These are reviewed studies whose abstracts concern Endometrioid Carcinoma. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Endometrioid Carcinoma. Most are early lab, animal, or small human studies, and findings often conflict.
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 20
The American journal of surgical pathology · Jun 2026 · retrospective case series
endometrioid carcinoma (ovary)endometrioid carcinoma (fallopian tube)
The authors reviewed 20 adnexal endometrioid carcinomas with sex cord-like morphology to describe their histology, immunohistochemistry, and genomics. They found most tumors were PAX8-negative, universally SOX17-positive, frequently showed nuclear beta-catenin staining, and 9 of 10 sequenced cases had activating CTNNB1 variants. These findings suggest SOX17 immunostaining and awareness of CTNNB1/beta-catenin alterations may help avoid misclassification of these tumors.
Reported effects: tumors identified 20 · ovarian_tumors 17 · +15 more
Key findings
- Twenty tumors (17 ovarian, 3 fallopian tube) were identified.
- Sex cord-like patterns included cords/trabeculae (n=17), small tubular glands (n=16), and "granulosa-like" nests (n=12).
- All tumors had conspicuous fibromatous stroma; 11 tumors had background endometrioid adenofibromas.
- Six tumors had associated endometriosis.
- PAX8 was positive in only 2/20 (diffuse in both).
- SOX17 was positive in all cases (focal in 1, diffuse in 19).
- Beta-catenin showed aberrant nuclear staining in 17/20.
- Of the 10 sequenced tumors, 9 showed activating pathogenic variants in CTNNB1; each of these also showed nuclear beta-catenin staining.
- All tumors lacked alterations in mismatch repair genes, TP53, and POLE (as reported).
Limitations: Small sample size (20 tumors).; Retrospective case series design with potential selection bias.; Genomic sequencing performed on a subset (10) of tumors only.; No control group of non-sex-cord-like endometrioid carcinomas presented for direct comparison.; No clinical outcome data or prospective validation reported..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 923
The journal of pathology. Clinical research · Mar 2026 · immunohistochemical study on tissue microarrays using the VENTANA FOLR1 CDx assay with standardized scoring criteria
tubo-ovarian tumorsendometrial tumorshigh-grade serous carcinoma (HGSC)low-grade serous carcinoma (LGSC)endometrial serous carcinomaserous borderline tumorendometrioid ovarian carcinomaclear cell ovarian carcinomamucinous ovarian tumorssex cord-stromal tumorsendometrial endometrioid carcinomasundifferentiated carcinomadedifferentiated carcinomaendometrial clear cell carcinoma
The study examined folate receptor alpha (FRα) expression by immunohistochemistry on tissue microarrays of 923 tubo-ovarian and endometrial tumors using the VENTANA FOLR1 CDx assay and standardized scoring. They found FRα expression most commonly in serous carcinomas (45% of HGSC, 25% LGSC) and less commonly in some endometrial serous and serous borderline tumors, while many other ovarian and endometrial tumor types were negative or rarely positive. The work is descriptive and does not report clinical outcomes or functional testing.
Reported effects: HGSC positive cases 45% · Low-grade serous carcinoma positive cases 25% · +4 more
Key findings
- HGSC (high-grade serous carcinoma): 45% positive cases
- Low-grade serous carcinoma: 25% positive cases
- Endometrial serous carcinoma: 11% positive cases
- Serous borderline tumor: 10% positive cases
- Endometrioid ovarian carcinoma: 2% positive cases
- Clear cell ovarian carcinoma: 1% positive cases
- Mucinous ovarian tumors, sex cord-stromal tumors, endometrial endometrioid carcinomas, undifferentiated and dedifferentiated carcinomas, and endometrial clear cell carcinomas were reported as negative
Limitations: Descriptive immunohistochemistry only — no functional assays or correlation with clinical outcomes reported in the abstract; Use of tissue microarrays may under-represent intratumoral heterogeneity; Cross-sectional/tissue-based study without longitudinal or therapeutic response data.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human
Cancers · Jan 2026
endometrial mixed carcinomaendometrial mixed-feature carcinomaendometrial serous carcinomaendometrioid carcinoma
This small cohort study compared clinical, histologic, and molecular features of mixed and mixed-feature endometrial carcinomas to pure serous and pure endometrioid carcinomas. The mixed tumors occurred in older patients, had shorter median disease-free survival, were high-grade and commonly composed of serous and endometrioid components, and showed identical TP53 and PIK3CA mutations between components consistent with a clonal origin. Mixed tumors also had additional alterations (e.g., TERT, MAP2K1) in higher-grade components, and ERBB2 amplifications were more frequent in the mixed groups.
Reported effects: median age 73 · median disease-free survival 23 mo · +2 more
Key findings
- Patients with mixed and mixed-feature carcinomas were older (median age: 73 years) and had worse disease-free survival (median: 23 months) than those with pure endometrioid carcinoma (median: 48 months).
- Mixed and mixed-feature carcinomas were histologically high-grade, most commonly comprising serous and endometrioid components.
- Molecular profiling supported a clonal origin, with identical TP53 and PIK3CA mutations between the two histologic components in each case.
- Additional gene mutations (e.g., TERT and MAP2K1) were found in higher-grade components.
- ERBB2 amplifications were more frequent in the mixed carcinoma groups (33%) compared to pure serous (11%) and pure endometrioid carcinomas (0%).
- Some mixed and mixed-feature carcinomas showed FBXW7 mutations not seen in pure endometrioid or pure serous carcinomas.
Limitations: Small cohort (described as a small cohort in the title/abstract).; No sample size or detailed study design reported in the abstract.; Observational design limits causal inference regarding outcomes.; Abstract gives no statistical measures (p-values, confidence intervals) or method details for molecular testing.; Potential limited genomic scope implied by the authors' call for targeted sequencing and larger cohorts..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 25
International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Jan 2026 · case series with centralized pathology review
endometrial carcinomaovarian endometrioid carcinoma
The authors reviewed 25 patients with synchronous endometrial and ovarian endometrioid carcinomas and compared staging under the FIGO 2009 versus FIGO 2023 classifications with centralized pathology review. Applying FIGO 2023 (and ESGO risk stratification) changed stage in 5 patients (20%), with 2 downstaged and 3 upstaged; among 11 patients with disease limited to uterus and ovaries, 5 met stage IA3 and none recurred, including 2 managed with surgery alone. The authors conclude FIGO 2023 IA3 can improve risk stratification, particularly for low-grade, ER-positive tumors with favorable molecular profiles, but note issues about adequate staging surgery and ovarian grading criteria.
Reported effects: stage_shifts 20%, n=25 · downstaged_count 2, n=25 · +4 more
Key findings
- Study cohort comprised 25 patients with concurrent endometrial and ovarian tumors.
- Applying FIGO 2023 classification and ESGO risk stratification led to stage shifts in 5 patients (20%): 2 were downstaged and 3 were upstaged.
- Among 11 patients whose disease was limited to the uterus and ovaries, 5 met criteria for stage IA3 and none experienced recurrence; this group included 2 patients managed with surgery alone.
- FIGO 2023 stage IA3 classification enables more precise risk stratification, particularly in low-grade, estrogen receptor-positive tumors with favorable molecular profiles (POLE-mutated or p53 wild-type / non-specific molecular profile).
- The new classification raises operational issues: the need for appropriate staging surgery and debate about the optimal grading system for ovarian endometrioid carcinoma.
Limitations: Small sample size (25 patients).; Observational case-series design with potential selection bias.; Follow-up duration and timing of recurrence assessment are not reported in the abstract.; Low event counts (no recurrences reported) limit strength of outcome conclusions.; Generalizability limited by small cohort and lack of multi-center data in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical
Oncology research · Nov 2025 · narrative review
ovarian endometrioid carcinomaepithelial ovarian cancer
This narrative review summarizes contemporary evidence about ovarian endometrioid carcinoma (OEC), applying the endometrial cancer molecular taxonomy (POLE‑ultramutated, MMRd, p53‑abnormal, NSMP) to OEC. The authors report that OEC is enriched for Lynch syndrome and recommend routine MMR testing; POLEmut/MMRd tumors generally have favorable outcomes and may be candidates for de‑escalation or immunotherapy, while p53‑abnormal/high‑grade tumors have poorer prognosis and may need intensified management or HRD‑directed strategies.
Reported effect: proportion_of_epithelial_ovarian_cancers 10%
Studied with: immune checkpoint inhibitors, HRD-directed strategies.
Key findings
- Ovarian endometrioid carcinoma (OEC) accounts for ~10% of epithelial ovarian cancers and displays broad morphologic diversity that complicates diagnosis and grading.
- The endometrial cancer molecular taxonomy (POLE‑ultramutated, MMRd, p53‑abnormal, NSMP) also applies to OEC.
- OEC is enriched for Lynch syndrome‑associated tumors, supporting routine MMR testing.
- Integrating morphology with molecular classification refines diagnosis and prognostication.
- POLEmut/MMRd subsets generally have excellent outcomes and are candidates for de‑escalation or immunotherapy.
- p53abn/high‑grade tumors carry a poorer prognosis and may warrant intensified management and trials of HRD‑directed strategies.
- Routine MMR immunohistochemistry with reflex germline testing improves Lynch detection.
- Future priorities include prospective validation and multi‑omics to refine NSMP and identify new targets.
Limitations: Narrative review rather than primary research; no new patient‑level data reported.; Recommendations (e.g., de‑escalation, therapeutic strategies) lack prospective validation in OEC as noted by the authors.; Broad morphologic diversity and diagnostic/grading challenges in OEC may limit generalizability of some recommendations.; NSMP group remains heterogeneous and requires further molecular refinement per the authors..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 3
Human pathology · Oct 2025 · case series
endometrial carcinomaendometrioid carcinomapilomatrix-like high-grade endometrioid carcinoma (PiMHEC)
The authors report three human cases of high-grade endometrioid carcinoma with pilomatrix-like features (PiMHEC) that lacked CTNNB1 exon 3 mutations and nuclear β-catenin by IHC. All tumors had characteristic pilomatrix-like morphology, presented at advanced stage, showed aggressive clinical behavior (two recurrences within 12 months), and targeted NGS identified alternative likely oncogenic alterations including FGFR4 p.T259A, TSC2 mutations, KRAS p.G12D, and MYC amplification.
Reported effects: number_of_cases 3, n=3 · patients_presenting_with_advanced_stage_disease 3, n=3 · +6 more
Key findings
- Three cases of high-grade endometrioid carcinoma with pilomatrix-like features were analyzed.
- All tumors demonstrated two components: a high-grade basaloid component with solid sheets of atypical basaloid cells, geographic necrosis, and focal "ghost" cells, and an associated low-grade FIGO grade 1 endometrioid carcinoma component.
- None of the three cases showed nuclear β-catenin expression by IHC, and all lacked CTNNB1 exon 3 mutations.
- All the patients presented with advanced-stage disease (stages IIC-IVB).
- Two patients had a recurrence within 12 months.
- NGS revealed no CTNNB1 mutations, but identified alternative likely oncogenic alterations: one tumor harbored an FGFR4 p. T259A mutation, two tumors had pathogenic TSC2 mutations, one had a KRAS p.G12D mutation, and two showed MYC amplification.
Limitations: Very small sample size (n=3) and single case-series design.; Case reports are descriptive and cannot establish causal relationships between identified mutations and the PiMHEC phenotype.; No functional validation provided to show that the alternative oncogenic alterations drive the pilomatrix-like phenotype.; Limited follow-up data reported (recurrence noted within 12 months for two patients), limiting assessment of long-term outcomes and prognostic significance..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMixed resultsModerate evidenceTier 3 · early humann = 390805
Gynecologic oncology · Sep 2025 · retrospective population-based registry analysis (SEER22, 2000-2019)
endometrial cancerendometrioid carcinomanon-endometrioid carcinomacarcinosarcomaclear cell carcinomaserous carcinomamixed carcinoma
This population-based study used SEER22 data from 2000–2019 (n=390,805) to estimate hysterectomy-corrected, age-specific incidence rates and five-year relative survival for individual endometrial cancer histotypes by race and ethnicity. It found that endometrioid carcinoma incidence was much higher in non-Hispanic White women aged 50+ (104.1 per 100,000) than in other groups, that non-endometrioid histotypes increased sharply around ages 50–54 (especially in non-Hispanic Black women), and that five-year relative survival was highest for endometrioid carcinomas (90.2%) and lower for other histotypes (range 39.6%–59.1%).
Reported effects: endometrioid carcinoma incidence rate, non-Hispanic White women ages 50+ (per 100,000) 104.1 · endometrioid carcinoma incidence rate, other groups ages 50+ (per 100,000) · +3 more
Key findings
- Estimated hysterectomy-corrected, age-specific incidence rates and five-year relative survival for endometrial cancer histotypes using SEER22 (N = 390,805).
- Endometrioid carcinoma rates were similar by race/ethnicity in younger women but much higher in non-Hispanic White women ages 50+ years (104.1 per 100,000) versus other groups (51.1-68.5).
- Non-endometrioid histotypes were rare in younger women, with mixed carcinomas being the most common among the non-endometrioid types.
- Carcinosarcoma, clear cell, and serous carcinoma rates increased sharply at ages 50-54, especially in non-Hispanic Black women.
- Median age at diagnosis was youngest in Hispanic and non-Hispanic Asian/Pacific Islander women, particularly for endometrioid carcinomas.
- Five-year relative survival: endometrioid carcinomas 90.2%; mixed carcinomas 77.0%; other non-endometrioid histotypes range 39.6%–59.1%.
Limitations: Observational registry study — cannot establish causal relationships between age/race/ethnicity and incidence or survival.; Potential for histotype or stage misclassification in registry data.; SEER lacks detailed individual-level risk factor, treatment, or molecular data to explain observed differences.; Hysterectomy-correction methods are estimations and may introduce uncertainty in incidence rates.; Findings are limited to populations covered by SEER and may not generalize to all US regions or internationally..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed
Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 1
International journal of surgical pathology · Sep 2025 · Case report
Endometrial endometrioid carcinomaPilomatrix-like high-grade endometrioid carcinoma
This is a single-patient case report of a 56-year-old woman whose high-grade endometrial endometrioid carcinoma showed complete transdifferentiation to a pilomatrix-like carcinoma pattern, with metastases to ovaries and lymph nodes. Pathology showed basaloid cells with ghost cell keratinization, aberrant cytoplasmic and nuclear β-catenin expression, focal CDX2, absent PAX8 and ER/PR, and NGS identified a CTNNB1 (p.Ser37Phe) mutation with a variant allele frequency of 18.6%. The authors note this tumor is rare, diagnostically challenging, presented at high stage, and it is unknown whether standard adjuvant therapies are effective for this subtype.
Reported effect: CTNNB1 variant allele frequency 18.6%, n=1
Key findings
- Hysterectomy specimen confirmed high-grade endometrioid carcinoma with secondary involvement of both ovaries, left tubo-ovarian ligament and obturator lymph nodes.
- Microscopically the tumor had a solid, nested/insular pattern with peripheral basaloid cells, central ghost cell keratinization, and extensive geographic necrosis.
- No low-grade endometrioid carcinoma component was identified in the primary tumor or metastases after extensive sampling.
- Immunohistochemistry showed aberrant cytoplasmic and nuclear expression of β-catenin, focal CDX2 expression, and negativity for PAX8 and estrogen and progesterone receptors (ER/PR).
- Next-generation sequencing found a CTNNB1 pathogenic mutation (p.Ser37Phe, c.110C > T) with a variant allele frequency of 18.6%.
- Based on morphology, immunohistochemistry and NGS analysis, the diagnosis of pilomatrix-like high-grade endometrioid carcinoma was established.
Limitations: Single-patient case report — findings may not be generalizable.; No data presented on treatment given or therapeutic outcomes for this patient.; Follow-up and clinical outcome details are not reported in the abstract.; Unable to assess effectiveness of standard adjuvant therapies for this subtype from this report..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 18
International journal of molecular sciences · Apr 2025
dedifferentiated endometrioid carcinomaendometrial cancer
This observational study analyzed 18 Japanese cases of dedifferentiated endometrioid carcinoma, with immunostaining on tumor components and whole-exome sequencing in three cases. The authors report that DDEC comprised 2.0% of endometrial cancers, had poor 5-year outcomes (PFS ≈40%, OS ≈30%), and that 66.7% of patients were mismatch repair deficient; they found differing mutation patterns between well-differentiated and undifferentiated components and suggest several targeted therapies could be relevant based on genetics.
Reported effects: incidence of DDEC among endometrial cancers 2% · 5-year progression-free survival 40% · +2 more
Key findings
- Incidence of DDEC was 2.0% among endometrial cancers.
- The 5-year progression-free survival for DDEC was approximately 40%.
- The 5-year overall survival for DDEC was approximately 30%.
- Immunohistochemistry indicated 66.7% of patients were mismatch repair deficient.
- The rate of p53 mutations in this series was higher than reported previously, and p53 mutations in undifferentiated components were associated with poor prognosis.
- Whole-exome sequencing (n = 3) showed different gene mutations and mutation signatures between well-differentiated and undifferentiated components.
- New genetic mutations in undifferentiated regions were uncommon in the three sequenced cases.
- Among the three sequenced cases: one showed homologous recombination deficiency, and the other two had MSI-high and hypermutator phenotypes.
- Authors suggest that immune checkpoint inhibitors, PARP inhibitors, and drugs targeting the p53 pathway may be therapeutically relevant to DDEC based on the genetic findings.
Limitations: Small overall sample size (18 cases); Whole-exome sequencing performed in only 3 cases; Observational, descriptive design with no interventional testing of suggested therapies; Single-country (Japanese) cohort which may limit generalizability; No functional validation of suggested therapeutic targets reported in the abstract.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 2
Pathologica · Feb 2025 · case report (two cases)
corded and hyalinized endometrioid carcinomaendometrioid carcinomaendometrial carcinoma
This paper reports two human cases of high-grade corded and hyalinized endometrioid carcinoma (CHEC) that showed a "no specific molecular profile" (NSMP). Both tumors had a markedly atypical, mitotically active corded component merging with FIGO G3 endometrioid carcinoma and squamous/morular differentiation, and both showed nuclear β-catenin accumulation, retained mismatch repair protein expression, wild-type p53 pattern, and no POLE mutations. The authors note heterogeneity in age and presentation (patients aged 25 and 81) and suggest these tumors be considered a variant of FIGO G3 endometrioid carcinoma.
Reported effects: number_of_cases 2 · tumor_size_case1 6 · +2 more
Key findings
- Both cases demonstrated a markedly atypical and mitotically active corded component merging with a FIGO G3 endometrioid component and accompanied by squamous/morular differentiation.
- Both tumors showed nuclear β-catenin accumulation, retained MMR protein expression, wild-type p53 pattern, and no POLE mutations.
- Case #1 was a 6-cm endometrial mass in a 25-year-old woman, infiltrating the deep myometrium and cervical stroma, with diffuse lymphovascular space invasion.
- Case #2 was an advanced, unresectable endometrial carcinoma involving the lower third of the vagina in an 81-year-old woman.
- The corded component was absent in the hysterectomy specimen of case #1 and in the vaginal biopsy specimen of case #2.
- Authors conclude these cases expand the clinical and molecular heterogeneity of high-grade CHEC and suggest considering them as a variant of FIGO G3 endometrioid carcinoma.
Limitations: Very small sample size (two cases) — case report-level evidence.; Descriptive pathology series without systematic follow-up or outcome data reported in the abstract.; No control or comparison group.; Methods for molecular testing (e.g., POLE testing) and detailed molecular data are not provided in the abstract.; Findings may not be generalizable..
Pathology case report that expands the morphological and molecular spectrum of high-grade corded and hyalinized endometrioid carcinoma (CHEC) by describing two human cases with NSMP.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 2
International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · Jan 2025 · Case report (2 cases)
Endometrial carcinomaCarcinosarcomaEndometrioid carcinoma
The authors report two cases that were morphologically suspicious for endometrial carcinosarcoma but did not meet essential diagnostic criteria. Molecular testing identified pathogenic POLE mutations in both cases, and the tumors were described as low-grade endometrioid carcinomas with a homologous sarcoma component. The report questions the existence of a true POLE-mutated carcinosarcoma entity.
Key findings
- Two cases had morphologic suspicion for endometrial carcinosarcoma but lacked essential criteria for that diagnosis.
- Pathogenic POLE mutations were detected on molecular testing in both cases.
- A descriptive diagnosis rendered was endometrial endometrioid carcinomas, low-grade, with a homologous sarcoma component.
- These observations challenge the existence of POLE-mutated 'carcinosarcoma.'
Limitations: Very small sample size (2 cases).; Case report design without a systematic series or controls.; No clinical follow-up, treatment, or outcome data reported in the abstract.; Abstract provides limited pathological and methodological detail..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismReported positiveModerate evidenceTier 3 · early humann = 122
Histopathology · Nov 2024 · immunohistochemical analysis of a cohort of human tumours (122 cases) including STK11 adnexal tumours and morphological mimics
STK11 adnexal tumourovarian neoplasmsovarian endometrioid carcinomatubo-ovarian high-grade serous carcinomaovarian mesonephric-like adenocarcinomaovarian carcinosarcomaperitoneal malignant mesotheliomapelvic plexiform leiomyomaovarian solid pseudopapillary tumourgranulosa cell tumourSertoli-Leydig cell tumourLeydig cell tumourSertoli cell tumoursteroid cell tumourfemale adnexal tumour of Wolffian originextra-ovarian sex cord-stromal tumour
Researchers performed STK11 (LKB1) immunohistochemistry on 122 human tumour samples, including 17 STK11 adnexal tumours and 105 morphological mimics. All 17 STK11 adnexal tumours showed complete loss of cytoplasmic STK11 staining. Nearly all other tumour types retained cytoplasmic STK11 staining, with the exception of one endometrioid carcinoma with mucinous differentiation showing complete loss and one high-grade serous carcinoma showing subclonal loss. The authors conclude STK11 IHC is a highly sensitive and specific marker for distinguishing STK11 adnexal tumour in the appropriate morphological context and could obviate confirmatory molecular testing.
Reported effects: total tumours tested 122, n=122 · STK11 adnexal tumours included 17, n=17 · +3 more
Key findings
- IHC for STK11 was performed on 122 tumours, including 17 STK11 adnexal tumours and 105 morphological mimics (full list of mimics given in abstract).
- All STK11 adnexal tumours showed complete loss of cytoplasmic staining for STK11.
- All other tumour types showed retained cytoplasmic staining, except for one endometrioid carcinoma with mucinous differentiation which showed complete loss of STK11 expression and a high-grade serous carcinoma with subclonal loss.
- Authors conclude STK11 IHC is a highly sensitive and specific immunohistochemical marker for distinguishing STK11 adnexal tumour from histological mimics and may obviate the need for confirmatory molecular studies in the appropriate morphological context.
Limitations: Small number of STK11 adnexal tumours (n=17), reflecting rarity of the entity.; Study reports a single cohort with no external validation cohort mentioned in the abstract.; Potential selection bias because tumour types were a selected set of morphological mimics.; Abstract does not report blinding, interobserver reproducibility, or diagnostic performance statistics (sensitivity/specificity values) beyond descriptive counts.; Two non-STK11 tumours showed loss/subclonal loss of STK11, indicating imperfect specificity in this cohort..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text