Research Radartracking 1,762 published studies · 471 human · 11 safety signals · 58 clinical trials · 44 cancer pages · updated Sep 2026Open the Research Map →

Clear Cell Carcinoma

A plain-English summary of the published research on Clear Cell 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 →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Jun 2026

Evidence at a glanceHuman trial / meta-analysisMixed results⚠ Studies disagree
90 published studies that name Clear Cell Carcinoma28 human studies approved & graded (trial, observational, or meta-analysis)57 human clinical studies in the Clear Cell Carcinoma corpus888 source documents in the Clear Cell Carcinoma corpus

last checked June 19, 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.

Studied, not standard - investigational
  • surgery
  • surgery + radiotherapy
  • radiotherapy
  • chemotherapy
  • temsirolimus
  • bevacizumab
  • immune checkpoint inhibitors
  • paclitaxel + carboplatin
  • sentinel lymph node mapping
  • gemcitabine

Read the guidelines

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

Treatment map: Clear Cell 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.

10
Interventions
0
Standard of care
4
Tested in people
1
Lab / animal
5
Named in lit.
5
Classes
Standard of care (0) Guideline option (0) Tested in people (4) Lab / animal only (1) Named in the literature (5)

Tested in people, by trial phase: 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
—
1
Radiotherapy
—
—
—
—
2
Chemotherapy
—
—
1
1
1
Targeted therapy
—
—
1
—
1
Immunotherapy
—
—
1
—
—

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

Investigational & adjunct compounds — detail (10)
Meta-analysis (4)
bevacizumaboff-label· Recurrent or later-lineimmune checkpoint inhibitorspaclitaxel + carboplatin· Adjuvant (after surgery)sentinel lymph node mapping
Named in the literature
surgerysurgery + radiotherapyradiotherapychemotherapy· Adjuvant (after surgery)temsirolimus
Lab / animal only
gemcitabineoff-label

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

Reported figures

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Snapshot

The essentials in ~60 seconds — every line is drawn from the cited sources below.

What it is
Clear cell carcinoma is a histologic pattern that occurs in different organs and behaves differently by site: uterine clear cell carcinoma (CCC) is an aggressive non‑endometrioid subtype that accounts for less than 5% of endometrial carcinomas; some head and neck clear cell carcinomas are rare, low‑grade, and typically indolent; ovarian clear cell carcinoma is a rare subtype with poor prognosis and intrinsic resistance to platinum chemotherapy. [1][2][3]
Survival
Prognosis varies by site: in one uterine CCC cohort 5‑year overall survival was 63% (vs 83% for endometrioid endometrial carcinoma); a historical ovarian series reported an overall 5‑year survival of 34% for clear cell tumors; a population analysis of salivary clear cell carcinoma reported 5‑, 10‑, and 20‑year disease‑specific survival of 81.3%, 69.6%, and 55.3%, respectively. [1][4][5]
Standard treatment
Initial management generally includes comprehensive surgical staging followed by adjuvant radiotherapy and/or chemotherapy for uterine CCC; guidelines recommend six cycles of postoperative adjuvant chemotherapy for high‑risk early‑stage disease including clear cell carcinoma and for advanced ovarian cancer. [1][6]
Key test
Targeted next‑generation sequencing to classify uterine CCC into POLE‑mutated, MSI, TP53‑wildtype, or TP53‑mutated molecular subgroups. [1]
Biggest challenge
Major challenges are biological heterogeneity and a high risk of recurrence, with intrinsic platinum resistance in ovarian clear cell carcinoma and only modest clinical activity of immune checkpoint inhibitors in clear cell gynecologic carcinomas. [1][3]

Ask about Clear Cell Carcinoma

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.

Key numbers & factors

Risk factors

  • ▲ increases riskEndometriosis — Associated with the tumor in 8 of 13 (62%) reported primary carcinomas arising in episiotomy scars; severe EMS shows transcriptomic similarity to OCCC. [7][8]
  • ▲ increases riskMale sex (prognostic) — Associated with worse prognosis (HR 4.74). [5]
  • ▲ increases riskRegional metastases (prognostic) — Associated with worse prognosis (HR 5.59). [5]
  • ▲ increases riskDistant metastases (prognostic) — Associated with worse prognosis (HR 8.9). [5]

Biomarkers

  • POLE mutation · Molecular subgroup classification of uterine CCC [1]
  • MSI · Molecular subgroup classification of uterine CCC (present in 5% of pure and 43% of mixed cases in one series) [1]
  • TP53 status · Molecular subgroup classification of uterine CCC (wildtype vs mutated) [1]
  • CA125 KELIM · Indicator of tumor intrinsic chemosensitivity and prognostic for 5‑year recurrence‑free and overall survival [9]

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

Overview5 points
  • Uterine clear cell carcinoma (CCC) is described as an aggressive subtype of non-endometrioid endometrial carcinoma and accounts for less than 5% of endometrial carcinomas. [1]
  • Some head and neck clear cell carcinomas (including hyalinizing clear cell carcinoma and clear cell odontogenic carcinoma) are described in the literature as rare, low-grade, and typically indolent malignancies. [2]
  • Clear cell ovarian carcinoma is a rare sub-type characterized by poor prognosis and intrinsic resistance to platinum-based chemotherapy. [3]
  • Clear cell ovarian carcinoma's distinct molecular profile suggests a potentially greater susceptibility to immunotherapy. [3]
  • Dynamic whole-body and dual-time-point FDG-PET/CT imaging demonstrated different FDG dynamics between clear cell renal cell carcinoma (ccRCC) and non-ccRCC. [10]
Epidemiology3 points
  • Among 13 published primary carcinomas arising in the episiotomy scar site, 8 of 13 (62%) were clear cell carcinomas, and endometriosis was associated with the tumor in eight (62%) cases. [7]
  • Endometrial carcinoma (EC) was reported as the fourth leading cancer in female patients in Europe with 121,600 new cases and 29,600 deaths in 2018. [1]
  • A population-based analysis reported an overall incidence of salivary clear cell carcinoma of 0.011 per 100 000 individuals. [5]
Key biomarkers4 points
  • In this study, targeted next-generation sequencing classified uterine clear cell carcinomas into POLE mutated, MSI, TP53 wildtype, or TP53 mutated molecular subgroups. [1]
  • Within the analyzed cases, MSI was present in 5% of pure uterine CCCs and in 43% of mixed uterine CCCs (p = 0.004). [1]
  • The CA125 ELIMination rate constant K (KELIM) is described as a pragmatic indicator of tumor intrinsic chemosensitivity in advanced epithelial ovarian cancer, and a favorable KELIM score (≥1.0) was associated with higher 5-year recurrence-free survival (68.3% vs 55.9%; HR 0.61, 95% CI 0.48 to 0.77) and 5-year overall survival (80.7% vs 72.8%; HR 0.50, 95% CI 0.36 to 0.68). [9]
  • Severe uterine endometriosis (EMS) showed greater transcriptomic similarity to OCCC than to non-endometriosis-associated ovarian cancer subtypes such as high-grade serous ovarian cancer (HGSOC). [8]
Biology & pathways3 points
  • The VEGF pathway and the mammalian Target of Rapamycin (mTOR) are frequently exploited targets in renal cell carcinoma, and temsirolimus is an mTOR inhibitor that binds FKBP-12; the resulting complex binds and inhibits mTOR. [11]
  • OCCC-specific genes were classified into EMS epithelial cell–specific and tumor microenvironment (TME)–related categories and implicated in pathways tied to tumor progression, invasion, and metabolic reprogramming. [8]
  • Spatial and transcriptomic profiling of ovarian tissue with coexisting endometriosis (EMS) and ovarian clear cell carcinoma (OCCC) support a progression pathway from EMS to OCCC and identify shared molecular features, including overexpression of genes related to tissue development and apoptosis. [8]
Standard management4 points
  • The Society of Gynecologic Oncology recommends comprehensive surgical staging and the use of adjuvant radiotherapy and/or chemotherapy for patients with uterine clear cell carcinoma because of the high incidence of recurrence. [1]
  • The NCCN Clinical Practice Guidelines recommend six cycles of postoperative adjuvant chemotherapy for patients with high-risk early-stage disease including clear cell carcinoma and for those with advanced ovarian cancer. [6]
  • Early and delayed maximum standardized uptake values (SUVe and SUVd) were significantly higher in non-ccRCC than in ccRCC in analyses of all tumors and of T3/4 tumors (both P < 0.05); metabolic rate of FDG (MR FDG) was significantly higher in T3/4 non-ccRCC than in T3/4 ccRCC (P = 0.04). [10]
  • In ROC analysis for differentiating ccRCC from non-ccRCC, delayed SUV (SUVd) showed the highest area under the curve (0.92-0.93 for all and T3/4 RCC) compared with other parameters (0.70-0.84). [10]
Treatments & compounds studied9 treatments

Chemotherapy

  • chemotherapy: Adjuvant (after surgery)Adjuvant chemotherapy is listed among therapies recommended by the Society of Gynecologic Oncology for uterine clear cell carcinoma. [1]
  • paclitaxel plus carboplatin: Adjuvant (after surgery)A reported patient received six cycles of adjuvant paclitaxel plus carboplatin after surgery for FIGO stage IC1 disease. [6]

Targeted therapy

  • temsirolimus: In a Phase III trial in renal cell carcinoma patients with poor prognosis, temsirolimus showed statistically significant advantages over interferon-alpha and was suggested as possibly useful in metastatic non-clear cell carcinoma in a subset analysis. [11]
    improvement in median overall survival vs IFN-α 49% vs IFN-α
    Source quote
    • “Median OS was improved 49% compared to IFN-α, and median PFS was approximately doubled.”
  • bevacizumab: Recurrent or later-lineBevacizumab-based combination therapy in advanced or recurrent ovarian clear cell carcinoma was associated with improved overall survival (HR = 0.51; 95% CI: 0.40-0.66), improved progression-free survival (HR = 0.42; 95% CI: 0.29-0.60), and an overall objective response rate of 49% (95% CI: 39-60%). [12]
    HR for overall survival 0.51 (95% CI 0.4–0.66)HR for progression-free survival 0.42 (95% CI 0.29–0.6)Overall objective response rate (ORR) 49% (95% CI 39–60)
    Source quotes
    • “Results showed that bevacizumab significantly improved overall survival (OS) (HR = 0.51; 95% CI: 0.40-0.66) and progression-free survival (PFS) (HR = 0.42; 95% CI: 0.29-0.60).”
    • “Results showed that bevacizumab significantly improved overall survival (OS) (HR = 0.51; 95% CI: 0.40-0.66) and progression-free survival (PFS) (HR = 0.42; 95% CI: 0.29-0.60).”
    • “The overall objective response rate (ORR), complete response (CR), and partial response (PR) were 49% (95% CI: 39-60%), 17% (95% CI: 9-25%), and 31% (95% CI: 22-41%).”

Immunotherapy

  • immune checkpoint inhibitors: Immune checkpoint inhibitors across clear cell gynecologic carcinomas had a pooled objective response rate of 24.5% (95% CI 18.3 to 32.7), with monotherapy ORR 14.6% (95% CI 8.8 to 24.2, n = 122) and dual blockade ORR 37.5% (95% CI 24.4 to 57.5, n = 77), pooled median progression-free survival 3.8 months and overall survival 18.8 months (n = 130), and grade ≥3 adverse events in 29.36% (N = 288, 95% CI 20.30 to 42.47). [3]
    Pooled objective response rate (all cohorts) 24.5% (95% CI 18.3–32.7), p < .01ORR for ICI monotherapy 14.6% (95% CI 8.8–24.2)ORR for dual blockade 37.5% (95% CI 24.4–57.5)Median progression-free survival (pooled) 3.8 monthsMedian overall survival (pooled) 18.8 monthsGrade ≥3 treatment-related adverse event rate 29.36% (95% CI 20.3–42.47)
    Source quotes
    • “The pooled objective response rate across all treatment cohorts was 24.5% (95% confidence interval [CI] 18.3 to 32.7, I2 = 61%, p < .01).”
    • “Specifically, 14.6% for immune checkpoint inhibitor monotherapy (n = 122, 95% CI 8.8 to 24.2, I2 = 38%, p = .15)”
    • “and 37.5% for dual blockage (n = 77, 95% CI 24.4 to 57.5, I2 = 42%, p = .16).”
    • “Four studies (n = 130) provided re-constructable survival data, yielding a pooled median progression-free survival of 3.8 months and overall survival of 18.8 months.”
    • “Four studies (n = 130) provided re-constructable survival data, yielding a pooled median progression-free survival of 3.8 months and overall survival of 18.8 months.”
    • “Severe treatment-related adverse events grade ≥3 occurred in 29.36% of patients (N = 288, 95% CI 20.30 to 42.47, I2 = 70%).”

Radiotherapy

  • surgery + radiotherapy: In the same series, combination radiation and surgery had a 10-year disease-specific survival of 57.6%. [5]
  • radiotherapy: Radiation monotherapy had a 10-year disease-specific survival of 18.75% in that population-based series. [5]

Procedures & devices

  • surgery: In a population-based study of salivary clear cell carcinoma, surgery alone was reported to have a 10-year disease-specific survival (10-year DSS) of 86.3%. [5]
  • sentinel lymph node mapping: Sentinel lymph node mapping alone did not increase recurrence or mortality versus systemic lymphadenectomy in patients with high-risk endometrial cancer, and subgroup analysis showed no increase in mortality for carcinosarcoma, serous carcinoma, and clear cell carcinoma (HR = 0.51; 95% CI: 0.38-0.67). [13]
    HR for mortality in subgroup (carcinosarcoma, serous, and clear cell) 0.51 (95% CI 0.38–0.67), p = .001 vs systemic lymphadenectomyHR for recurrence (overall comparison SLNM vs LND) 0.89 (95% CI 0.74–1.07), p < 1.00 vs systemic lymphadenectomy
    Source quotes
    • “Subgroup analysis according to histology with mortality data showed no increase in mortality with carcinosarcoma, serous carcinoma, and clear cell carcinoma (HR = 0.51; 95% CI: 0.38-0.67; I2 = 0.0; p = .001).”
    • “No significant differences in recurrence (hazard ratio (HR) = 0.89; 95% confidence interval (CI): 0.74-1.07; I2 = 0; p < 1.00) and mortality (HR = 0.72; 95% CI: 0.56-1.01; I2 = 63.3; p = .001) were observed between the 2 groups.”
Staging & risk2 points
  • In a uterine clear cell carcinoma cohort, stage of disease was assigned based on the 2009 International Federation of Gynecology and Obstetrics (FIGO) endometrial cancer criteria. [1]
Show 1 lab & early-research finding
  • According to the 2021 FIGO staging system, surgical spill in the reported case classified the disease as FIGO stage IC1. [6]
Prognosis5 points
  • In a uterine clear cell carcinoma cohort, reported 5-year overall survival (OS) was 63% compared to 83% in the endometrioid endometrial carcinoma (EEC) population; in the same cohort 11 patients (50%) with pure uterine CCC died during follow-up compared to 4 patients (19%, p = 0.033) with mixed uterine CCC. [1]
  • When compared stage for stage in a historical ovarian series, clear cell tumors were associated with poorer 5-year survival rates with an overall 5-year survival rate of 34%. [4]
  • The pragmatic KELIM score is reported as an independent prognostic factor in patients with a non-mucinous stage I to II ovarian cancer optimally resected and treated with adjuvant chemotherapy and may help identify patients at higher risk of relapse and death. [9]
  • Immune checkpoint inhibitors are reported to demonstrate modest clinical activity in clear cell gynecologic carcinomas, with higher response rates observed for dual-agent regimens. [3]
  • A population-based analysis of salivary clear cell carcinoma reported 5-, 10-, and 20-year disease-specific survival (DSS) rates of 81.3%, 69.6%, and 55.3%, respectively; male sex and regional or distant metastases were associated with worse prognosis with reported hazard ratios of 4.74 for men, 5.59 for regional metastases, and 8.9 for distant metastases. [5]
Safety & interactions2 points

Key figures

Survival & outcomes
OutcomeValue95% CI
Grade ≥3 adverse event rate with immune checkpoint inhibitors29.36%20.3–42.47
Source quotes
  • “Severe treatment-related adverse events grade ≥3 occurred in 29.36% of patients (N = 288, 95% CI 20.30 to 42.47, I2 = 70%).”
  • Severe treatment-related adverse events grade ≥3 occurred in 29.36% of patients receiving immune checkpoint inhibitors in pooled clear cell gynecologic cohorts (N = 288, 95% CI 20.30 to 42.47). [3]
  • Hyalinizing clear cell carcinoma (HCCC) is molecularly distinct but has a propensity for locoregional recurrence. [14]
What we don't know yet3 points
  • Sources describe that pure uterine clear cell carcinoma is molecularly heterogeneous and that this heterogeneity could have consequences for the extent of adjuvant therapy. [1]
  • Substantial heterogeneity and limited survival data support the need for biomarker-driven prospective trials to better define which patients benefit most from immune checkpoint inhibitors in clear cell gynecologic carcinomas. [3]
  • The source describes transcriptomic characterization of coexisting EMS and OCCC that suggests strategies for targeted therapy and improved diagnostics. [8]

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 19, 2026.

  1. Clinical trialPure and mixed clear cell carcinoma of the endometrium: A molecular and immunohistochemical analysis study · 2023
  2. Clinical trialClear cell carcinoma and clear cell odontogenic carcinoma: a comparative clinicopathologic and immunohistochemical study · 2011
  3. Meta-analysisImmune checkpoint inhibitors in clear cell ovarian carcinoma and mixed gynecologic clear cell cohorts: a systematic review and meta-analysis · 2026
  4. Clinical trialClear cell adenocarcinoma of the ovary: a clinical analysis and comparison with serous carcinoma · 1989
  5. Clinical trialSalivary Clear Cell Carcinoma Clinicopathologic Characteristics and Outcomes: A Population-Based Analysis · 2019
  6. Systematic reviewDual TP53 mutations in ovarian high-grade serous carcinoma combined with squamous cell carcinoma: a case report and systematic literature review · 2026
  7. Systematic reviewPrimary Carcinomas of the Episiotomy Scar Site: A Systematic Literature Review · 2025
  8. StudyTranscriptomic landscape of coexisting ovarian clear cell carcinoma and endometriosis: Insights into malignant transformation · 2026
  9. Meta-analysisIdentifying high-risk relapse in early-stage I to II ovarian cancer using the CA125 ELIMination rate constant K (KELIM) score: a Gynecologic Cancer InterGroup individual patient-data meta-analysis · 2026
  10. Clinical trialFour-dimensional parametric and dual-time-point FDG-PET/CT imaging in metabolically active renal cell carcinoma: a comparison of clear cell and non-clear cell carcinoma · 2026
  11. Clinical trialTemsirolimus: a safety and efficacy review · 2012
  12. Meta-analysisSystematic Review and Single-Arm Meta-Analysis of Bevacizumab Combined with Chemotherapy or Immunotherapy for Oncological Outcomes in Advanced/Recurrent Ovarian Clear Cell Carcinoma · 2026
  13. Meta-analysisSentinel Lymph Node Mapping Versus Systemic Lymphadenectomy in High-Risk Endometrial Cancer Patients: A Meta-Analysis of Oncologic Outcomes · 2026
  14. Clinical trialReappraising hyalinizing clear cell carcinoma: A population-based study with molecular confirmation · 2017

What supports this page

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

Guideline
7
Meta-analysis
28
Systematic review
18
Randomized trial
1
Clinical trial
16
Observational
2
Case report
216
Review
569
Preclinical
0
Other
31

Living document — last change June 19, 2026: Cancer page updated. 3 recent updates logged.

Pooled evidence across studies

PubMed
  • PRAME immunoreactivity rate: 76% (60–90 across studies) · PRAME (Preferentially expressed antigen in melanoma)
    13 studies · 62% agree · moderate35973038
  • 10-year Disease-specific survival at 10 years: 86.3% (69.6–86.3 across studies) · (regimen unspecified)
    3 studies · 67% agree · moderate · 1 flagged31142129
  • Disease-specific survival: HR 5.59 (4.74–8.9 across studies) · (regimen unspecified)
    3 studies · 33% agree · heterogeneous · 1 flagged31142129
  • Five-year relative survival: 83.6% (77–90.2 across studies) · (regimen unspecified)
    2 studies · 100% agree · consistent40752271
  • 5-year Disease-specific survival at 5 years: 88.83% (81.3–96.36 across studies) · (regimen unspecified)
    2 studies · 100% agree · consistent31142129
  • Risk of recurrence (subgroup): HR 0.705 (0.7–0.71 across studies) · (regimen unspecified)
    2 studies · 100% agree · consistent20629008

Numbers pooled deterministically across 76 published studies that passed our figure-accuracy checks — a quick synthesis, not a formal meta-analysis. Updated 9/4/2026.

Medicines & supplements studied for Clear Cell Carcinoma

PubMedFDAClinicalTrials.gov

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

Medicines · 1

GemcitabineInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Treatment Strategies for ARID1A-Deficient Ovarian Clear Cell Carcinoma

No human studies yet · No numeric effect sizes reported.
ChemotherapyFDA off-label2 studiesFull profile →

What recent studies report in Clear Cell Carcinoma

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

60 studies24 human4 animal2 lab⚠ Conflicting evidenceMechanism (43)Supportive care (1)

Tracking 60 published studies of Clear Cell Carcinoma: 24 in humans, 4 in animals, 2 in the lab, 30 reviews/other.

Reported direction across studies: 22 positive, 12 mixed, 3 negative, 23 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 Clear Cell Carcinoma.

Compounds with studies mentioning Clear Cell Carcinoma

Gemcitabine (2)
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 923

Folate receptor alpha (FRα) expression in tubo-ovarian and endometrial tumors: a study of 923 cases

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 positiveModerate evidenceTier 3 · early human

IRF7 is a novel prognostic biomarker in kidney renal clear cell carcinoma

Scientific reports · Jan 2026 · Multi-omics retrospective analysis of public cohorts (TCGA, GTEx, CPTAC) with tissue microarray validation and bioinformatic functional analyses

kidney renal clear cell carcinoma (KIRC)

This study used multi-omics analyses of public datasets and tissue microarrays to evaluate IRF7 in cancers, focusing on kidney renal clear cell carcinoma (KIRC). IRF7 was dysregulated across cancers and higher IRF7 expression in KIRC was associated with worse survival; tissue microarrays confirmed higher IRF7 in tumors versus normal tissue. Functional analyses linked IRF7 to immune checkpoints, T-cell activity, methylation, fatty acid metabolism, oxidative phosphorylation, and drug sensitivity. A KIRC-specific prognostic nomogram including IRF7 predicted overall survival with high accuracy.

Reported effects: KIRC differential expression p-value, p p&#x2009;&lt;&#x2009;0.001 · Association of elevated IRF7 expression with poor survival, p p&#x2009;&lt;&#x2009;0.01 · +1 more

Key findings
  • IRF7 was dysregulated in 22 cancers (KIRC: p&#x2009;&lt;&#x2009;0.001).
  • Elevated IRF7 expression in KIRC correlated with poor survival (p&#x2009;&lt;&#x2009;0.01).
  • IRF7 expression associated with immune checkpoints, epigenetic modifiers, T-cell activity, and methylation.
  • Functional analyses implicated IRF7 in fatty acid metabolism, oxidative phosphorylation, and drug sensitivity.
  • A KIRC-specific nomogram predicted overall survival with high accuracy.
  • Tissue microarrays confirmed IRF7 overexpression in KIRC versus normal tissues (p&#x2009;&lt;&#x2009;0.001), linked to reduced survival.
Limitations: Observational, retrospective bioinformatic analysis without prospective validation.; Abstract does not report sample sizes, effect sizes, or metrics for the nomogram performance.; Association data cannot establish causality or therapeutic predictive value.; No functional in vivo experiments or interventional data reported in the abstract..

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

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

Transcriptomic landscape of coexisting ovarian clear cell carcinoma and endometriosis: Insights into malignant transformation

Cancer treatment and research communications · Jan 2026 · Spatial transcriptomics profiling integrated with single-cell RNA sequencing (scRNA-seq) of tissues containing coexisting endometriosis and ovarian clear cell carcinoma regions

endometriosisovarian clear cell carcinomahigh-grade serous ovarian cancer

This study used spatial transcriptomics combined with single-cell RNA sequencing to compare molecular profiles of coexisting endometriosis and ovarian clear cell carcinoma (OCCC) regions in human tissue. The authors report shared molecular features between EMS and OCCC, greater transcriptomic similarity of severe uterine EMS to OCCC than to HGSOC, and classification of OCCC-specific genes into EMS epithelial cell-specific and tumor microenvironment-related groups that are associated with pathways linked to progression, invasion, and metabolic reprogramming.

Key findings
  • Spatial transcriptomic profiling revealed shared molecular features between OCCC and EMS, including overexpression of genes related to tissue development and apoptosis.
  • Integration with scRNA-seq data showed severe uterine EMS exhibited greater transcriptomic similarities to OCCC than to non-EAOC ovarian cancer subtypes such as HGSOC.
  • OCCC-specific genes were classified into EMS epithelial cell-specific and tumor microenvironment-related categories.
  • Identified gene sets and categories are associated with pathways implicated in tumor progression, invasion, and metabolic reprogramming.
  • Findings support a transcriptomic progression pathway from EMS to OCCC and provide molecular insights relevant to etiology, diagnostics, and potential targeted strategies.
Limitations: Sample size and cohort details are not reported in the abstract.; Observational, transcriptomic profiling only — correlative data that cannot establish causal malignant transformation.; No functional validation experiments (e.g., in vitro/in vivo perturbation) are reported in the abstract to confirm mechanistic roles of identified genes or pathways.; Generalizability is unclear because the abstract does not describe the number or diversity of patients/tissues analyzed..

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

ReviewInconclusiveLimited evidenceTier 4 · clinical

Genomics of ovarian cancers and the potential of precision medicine

Therapeutic advances in medical oncology · Dec 2025 · review

epithelial ovarian cancerhigh-grade serous ovarian cancerovarian clear cell carcinomaendometrioid ovarian carcinomamucinous ovarian carcinomalow-grade serous ovarian carcinomaovarian carcinosarcoma

This review describes the main genomic subtypes of epithelial ovarian cancer and how those differences may help match patients to targeted therapies. It highlights PARP inhibitors, MAPK pathway inhibitors, cell cycle checkpoint inhibitors, immune checkpoint inhibitors, and antibody-drug conjugate approaches that are being investigated for specific ovarian cancer types. The article also notes that resistance to PARP inhibitors remains a problem and that more evidence is needed for effective combination therapies.

Key findings
  • High-grade serous ovarian cancer is linked mainly to homologous recombination repair gene alterations such as BRCA1 and BRCA2.
  • Ovarian clear cell carcinoma is associated with ARID1A and PIK3CA alterations; endometrioid ovarian carcinoma with PIK3CA and KRAS; mucinous ovarian carcinoma with CDKN2A and KRAS; and low-grade serous ovarian carcinoma with MAPK pathway genes such as BRAF and KRAS.
  • PARP inhibitor therapy has improved survival for women with homologous recombination repair defects in high-grade serous ovarian cancer, but acquired resistance remains an issue.
  • The review emphasizes that genomically targeted combination therapies are urgently needed and that some reported responses are preliminary.
Limitations: Review article only; no new experimental or clinical data presented in the abstract.; No quantitative outcomes or effect sizes are reported in the abstract.; The abstract is broad and does not provide trial-level details, sample sizes, or follow-up durations.; Some therapies discussed are preliminary and require further evidence..

The article is about ovarian cancer genomics and targeted therapies, not a single compound experiment.

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 humann = 48

Napsin-A Expression in Mesonephric and Mesonephric-like Adenocarcinomas: Implications for Distinction From Clear Cell Carcinoma

International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · Nov 2025 · case series

mesonephric adenocarcinomamesonephric-like adenocarcinomaclear cell carcinomamesonephric carcinosarcoma

The authors performed Napsin-A immunohistochemistry on whole-slide sections from 48 mesonephric and mesonephric-like adenocarcinomas and carcinosarcomas. Napsin-A was positive in 17/48 cases (35.4%), with focal granular cytoplasmic staining in 1–40% of cells; positivity occurred in 13/32 MLAs, 2/13 MAs, and 2/3 carcinosarcomas. The study concludes that Napsin-A is expressed in a substantial subset of these tumors and that reliance on a single marker could lead to misclassification as clear cell carcinoma.

Reported effects: Napsin-A positive overall 35.4%, n=48 · Range of focal granular cytoplasmic expression · +3 more

Key findings
  • Napsin-A staining was positive in 17 of 48 cases (35.4%), with focal granular cytoplasmic expression ranging from 1% to 40%.
  • 13/32 (40.6%) mesonephric-like adenocarcinomas (MLAs) were Napsin-A positive.
  • 2/13 (15.4%) mesonephric adenocarcinomas (MAs) were Napsin-A positive.
  • 2/3 (66.7%) mesonephric or mesonephric-like carcinosarcomas were Napsin-A positive.
  • Because of morphologic and immunohistochemical overlap, Napsin-A expression in MA/MLA may contribute to misclassification as clear cell carcinoma.
Limitations: Observational pathology series without reported clinical outcome correlation; Relatively small overall sample size and very small subgroup sizes (e.g., n=3 carcinosarcomas); Findings are based solely on immunohistochemistry on tissue sections; no clinical or molecular correlation reported in the abstract.

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

Animal studyReported positivePreclinical onlyTier 2 · animal

The effectiveness of anti-PD-L1 treatment and the underlying regulatory mechanism in ovarian clear cell carcinoma

International immunopharmacology · Oct 2025 · in vitro cell experiments and mouse in vivo experiments with molecular assays (western blot, RT-PCR, RNA pull-down, RIP)

ovarian clear cell carcinoma

This laboratory study used cell-based assays and mouse models to test anti-PD-L1 treatment in ovarian clear cell carcinoma (OCCC). The authors report that anti-PD-L1 showed effectiveness in OCCC, that PD-L1 is highly expressed and associated with proliferation, invasion and metastasis, and that the lncRNA ZFPM2-AS1 binds HNRNPC and the ZFPM2-AS1/HNRNPC axis modulates the response to anti-PD-L1. The work is preclinical and uses molecular, cellular and animal experiments.

Key findings
  • The study identified effectiveness of anti-PD-L1 treatment in OCCC (reported in vitro and in vivo).
  • PD-L1 was highly expressed in OCCC and was closely related to proliferation, invasion and metastasis in vitro and in vivo.
  • ZFPM2-AS1 was overexpressed in OCCC and can bind HNRNPC.
  • The ZFPM2-AS1/HNRNPC axis participates in regulating the effectiveness of anti-PD-L1 treatment.
Limitations: Preclinical study only (cellular assays and animal models); no human trial or clinical data reported in the abstract.; Abstract does not report sample sizes, numerical effect sizes, or statistical significance.; Details of experimental controls, doses, and treatment schedules are not provided in the abstract..

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

Age-specific incidence and five-year relative survival of endometrial cancer histotypes by race and ethnicity among US women, 2000 to 2019

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

Lab · in vitroMechanismMixed resultsPreclinical onlyTier 1 · lab

Proteomic Analysis of ARID1A-Deficient Ovarian Clear Cell Carcinoma Cells Reveals Differential Mitochondria ETC Subunit Abundances and Targetable Mitochondrial Pathways

International journal of molecular sciences · Jun 2025

ovarian clear cell carcinoma

The authors performed biochemical and proteomic analyses on ARID1A-deficient ovarian clear cell carcinoma cells. They found marked upregulation of specific subunits of mitochondrial electron transport chain Complexes I, III, and IV. Despite this upregulation, the cells did not show increased sensitivity to broad-spectrum inhibitors of these complexes. The authors suggest that selectively inhibiting specific ETC subunits might better exploit metabolic vulnerabilities in ARID1A-deficient cells.

Key findings
  • ARID1A-deficient ovarian clear cell carcinoma cells depend heavily on mitochondrial respiration (as stated by the authors).
  • Proteomic and biochemical analyses revealed marked upregulation of specific subunits within mitochondrial ETC Complexes I, III, and IV in ARID1A knockout cells.
  • Upregulation of these ETC subunits did not translate into increased sensitivity to broad-spectrum inhibitors targeting the complexes.
  • Authors propose that selective inhibition of specific ETC subunits could be a more promising approach than broad-spectrum mitochondrial inhibitors.
Limitations: In vitro cell-line study only; no in vivo or clinical data reported in the abstract.; Abstract does not report sample sizes, quantitative metrics, or statistical results.; No specific inhibitors or compounds are named or characterized in the abstract.; Functional or therapeutic efficacy of selective ETC subunit inhibition is suggested but not demonstrated in this study..

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

Animal studyMechanismReported positivePreclinical onlyTier 2 · animaln = 5

Establishment and characterization of ovarian clear cell carcinoma patient-derived xenografts

Scientific reports · Feb 2025 · Establishment and molecular characterization of patient-derived xenografts (PDXs) from ovarian clear cell carcinoma

ovarian clear cell carcinomaOCCC

The authors established five subcutaneous patient-derived xenografts (PDXs) from ovarian clear cell carcinoma (OCCC) and characterized their morphology and molecular features. They found that PDXs retained key mutations (ARID1A, PTEN, ATM, BRCA1, PIK3CA), ARID1A protein loss, copy number alterations, and overall DNA methylation signatures similar to the matched patient tumors, though a small set of promoter CpG islands gained methylation in PDXs. Human stroma was replaced by mouse stroma in at least one PDX, and glycogen accumulation was confirmed in tumors and PDXs. The authors conclude these PDXs may serve as potential preclinical models for translational OCCC research.

Reported effects: engraftment success rate PDX.F1, p over 30% · promoter CpG island methylation gain (Δβ threshold), p &#x25b3;&#x3b2;-value&#x2009;&gt;&#x2009;0.4

Key findings
  • Five subcutaneous OCCC PDXs were established; "The PDX.F1 engraftment success rate was over 30% with similar latency time and growth speed of PDX.F2."
  • ARID1A, PTEN, ATM, BRCA1 and PIK3CA mutations were found in matched tumors and PDXs.
  • ARID1A protein loss was verified by immunohistochemical staining.
  • Cyclophilin A staining showed replacement of human stroma by mouse stroma in PDX.F2.
  • PAS/PAS-D staining confirmed cellular glycogen accumulation in OCCC tumors and PDXs.
  • SNP array and Infinium MethylationEPIC BeadChip array analyses demonstrated that copy number alterations and DNA methylation signatures of genome-wide and tumor-driver genes in PDXs generally resembled their patients' tumors.
  • Promoter CpG islands of a small number of genes, enriched in PRC2/histone methylation related gene-sets, gained methylation (△β-value > 0.4) in PDXs vs patient tumors: "Promoter CpG islands of a small number of genes, enriched in PRC2/histone methylation related gene-sets, gained methylation (&#x25b3;&#x3b2;-value&#x2009;&gt;&#x2009;0.4) in PDXs vs patient tumors."
  • Conclusion stated: the high phenotypic and molecular similarity allows the established PDXs to serve as potential preclinical models for future translational research of OCCC.
Limitations: Preclinical animal study (mouse PDXs) so findings may not fully predict patient responses.; Small number of PDX models established (five), limiting generalizability.; Human tumor stroma was replaced by mouse stroma in PDXs, which may alter tumor microenvironment and affect translational relevance.; A small number of genes showed promoter CpG island methylation gains in PDXs, indicating possible epigenetic drift during engraftment.; No therapeutic or functional response data reported in the abstract to validate PDX utility for treatment testing..

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 human

Neuroendocrine gene subsets are uniquely dysregulated in prostate adenocarcinoma

Cancer biology & therapy · Dec 2024 · bioinformatic analysis of RNA expression across five cancer types and observational profiling of plasma small extracellular vesicles (sEVs) from prostate cancer patients and healthy donors

prostate adenocarcinomabreast cancerkidney chromophobekidney renal clear cell carcinomakidney renal papillary cell carcinoma

This study used bioinformatic analysis to evaluate RNA expression of neuroendocrine genes across five cancer types and examined small extracellular vesicles (sEVs) from plasma. The authors report that specific neuroendocrine genes are significantly dysregulated in these tumors, that synaptophysin (SYP) is upregulated in prostate adenocarcinoma and breast cancer, and that SYP is present in sEVs from prostate cancer patients but absent in sEVs from healthy donors.

Key findings
  • Specific neuroendocrine genes are significantly dysregulated in the analyzed tumors, suggesting a role in cancer progression.
  • Synaptophysin (SYP) is upregulated in prostate adenocarcinoma (PRAD) and breast cancer (BRCA).
  • SYP is enriched in small extracellular vesicles (sEVs) derived from plasma of PRAD patients, but it is absent in sEVs derived from plasma of healthy donors.
  • Classical sEV markers are enriched in sEVs derived from plasma of prostate cancer patients, but weakly detectable in sEVs derived from plasma of healthy donors.
  • Authors suggest these findings could support exploration of diagnostic strategies based on neuroendocrine gene expression in tumors or plasma sEVs.
Limitations: Abstract provides no sample sizes or quantitative performance metrics (e.g., sensitivity/specificity) for the sEV findings.; Observational and bioinformatic study design limits causal inference and clinical applicability.; No clinical validation or functional experiments reported in the abstract to confirm biological role of dysregulated genes.; Details of patient selection, cohort characteristics, and methods for sEV isolation/characterization are not provided in the abstract..

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

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 47

SOX17 expression in ovarian clear cell carcinoma

Journal of ovarian research · Nov 2024 · Immunohistochemical analysis of 47 OCCC whole-tissue specimens combined with immunoblotting and cell-line experiments

ovarian clear cell carcinoma

The authors examined SOX17 protein expression by immunohistochemistry in 47 ovarian clear cell carcinoma (OCCC) tissue specimens and studied SOX17 expression and regulation in OCCC cell lines. SOX17 expression was heterogeneous across tumors and cell lines; high SOX17 immunoreactivity trended toward worse patient outcomes but this was not statistically significant. In cell lines, SOX17 was abundant in OVISE and RMG-V but low in OVTOKO, where polyubiquitinated SOX17 accumulated after proteasome inhibition. Knockdown of the deubiquitinase UCHL1 in OVISE increased SOX17 polyubiquitination and subsequent proteasome degradation, suggesting impaired ubiquitin-mediated degradation can stabilize SOX17 in some OCCC cells.

Key findings
  • SOX17-high immunoreactivity tended to be related to unfavorable patient outcomes, although not statistically significant.
  • Double immunofluorescence staining demonstrated that SOX17 immunoreactivity was not associated with ARID1A immunoreactivity.
  • Immunoblotting revealed that SOX17 was abundantly expressed in cultured OVISE and RMG-V OCCC cells, but not in OVTOKO OCCC cells.
  • Polyubiquitinated bands of SOX17 were observed in MG132 treated OVTOKO, but not in OVISE or RMG-V OCCC cells.
  • si-RNA-mediated knockdown of a deubiquitinase enzyme, ubiquitin C-terminal hydrolase L1, increased polyubiquitination followed by proteasome degradation of SOX17 in OVISE.
Limitations: Observational, descriptive study of human tumor specimens without functional in vivo validation.; Prognostic association (SOX17-high vs outcomes) was not statistically significant.; Relatively small specimen cohort (n=47) limits generalizability and statistical power.; Cell-line findings (three lines) may not represent tumor heterogeneity in patients..

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

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 1

Mixed Mesonephric-like Adenocarcinoma, Clear Cell Carcinoma, and Endometrioid Carcinoma Arising from an Endometriotic Cyst

International journal of surgical pathology · Sep 2024 · case report

ovarian neoplasmmesonephric-like adenocarcinomaclear cell carcinomaendometrioid carcinomaendometriosis-associated neoplasm

This case report describes a 48-year-old woman with an ovarian mixed carcinoma composed of mesonephric-like adenocarcinoma, clear cell carcinoma, and endometrioid carcinoma arising in an endometriotic cyst. Each component had distinct immunophenotypes; the mesonephric-like component was PAX8- and GATA3-positive and ER/PR-negative, with wild-type p53 and complete loss of ARID1A expression. Manual macrodissection and Sanger sequencing found identical KRAS and PIK3CA mutations in all three tumor components, which the authors state supports that mesonephric-like adenocarcinoma can be an endometriosis-associated neoplasm.

Key findings
  • Mixed ovarian carcinoma composed of mesonephric-like adenocarcinoma, clear cell carcinoma, and endometrioid carcinoma arising from an endometriotic cyst.
  • Mesonephric-like adenocarcinoma showed diffuse positive staining for PAX8 and GATA3 and negative staining for estrogen and progesterone receptors.
  • p53 staining exhibited wild-type immunoreactivity.
  • Complete loss of ARID1A expression was observed, suggestive of ARID1A mutation.
  • Manual macrodissection and Sanger sequencing revealed identical KRAS and PIK3CA mutations in all three components.
  • Authors state this is the first report of mesonephric-like adenocarcinoma combined with clear cell and endometrioid carcinoma, supporting an endometriosis-associated origin.
Limitations: Single-patient case report limits generalizability.; No functional studies to demonstrate the biological consequence of the identified mutations.; Clinical staging, treatment, and follow-up outcomes are not reported in the abstract.; Molecular analysis used manual macrodissection and Sanger sequencing; extent of sampling and clonality assessment are limited..

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

Browse all studies mentioning Clear Cell Carcinoma →

Study mix

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

28 Human4 Animal2 Lab56 Review/other
Reported directionReported positive32Mixed results17Reported negative3Inconclusive38

Compounds with reported-positive results in Clear Cell 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.

Preclinical only: lab / animal (1)
Gemcitabine1 positive
Limitations: This is a review article and does not present primary trial data within the abstract.; The abstract emphasizes molecular and preclinical vulnerabilities (synthetic lethality) rather than reporting results from controlled clinical trials.; No sample sizes, study designs, or quantitative patient outcomes are reported in the abstract.; Clinical benefit in patients is presented as a possibility or recent evidence without details (limiting assessment of clinical applicability)..
Cited positive studies (1)

Evidence at a glance: compounds studied in Clear Cell 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.

GemcitabineInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Treatment Strategies for ARID1A-Deficient Ovarian Clear Cell Carcinoma

No human studies yet · No numeric effect sizes reported.

What the research shows for Clear Cell Carcinoma

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

  • These studies report that many ovarian clear cell carcinomas (OCCC) are thought to arise from malignant transformation of endometriosis; a human spatial transcriptomics and single-cell RNA‑sequencing study and several reviews described shared molecular features between coexisting endometriosis and OCCC tissue.
  • These studies report that OCCC has distinctive molecular and genomic features compared with other ovarian subtypes, with frequent alterations such as ARID1A and PIK3CA and typically lacking TP53 mutations, as summarized in multiple reviews.
  • These studies report that OCCC is noted to have relatively poor responses to conventional platinum‑based chemotherapy in clinical practice, a point emphasized across reviews of the disease.
  • These studies report that a range of targeted and immune‑based therapeutic strategies (examples discussed include PARP inhibitors, MAPK pathway inhibitors, cell‑cycle checkpoint inhibitors, and immune checkpoint inhibitors) have been proposed based on molecular profiles, but clinical evidence specific to OCCC is limited and inconclusive.
  • These studies report that the published literature on OCCC is heterogeneous and largely comprised of narrative reviews and small observational molecular studies, and that rare ovarian tumor subtypes suffer from limited data overall.

Supportive & alternative options discussed

  • Hyperthermia (heat): Also discussed as an adjunctive approach in ovarian cancer care (for example, hyperthermic intraperitoneal chemotherapy/HIPEC); evidence specific to ovarian clear cell carcinoma (OCCC) remains limited.
  • Mistletoe (VAE): Also discussed as an integrative/supportive therapy in ovarian cancer settings; evidence specific to OCCC is limited and not established by the studies above.
  • Ketogenic / metabolic therapy: Also discussed as a metabolic/dietary approach in oncology contexts; the studies above do not provide conclusive evidence for the ketogenic diet in OCCC.
  • Acupuncture: Also discussed as a supportive option for symptom management (e.g., pain, nausea, neuropathy) in ovarian cancer care; these studies do not provide OCCC-specific efficacy data.
  • Exercise / prehabilitation: Also discussed as supportive for quality of life, functional status, and survivorship in ovarian cancer; the studies above do not establish OCCC-specific outcomes.
  • Mind–body (MBSR / CBT): Also discussed as supportive for stress reduction, anxiety, and quality-of-life in cancer care; these studies do not provide evidence specific to OCCC.

What we don’t know yet

  • These studies do not establish which targeted or immune therapies (if any) improve clinical outcomes specifically for patients with OCCC in randomized trials.
  • These studies do not validate predictive biomarkers that reliably identify which OCCC patients might benefit from specific targeted treatments.
  • These studies do not define optimal treatment sequencing or management strategies for OCCC given its relative chemotherapy resistance.
  • These studies do not clarify the mechanistic steps or risk factors that drive malignant transformation of endometriosis into OCCC in humans.
  • These studies do not provide long‑term outcome, safety, dosing, or patient‑selection data for proposed novel therapies in OCCC.
  • These studies do not overcome limitations of small sample sizes, heterogeneous study designs, and the predominance of narrative reviews in the literature base.
Overall, the evidence summarized in these studies is preliminary—primarily narrative reviews and limited human molecular/observational work—and does not establish proven clinical therapies for ovarian clear cell carcinoma.

Clinical trials in Clear Cell Carcinoma

62 ongoing · 96 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
34 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Clear Cell 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.

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