Human · observationalMechanismReported positiveModerate evidenceTier 3 · early human
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 < 0.001 · Association of elevated IRF7 expression with poor survival, p p < 0.01 · +1 more
Key findings
- IRF7 was dysregulated in 22 cancers (KIRC: p < 0.001).
- Elevated IRF7 expression in KIRC correlated with poor survival (p < 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 < 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
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
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
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
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
Lab · in vitroMechanismMixed resultsPreclinical onlyTier 1 · lab
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
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 47
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
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 18
Cell death & disease · Aug 2024 · Single-cell RNA sequencing of 18 human endometrial cancer samples across multiple pathological types, with patient-derived organoid drug testing and in vitro validation experiments
endometrial canceruterine clear cell carcinomaendometrioid endometrial carcinomauterine serous carcinoma
The authors performed single-cell RNA sequencing on 18 endometrial cancer samples across different pathological subtypes to map tumor-cell and microenvironment heterogeneity. They report pathology-specific tumor cell programs (immune-, proliferation-, or metabolism-modulating) and distinct microenvironment compositions, identified candidate drugs for each pathological group and confirmed drug activity in patient-derived organoids, and validated oncogenic effects of SOD2+ inflammatory cancer-associated fibroblasts in vitro. These findings provide descriptive molecular and cellular maps that may guide future, but not yet clinical, personalized approaches.
Reported effect: n_samples 18, n=18
Key findings
- scRNA-seq was performed on 18 endometrial cancer samples from multiple pathological types.
- Cancer cells showed pathology-associated hallmarks: immune-modulating in uterine clear cell carcinoma (UCCC), proliferation-modulating in well-differentiated endometrioid endometrial carcinoma (EEC-I), and metabolism-modulating in uterine serous carcinoma (USC).
- Cancer cells from UCCC exhibited the greatest heterogeneity among the groups studied.
- Potential effective drugs were predicted for each pathological group and their effectiveness was confirmed using patient-derived endometrial cancer organoids.
- Tumor microenvironment differences: normal endometrium had prognostically favorable CD8+ cytotoxic T cells and NK cells, whereas tumors were dominated by CD4+ regulatory T cells, CD4+ exhausted T cells, and CD8+ exhausted T cells.
- CXCL3+ macrophages with an M2 signature and angiogenesis association were found exclusively in tumors.
- Epithelium-specific CAFs (eCAFs) predominated in EEC-I while SOD2+ inflammatory CAFs (iCAFs) predominated in UCCC.
- The oncogenic effects of SOD2+ iCAFs were validated in vitro.
Limitations: Relatively small sample size (18 samples) limits generalizability.; Observational single-cell profiling: no prospective clinical outcome data or in vivo validation reported.; Drug effectiveness was confirmed in patient-derived organoids (ex vivo) but not in patients or animal models.; In vitro validation of SOD2+ iCAFs does not establish causality in vivo or clinical relevance.; Abstract does not report specific drug names, doses, or safety data..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text