key papersKey paper
The molecular origin and taxonomy of mucinous ovarian carcinoma
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.
Overview
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.
Translational studyChanged practice227 participants
Authors
Cheasley D, Wakefield MJ, Ryland GL, et al.
Published
Nature Communications, 2019
Findings
- KRAS mutation in about 65 percent, TP53 in 64 percent and CDKN2A loss in 76 percent of carcinomas.
- HER2 amplification in about 26 percent of carcinomas.
What it means
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.
Caveats
- Treatment implications remain under investigation.