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Genomic analysis of over 200 mucinous ovarian tumours showed they arise in the ovary from benign and borderline precursors through KRAS, TP53 and CDKN2A changes, and are genuinely different from the gastrointestinal cancers they resemble.
Genomic study of 227 mucinous ovarian tumours (benign, borderline and carcinoma) identifying a progression model with KRAS mutation and CDKN2A loss early, TP53 mutation and copy-number gains including HER2 amplification in carcinomas, and a distinct profile from colorectal, gastric and pancreatic cancers.
Mucinous ovarian carcinoma is confirmed as a primary ovarian disease with its own biology; HER2 amplification in about a fifth of cases is a possible treatment target.