Critical molecular abnormalities in high-grade serous carcinoma of the ovary.
Ovarian carcinomas show more morphological heterogeneity than adenocarcinomas of any other body site. It has recently become clear that the morphologically defined subtypes of ovarian carcinoma are distinct diseases, with different risk factors, molecular events during oncogenesis, likelihood of spread, responses to chemotherapy, and outcomes. This review focuses on molecular abnormalities (in genes expressing BRCA1/2, TP53 and RB1/CCND1/CDKN2A/E2F) found in high-grade serous carcinomas of the ovary, which account for most ovarian cancer deaths. These highly aggressive but chemosensitive tumours are associated with perturbation of molecular pathways leading to genomic instability and extreme mutability and present unique challenges in oncological research and practice.
Köbel
Martin
M
Genetic Pathology Evaluation Centre of the Prostate Research Centre, Department of Pathology, Vancouver General Hospital and British Columbia Cancer Agency, Vancouver BC, Canada.
Huntsman
David
D
Gilks
C Blake
CB
D000818:Animals; D019927:Cyclin E / Q000235:genetics / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics / Q000378:metabolism; D018284:Cystadenocarcinoma, Serous / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D005260:Female; D019398:Genes, BRCA1; D024522:Genes, BRCA2; D016158:Genes, p53; D006801:Humans; D009154:Mutation; D010051:Ovarian Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D010053:Ovary / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
D019927:Cyclin E; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016271:Proto-Oncogene Proteins c-myc