ArticleGynecologic oncology2023
Germline drivers of gynecologic carcinosarcomas.
Article in Gynecologic oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- A rare case of uterine carcinosarcoma in a 21-year-old woman with hereditary breast and ovarian cancer syndrome: A case report.Oncology letters · 2026Article
- Molecular characteristics of tubo-ovarian carcinosarcoma at different anatomic locations.Virchows Archiv : an international journal of pathology · 2024Article
- Mainstreaming in parallel with ovarian cancer tumor testing to improve genetic testing uptake.Gynecologic oncology · 2024Article
- Ovarian carcinosarcomas: p53 status defines two distinct patterns of oncogenesis and outcomes.Frontiers in oncology · 2024Article
- Response of low HER2-expressing ovarian carcinosarcoma to trastuzumab deruxtecan, a case report.Gynecologic oncology reports · 2023Article
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Authors and funding
27 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesTo describe the prevalence of germline pathogenic variants (gPVs) in endometrial and ovarian carcinosarcomas and determine if gPVs are drivers of carcinosarcoma.
methodsPatients with endometrial or ovarian carcinosarcomas who underwent clinical tumor-normal sequencing from 1/1/2015 to 6/1/2021 and consented to germline assessment of ≥76 cancer predisposition genes were included. In patients with gPVs, biallelic inactivation was identified through analysis of loss of heterozygosity and somatic pathogenic alterations.
resultsOf 216 patients identified, 167 (77%) were diagnosed with endometrial carcinosarcoma and 49 (23%) with ovarian carcinosarcoma. Overall, 33 gPVs were observed in 29 patients (13%); 20 gPVs (61%) had biallelic loss in tumors. The rate of high-penetrance gPVs overall was 7% (16 of 216); 88% of high-penetrance gPVs had biallelic loss. In the endometrial carcinosarcoma cohort, 22 gPVs were found in 19 (11%) of 167 patients; 12 gPVs (55%) had biallelic loss in tumors, including 8 (89%) of 9 in high-penetrance gPVs. Among the ovarian carcinosarcoma cohort, 11 gPVs were found in 10 (20%) of 49 patients; 8 gPVs (73%) had biallelic loss in tumors, and all evaluable high-penetrance gPVs (n = 6) had biallelic loss. All gPVs in homologous recombination (BRCA1, BRCA2, RAD51C) and Lynch syndrome (MSH2, MSH6) genes had biallelic loss in tumors (n = 15).
conclusionsgPVs in genes affecting homologous recombination- or Lynch-associated mismatch repair exhibited biallelic inactivation within tumors, suggesting likely drivers of gynecologic carcinosarcoma. Our data support germline testing for patients with gynecologic carcinosarcomas, given implications for treatment and risk-reduction in patients and at-risk family members.
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