profile →
TopotecanInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
OtherFDA off-label1 studyFull profile →

What recent studies report in Ovarian Epithelial Carcinoma

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

25 studies11 human1 animal5 lab⚠ Conflicting evidenceMechanism (17)Trial (3)

Tracking 25 published studies of Ovarian Epithelial Carcinoma: 11 in humans, 1 in animals, 5 in the lab, 8 reviews/other.

Reported direction across studies: 15 positive, 5 mixed, 5 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 Ovarian Epithelial Carcinoma.

Compounds with studies mentioning Ovarian Epithelial Carcinoma

Bevacizumab (2)Olaparib (2)Anastrozole (1)Cisplatin (1)Gemcitabine (1)Topotecan (1)Niraparib (1)Carboplatin (1)Liposomal doxorubicin (1)Paclitaxel (1)Tamoxifen (1)Rucaparib (1)Relacorilant (1)
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 381

FOXA1 expression and its association with mucin expression and KRAS mutation in ovarian mucinous tumors: implications for tumor progression and differentiation

Virchows Archiv : an international journal of pathology · Sep 2025

ovarian mucinous tumorsovarian epithelial carcinomas

The authors examined FOXA1 protein expression by immunohistochemistry and KRAS mutation status across normal/benign ovarian tissues, mucinous ovarian tumors, and other ovarian epithelial carcinomas (total n=381). FOXA1 was commonly expressed in mucinous tumors and its expression correlated with MUC2; KRAS mutations increased with malignancy but were relatively enriched in FOXA1-negative cystadenomas. The authors propose that co-occurrence of KRAS mutation and FOXA1 expression may relate to tumor progression and intestinal-type differentiation.

Reported effects: FOXA1 expression in cystadenomas 73.6% · FOXA1 expression in borderline tumors 91.4% · +7 more

Key findings
  • FOXA1 expression was significantly associated with mucinous histology in ovarian epithelial carcinomas (P < 0.001).
  • In mucinous tumors, FOXA1 was expressed in 73.6% of cystadenomas, 91.4% of borderline tumors, 100% of borderline tumors with intraepithelial carcinomas, and 87.5% of carcinomas.
  • MUC2 expression progressively increased from mucinous cystadenomas to borderline tumors (P < 0.050) and significantly correlated with FOXA1 expression (P = 0.024).
  • The prevalence of KRAS mutations tended to increase with the malignancy of mucinous tumors (P < 0.050).
  • KRAS mutations were significantly enriched in FOXA1-negative cystadenomas compared with FOXA1-positive cystadenomas (P < 0.050).
  • A stepwise increase was noted in the percentage of both KRAS mutations and FOXA1 expression from cystadenoma to carcinoma.
Limitations: Observational analysis of tumor specimens only (no functional or mechanistic experiments reported).; No clinical outcome or survival data were reported to link findings to prognosis.; Causality between FOXA1 expression, KRAS mutation, and tumor progression or differentiation cannot be established from the methods described..

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

ReviewTrialInconclusiveLimited evidenceTier 4 · clinicaln = 11

Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

Revista colombiana de obstetricia y ginecologia · Jun 2024 · expert consensus / practice guideline based on literature review

BevacizumabAnastrozoleCisplatinGemcitabineTopotecanOlaparibNiraparibCarboplatinLiposomal-doxorubicinPaclitaxelTamoxifenRucaparibadvanced or metastatic high-grade epithelial ovarian cancerhigh-grade epithelial ovarian cancerovarian epithelial carcinoma

This paper is an expert consensus, not a clinical study of a single drug. Eleven specialists reviewed the literature and issued recommendations for managing advanced or metastatic high-grade epithelial ovarian cancer, including surgery, chemotherapy, genetic testing, bevacizumab, and PARP inhibitors. It does not report new patient outcomes from a trial. The document mainly summarizes what the panel suggested based on existing guidelines and evidence.

Studied with: platinum-based chemotherapy, bevacizumab, paclitaxel, carboplatin.

Key findings
  • The panel suggested primary cytoreductive surgery as the initial approach when complete resection is feasible.
  • Neoadjuvant chemotherapy followed by interval surgery was suggested when complete cytoreduction is unlikely or the patient has poor functional status/comorbidities.
  • Bevacizumab was suggested with platinum-based chemotherapy for high-risk disease, with maintenance only if it was part of first-line therapy.
  • PARP inhibitors (olaparib, niraparib, rucaparib) were suggested as maintenance in selected BRCA/HRD-defined groups.
  • For platinum-resistant relapse, sequential non-platinum single-agent chemotherapy and best supportive care for poor performance status were suggested.
Limitations: This is a consensus statement/practice guideline, not an original comparative trial.; No new efficacy or safety data are reported in the abstract.; Recommendations are based on literature review and expert agreement, so they are subject to guideline-selection and expert-opinion bias.; The abstract does not provide patient-level outcomes, follow-up, or effect estimates.; Several recommendations are conditional/suggested rather than based on direct evidence from this paper..

Provides management recommendations for advanced/metastatic epithelial ovarian cancer, including several anticancer agents and maintenance strategies.

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

Human trialTrialMixed resultsModerate evidenceTier 4 · clinicaln = 178

Relacorilant + Nab-Paclitaxel in Patients With Recurrent, Platinum-Resistant Ovarian Cancer: A Three-Arm, Randomized, Controlled, Open-Label Phase II Study

Journal of clinical oncology : official journal of the American Society of Clinical Oncology · Oct 2023 · three-arm, randomized, controlled, open-label phase II study

Relacorilantovarian cancerovarian epithelial carcinomaprimary peritoneal cancerfallopian tube cancerovarian carcinosarcoma

This phase II study tested relacorilant added to nab-paclitaxel in women with recurrent platinum-resistant or refractory ovarian and related cancers. The intermittent relacorilant schedule improved progression-free survival and duration of response compared with nab-paclitaxel alone, while overall response rate was similar across groups. Side effects were broadly comparable between arms, and the study did not meet its prespecified statistical threshold after multiplicity adjustment.

Reported effects: PFS HR 0.66, p P = .038, n=178 · DOR HR 0.36, p P = .006, n=178 · +1 more

Studied with: nab-paclitaxel.

Key findings
  • Intermittent relacorilant plus nab-paclitaxel improved PFS versus nab-paclitaxel monotherapy (HR 0.66; P = .038).
  • Intermittent relacorilant plus nab-paclitaxel improved DOR versus nab-paclitaxel monotherapy (HR 0.36; P = .006).
  • ORR was similar across arms.
  • At the preplanned OS analysis, the OS HR was 0.67 with P = .066 for the intermittent arm versus nab-paclitaxel monotherapy.
  • Continuous relacorilant plus nab-paclitaxel showed numerically improved median PFS but no significant improvement over monotherapy.
  • Adverse events were comparable across study arms; common grade ≥3 events included neutropenia, anemia, peripheral neuropathy, and fatigue/asthenia.
Limitations: Phase II study with relatively small sample size.; Open-label design.; Primary end point did not reach statistical significance after protocol-prespecified Hochberg step-up multiplicity adjustment.; Median follow-up was limited for PFS and OS analyses.; Safety and efficacy were compared against nab-paclitaxel monotherapy, but the abstract does not provide detailed absolute event rates..

Relacorilant was studied as an add-on to chemotherapy in recurrent platinum-resistant ovarian cancer.

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 = 203

Are ROMA and HE4 More Accurate than CA-125, in Predicting of Ovarian Epithelial Carcinoma?

Advanced biomedical research · Jun 2023 · cross-sectional study

ovarian epithelial carcinomaovarian epithelial masses

This cross-sectional study compared three blood markers—HE4, ROMA, and CA-125—in 203 people with ovarian epithelial masses before surgery. The markers were higher in malignant tumors than in benign or borderline tumors. The study also reported that CA-125 had the highest sensitivity overall, while HE4 and ROMA had higher specificity in some groups.

Reported effect: P value for higher marker levels in malignant tumors, p < 0.001, n=203

Key findings
  • All three markers were significantly higher in malignant tumors than in benign or borderline tumors (P < 0.001 for all).
  • CA-125 had the highest sensitivity overall in pre- and post-menopausal patients (90.7%).
  • HE4 and ROMA had higher specificity than CA-125 overall (98.1% and 97.5% vs 86.9%).
  • In postmenopausal patients, HE4 and ROMA sensitivities were both 90.5%, while CA-125 specificity and sensitivity were the highest (95.2% and 100%).
  • In premenopausal patients, ROMA sensitivity was 90.9% and HE4 specificity was 100%.
Limitations: Cross-sectional design limits causal inference.; Single study with a modest sample size.; Diagnostic accuracy was assessed against pathology, not patient outcomes.; The abstract does not provide confidence intervals for the reported sensitivities/specificities.; The study evaluates biomarkers for prediction/diagnosis rather than effects on cancer growth or survival..

This study evaluates blood markers for predicting malignant ovarian epithelial masses before surgery.

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

The diverse morphology and immunophenotype of ovarian endometrioid carcinomas

Pathology · Apr 2023 · review

ovarian endometrioid carcinomaovarian epithelial carcinomaovarian neoplasmssex cord-gonadal stromal tumours

This narrative review summarizes the wide range of morphologies and immunophenotypes seen in ovarian endometrioid carcinoma, including metaplastic changes, spindle cell/corded and hyalinised features, and sex cord-like formations. It notes that these tumours can undergo transdifferentiation (for example an association with a somatically derived yolk sac tumour) and that aberrant immunohistochemical profiles may complicate distinction from other ovarian tumours. The review also discusses genomic characteristics and the recent incorporation of seromucinous carcinoma into the endometrioid carcinoma category.

Key findings
  • Ovarian endometrioid carcinoma (EC) comprises approximately 10-12% of ovarian epithelial malignancies (stated in abstract).
  • EC displays protean and diverse morphologies, including metaplastic changes, spindle cell differentiation/corded and hyalinised features, and sex cord-like formations.
  • Ovarian ECs show propensity for transdifferentiation; one example discussed is an association with a somatically derived yolk sac tumour.
  • Immunohistochemistry is useful for diagnosing EC and distinguishing it from other ovarian epithelial malignancies, metastases, and sex cord-stromal tumours, but ECs may exhibit aberrant immunophenotypes that increase diagnostic uncertainty.
  • The review discusses the genomic characteristics of these tumours and the recent incorporation of seromucinous carcinoma into the EC category.
Limitations: Review article—no new primary data or experiments reported in this paper.; Narrative review (not stated as systematic); potential for selection or reporting bias in which studies/features are emphasized.; Findings are descriptive and focused on diagnostic morphology/immunophenotype; no quantitative synthesis or prospective validation presented..

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

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 855

Stage, treatment and survival of low-grade serous ovarian carcinoma in the Netherlands: A nationwide study

Acta obstetricia et gynecologica Scandinavica · Mar 2023 · retrospective population-based registry study (Netherlands Cancer Registry)

low-grade serous ovarian carcinomaovarian epithelial carcinoma

This retrospective, registry-based study examined stage at diagnosis, primary surgical treatment (primary vs interval debulking) and 5-year relative survival in 855 patients with low-grade serous ovarian carcinoma in the Netherlands (2000–2019). Over time tumors were more often stage III–IV and interval debulking was used more frequently; overall 5-year relative survival was 61%. Patients who underwent primary debulking surgery had higher 5-year survival than those who underwent interval debulking (60% vs 34%), and absence of macroscopic residual disease after surgery was associated with the best survival.

Reported effects: Stage III (trend), p <0.001 · Stage IV (trend), p <0.001 · +10 more

Key findings
  • LGSC was increasingly diagnosed as stage III (39.9%-59.0%) and IV (5.7%-14.4%) and less often as stage I (34.6%-13.5%; p < 0.001).
  • Primary debulking surgery was the most common strategy (76.2%), but use of interval debulking increased from 10.6% to 31.1% (p < 0.001).
  • Following primary surgery >1 cm residual disease occurred in 15/252 patients (6%) compared with 17/95 patients (17.9%) after interval surgery.
  • Full cohort 5-year relative survival was 61%.
  • Five-year survival after primary debulking surgery was 60% versus 34% after interval debulking surgery.
  • After primary debulking surgery, 5-year survival was 73% with no macroscopic residual disease, 47% with ≤1 cm residual disease and 22% with >1 cm residual disease.
  • After interval debulking surgery, 5-year survival was 51% with no macroscopic residual disease versus 24% with >1 cm residual disease.
  • Except for FIGO stage II (85%-92%), survival did not change significantly over time.
Limitations: Retrospective, observational design using registry data (cannot establish causality).; Potential selection bias and confounding in choice of primary versus interval debulking (non-randomized comparison).; Single-country (Netherlands) data may limit generalizability to other settings.; Abstract does not report details on systemic therapies, performance status, or reasons for choosing surgical strategy (potential unmeasured confounders)..

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

Molecular characteristics and clinical behaviour of epithelial ovarian cancers

Cancer letters · Feb 2023 · review

ovarian epithelial carcinomaovarian neoplasmshigh grade serous ovarian carcinomaendometrioid ovarian carcinomaclear cell ovarian carcinomamucinous ovarian carcinomalow grade serous ovarian carcinoma

This review discusses how ovarian epithelial cancers differ by histotype in their molecular features and clinical behavior. It notes that knowledge of high-grade serous ovarian cancer has led to advances such as PARP inhibitor use, but that these agents are not suitable for all patients, especially many with rare histotypes. The paper emphasizes that more molecular profiling is needed to find additional targeted strategies for these cancers.

Key findings
  • Ovarian carcinoma comprises multiple distinct histotypes with different developmental origins, clinical behavior, and molecular profiles.
  • Knowledge of driver events in high-grade serous ovarian cancer has led to major advances in treatments, including PARP inhibitor use.
  • PARP inhibitors are not suitable for all patients, notably many with rare ovarian cancer histotypes.
  • Genomic characterization in endometrioid, clear cell, mucinous, and low-grade serous ovarian cancer has expanded understanding of mutational events.
  • Substantial knowledge gaps remain, and the review calls for histotype-specific targeted therapeutic strategies.
Limitations: Review article; no original experimental or clinical data.; No quantitative outcomes reported.; Does not evaluate a specific intervention in a controlled study.; Conclusions are based on synthesis of prior literature..

Provides a review of molecular characteristics and clinical behavior of ovarian epithelial cancers, with mention of PARP inhibitors as part of the broader treatment landscape.

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

Human trialTrialReported positiveLimited evidenceTier 4 · clinicaln = 84⚠ Retracted

Effect of PARP Inhibitor Combined with Bevacizumab on Platinum-Resistant Recurrent Ovarian Epithelial Carcinoma

Computational and mathematical methods in medicine · Jun 2022 · randomized controlled trial

OlaparibBevacizumabplatinum-resistant recurrent ovarian epithelial carcinoma

This randomized study assigned 84 patients with platinum-resistant recurrent ovarian epithelial carcinoma to receive olaparib plus bevacizumab (n=42) or albumin-bound paclitaxel plus bevacizumab (n=42). The authors report higher overall response rate, disease control rate, greater reductions in CA125/CA199/HE4 and changes in measured miRNAs, better quality-of-life improvement, and higher 1-, 2-, and 3-year survival rates in the olaparib+bevacizumab group. The abstract contains inconsistent P-value statements for survival (reports higher survival rates but lists "all P > 0.05"), and detailed dosing, adverse-event counts, and blinding are not provided.

Reported effects: Overall response rate (ORR) 69.05%, p both P < 0.05, n=84 · Disease control rate (DCR) 88.1%, p both P < 0.05, n=84 · +3 more

Studied with: bevacizumab.

Key findings
  • Overall response rate (ORR) in the observation group was 69.05% versus 40.48% in the control group (both P < 0.05 as reported).
  • Disease control rate (DCR) in the observation group was 88.10% versus 66.67% in the control group (both P < 0.05 as reported).
  • After treatment, reductions in serum CA125, CA199, HE4 and changes in miRNA124, miRNA-21, and miRNA-203 were greater in the observation group than the control group (all P < 0.05 as reported).
  • Quality-of-life improvement (FACT-G) was greater in the observation group than the control group (P < 0.05 as reported).
  • Reported 1-, 2-, and 3-year survival rates were higher in the observation group (97.62%, 88.10%, 80.95%) than the control group (71.43%, 57.14%, 47.62%); the abstract states "with statistical significances (all P > 0.05)".
Limitations: Single-hospital (single-center) patient cohort as stated ('treated in our hospital'), limiting generalizability.; Small sample size (84 patients total; 42 per arm).; Abstract does not report doses or administration details of olaparib, bevacizumab, or albumin-bound paclitaxel.; Adverse event incidence was compared but numerical adverse-event data are not provided in the abstract.; Inconsistent P-value reporting for survival outcomes in the abstract (survival described as "with statistical significances (all P > 0.05)", which contradicts conventional significance thresholds).; Publication is marked as a retracted publication in the PubMed metadata..

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

ReviewMechanismMixed resultsLimited evidenceTier 1 · lab

Nucleobindin-2/Nesfatin-1-A New Cancer Related Molecule?

International journal of molecular sciences · Aug 2021 · review

breast cancercolon cancerprostate cancerendometrial cancerthyroid cancerbladder cancerglioblastomaadrenocortical carcinomaovarian epithelial carcinoma

This review discusses nucleobindin-2/nesfatin-1 (NUCB2/NESF-1) as a cancer-related molecule. It summarizes reports that higher expression is linked with poorer outcomes and with increased cancer cell proliferation, migration, and invasion in several cancers, while other reports suggest it may inhibit growth in some cancer cell types. The article does not present new experimental data.

Key findings
  • High NUCB2/NESF-1 expression has been associated with poor outcomes in several cancers.
  • Reported effects include increased cell proliferation, migration, and invasion in breast, colon, prostate, endometrial, thyroid, and bladder cancers, and glioblastoma.
  • The review also notes conflicting findings where nesfatin-1 inhibited proliferation in human adrenocortical carcinoma and ovarian epithelial carcinoma cells.
  • The authors propose NUCB2/NESF-1 as a prognostic and predictive marker in cancers.
Limitations: Review article; no original experimental or clinical data.; The abstract summarizes heterogeneous prior studies with conflicting findings.; No quantitative effect estimates are reported in the abstract.; No details on study quality, sample sizes, or methods of the cited studies are provided..

This is a review of a molecule reported to be associated with cancer progression and prognosis, not a primary intervention study.

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

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human⚠ Retracted

Differential expression of miR-130a-3p modulate ovarian epithelial carcinoma (OEC) cell development and could be a biomarker for OEC

Journal of reproductive immunology · Jun 2021

ovarian epithelial carcinoma (OEC)

The study measured miR-130a-3p expression by qRT-PCR in ovarian epithelial carcinoma (OEC) tissues and cell lines, analyzed associations with clinicopathologic features and overall survival, and performed in vitro functional assays. miR-130a-3p expression was reported as lower in OEC samples compared with adjacent normal tissue, low expression associated with worse survival/advanced clinicopathologic features, and overexpression in cell lines reduced proliferation and affected the cell cycle. The authors propose miR-130a-3p as a prognostic biomarker and potential therapeutic target, but clinical validation is not provided.

Key findings
  • miR-130a-3p expression was assessed by qRT-PCR in OEC tissues and cell lines.
  • Expression of miR-130a-3p was found to be lower in 7 OEC samples compared with adjacent normal tissues.
  • Low miR-130a-3p expression was associated with lower overall survival and with FIGO stage and lymph node metastasis (clinicopathologic features).
  • Multivariate Cox analysis identified miR-130a-3p as an independent candidate for predicting prognosis in OEC patients.
  • Over-expression of miR-130a-3p in OEC cell lines inhibited cell proliferation and altered the cell cycle in vitro.
Limitations: Abstract does not report total cohort/sample size (only notes lower expression in 7 OEC samples), so the patient sample size and statistical power are unclear.; Prognostic associations are observational and may be subject to confounding; causality is not established.; Functional experiments were performed in vitro (cell lines) with no in vivo or clinical intervention data presented.; Abstract lacks detailed statistical values (HRs, CIs, p-values) and methodological details in the text provided..

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

Lab · in vitroMechanismReported positivePreclinical onlyTier 1 · lab

LncRNA TONSL-AS1 regulates miR-490-3p/CDK1 to affect ovarian epithelial carcinoma cell proliferation

Journal of ovarian research · May 2020 · TCGA dataset analysis combined with in vitro cell line experiments (OVCAR3)

ovarian epithelial carcinoma

The authors analyzed TCGA data and found that the long noncoding RNA TONSL-AS1 is upregulated in ovarian epithelial carcinoma and that higher expression is associated with worse survival. In OVCAR3 ovarian cancer cells, TONSL-AS1 directly interacts with miR-490-3p and its overexpression increased CDK1 expression and cell proliferation. Overexpression of miR-490-3p reduced proliferation and attenuated the effects of TONSL-AS1 and CDK1 overexpression.

Key findings
  • TONSL-AS1 was upregulated in EOC tumor tissues from EOC patients and its high expression level was correlated with poor survival (TCGA analysis).
  • Dual luciferase assay and RNA interaction prediction indicated a direct interaction between TONSL-AS1 and miR-490-3p.
  • Overexpression of TONSL-AS1 resulted in upregulation of CDK1 mRNA and protein in OVCAR3 cells.
  • Overexpression of TONSL-AS1 and CDK1 increased proliferation rate of OVCAR3 cells in CCK-8 assays.
  • Overexpression of miR-490-3p reduced proliferation and counteracted the proliferative effects of TONSL-AS1 and CDK1 overexpression.
Limitations: Functional experiments were performed in a single in vitro cell line (OVCAR3) with no in vivo validation.; Survival association was based on TCGA dataset only; no independent clinical validation cohort or patient-level details provided.; Abstract does not report sample sizes, effect sizes, or statistical values for the findings.; Mechanistic evidence is limited to luciferase assay, interaction prediction, and overexpression experiments; endogenous loss-of-function experiments not reported in the abstract..

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

ReviewMixed resultsLimited evidenceTier 3 · early human

Surgical prevention strategies in ovarian cancer

Gynecologic oncology · Oct 2018 · narrative review

ovarian cancerovarian epithelial carcinomahigh-grade serous carcinomaendometriosis-associated carcinoma

This narrative review summarizes current understanding of the origins and precursor lesions of ovarian epithelial carcinomas (especially high-grade serous and endometriosis-associated carcinomas) and implications for surgical prevention. It reviews epidemiologic evidence on endometriosis excision, tubal procedures, and bilateral salpingo-oophorectomy and discusses short- and long-term consequences for women's health and quality of life. The authors provide recommendations for women with high-risk genetic mutations and average-risk women and highlight remaining gaps and ongoing research needed to define optimal surgical approaches.

Key findings
  • Effective screening for ovarian cancer is lacking, and surgical removal of at-risk tissue is described as the most successful strategy to decrease risk of cancer development.
  • Optimal timing of surgery, which tissues to remove, and appropriate patient selection for preventive procedures are poorly understood.
  • The review discusses origins and precursor lesions of ovarian epithelial carcinomas, focusing on high-grade serous and endometriosis-associated carcinomas.
  • The authors summarize epidemiologic evidence on surgical prevention strategies including endometriosis excision, tubal procedures, and bilateral salpingo-oophorectomy and consider short- and long-term consequences on women's health and quality of life.
  • The review concludes with recommendations for women with high-risk genetic mutations and for average-risk women and notes ongoing research to clarify optimal approaches that balance risk reduction with quality of life.
Limitations: This is a narrative review and does not present new primary data.; The epidemiologic evidence reviewed is likely observational in nature (as stated) and subject to limitations of such studies.; The abstract states important knowledge gaps remain (optimal timing, tissues to remove, and patient selection), limiting definitive guidance.; Potential short- and long-term consequences for quality of life mean risk-reduction benefits must be balanced against harms; the review does not resolve these trade-offs..

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

Browse all studies mentioning Ovarian Epithelial Carcinoma →

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
Bevacizumab11—2
Olaparib11—2
Relacorilant11—1
Anastrozole—1—1
Carboplatin—1—1
Cisplatin—1—1
Gemcitabine—1—1
Liposomal Doxorubicin—1—1
Niraparib †Rx—1—1
Paclitaxel—1—1
Rucaparib—1—1
Tamoxifen—1—1
Topotecan—1—1

Study mix

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

11 Human1 Animal5 Lab8 Review/other
Reported directionReported positive15Mixed results5Inconclusive5

Compounds with reported-positive results in Ovarian Epithelial Carcinoma

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

Bevacizumab1 positive1 human
Limitations: Single-hospital (single-center) patient cohort as stated ('treated in our hospital'), limiting generalizability.; Small sample size (84 patients total; 42 per arm).; Abstract does not report doses or administration details of olaparib, bevacizumab, or albumin-bound paclitaxel.; Adverse event incidence was compared but numerical adverse-event data are not provided in the abstract.; Inconsistent P-value reporting for survival outcomes in the abstract (survival described as "with statistical significances (all P > 0.05)", which contradicts conventional significance thresholds).; Publication is marked as a retracted publication in the PubMed metadata..
Cited positive studies (1)
Olaparib1 positive1 human
Limitations: Single-hospital (single-center) patient cohort as stated ('treated in our hospital'), limiting generalizability.; Small sample size (84 patients total; 42 per arm).; Abstract does not report doses or administration details of olaparib, bevacizumab, or albumin-bound paclitaxel.; Adverse event incidence was compared but numerical adverse-event data are not provided in the abstract.; Inconsistent P-value reporting for survival outcomes in the abstract (survival described as "with statistical significances (all P > 0.05)", which contradicts conventional significance thresholds).; Publication is marked as a retracted publication in the PubMed metadata..
Cited positive studies (1)

Evidence at a glance: compounds studied in Ovarian Epithelial Carcinoma

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.

BevacizumabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: Overall response rate (ORR) 69.05%, p both P < 0.05, n=84 PMID 35720032 · response rates 69.05–97.62 across 5 studies

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

Effect sizes reported in only 1 of 2 studies · Includes a retracted study.
OlaparibHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: Overall response rate (ORR) 69.05%, p both P < 0.05, n=84 PMID 35720032 · response rates 69.05–97.62 across 5 studies

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

Effect sizes reported in only 1 of 2 studies · Includes a retracted study.
RelacorilantHuman trial / meta-analysisMixed results1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: PFS HR 0.66, p P = .038, n=178 PMID 37364223 · hazard ratios 0.36–0.67 across 3 studies

Most authoritative study: Relacorilant + Nab-Paclitaxel in Patients With Recurrent, Platinum-Resistant Ovarian Cancer: A Three-Arm, Randomized, Controlled, Open-Label Phase II Study

Based on a single study.
AnastrozoleInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
CarboplatinInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
CisplatinInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
GemcitabineInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Liposomal DoxorubicinInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Niraparib †RxInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
PaclitaxelInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
RucaparibInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
TamoxifenInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
TopotecanInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Expert consensus: Profiling and management of advanced or metastatic epithelial ovarian cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.

Clinical trials in Ovarian Epithelial Carcinoma

60 ongoing · 125 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
37 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Ovarian Epithelial Carcinoma — 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 Foundation ↗ — Copay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell Foundation ↗ — Copay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistance ↗ — Limited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family Reach ↗ — Help with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMeds ↗ — Searchable 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.

Help paying for the medicines on this page

Second opinions

Caregiver support

We list only non-profit and government resources — never product sellers — and take no affiliate fees. If a link is broken or a resource doesn't meet that bar, tell us.

Interactions & safety to check: Ovarian Epithelial Carcinoma

This is not a complete interaction check. It only covers the compounds we track and the signals reported in studies. A drug or supplement not listed here is not therefore safe. Bring your full medication and supplement list to your pharmacist and oncologist before changing anything.

Potential interactions: highest-stakes first

  • Niraparib †Rx×CYP1A2 inhibitorshigh-stakeslow
    Monitor: Modest exposure increase (e.g., fluvoxamine).
  • Niraparib †Rx×P-gp substrateshigh-stakeslow
    Monitor: Potential competition (e.g., digoxin).
  • Niraparib †Rx×Bevacizumablow
    Synergize: Complementary PFS extension in ovarian.

Safety considerations

Heading to an appointment? Get a printable one-page summary — studied compounds, open trials, interactions, and questions to ask.
Bring this to your appointment →