Oncogenic events associated with endometrial and ovarian cancers are rare in endometriosis

Anna Lindeløv Vestergaard, Katrine Thorup, Ulla B Knudsen, Torben Munk, Hanne Rosbach, Jesper Bjørn Gorm Poulsen, Per Guldberg, Pia Møller Martensen

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Endometriosis displays some features that resemble malignant processes, including invasive growth, resistance to apoptosis and distant implantation. The objective of this study was to investigate whether gene alterations that are frequent in endometrial and/or ovarian cancers contribute to the pathogenesis of endometriosis. Biopsies were obtained from ectopic endometriosis lesions from 23 patients with revised American Fertility Score stage 1 (n= 1), 2 (n= 10), 3 (n= 11) or 4 (n= 1) endometriosis. Six genes (APC, CDKN2A, PYCARD, RARB, RASSF1 and ESR1) were analyzed for promoter hypermethylation using methylation-specific melting curve analysis, and 9 genes (BRAF, HRAS, NRAS, CTNNB1, CDK4, FGFR3, PIK3CA, TP53 and PTEN) were analyzed for mutations using denaturing gradient gel electrophoresis and direct sequencing. An oncogenic mutation in KRAS (c.34G > T; p.G12C) was detected in a single lesion. No gene alterations were found in the remaining samples. Our data suggest that genetic and epigenetic events contributing to endometrial and ovarian cancers are rare in endometriosis. However, other proto-oncogenes and tumor suppressor genes should be tested for alterations in order to identify the molecular basis of the susceptibility of endometriosis to malignant transformation.
Original languageEnglish
JournalMolecular Human Reproduction
Volume17
Issue number12
Pages (from-to)758-761
ISSN1460-2407
DOIs
Publication statusPublished - 2011

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