Abstract
Background: Aberrations in mediators of Ras signaling may increase the risk of developing recurrent endometrial carcinoma. Patients and methods: Primary tumors of patients with (n = 44) and without (n = 44) recurrent stage I endometrioid endometrial carcinoma were compared regarding the presence of K-ras mutations (codons 12 and 13), B- raf mutations (V599), and RASSF1A gene promoter methylation. Results: K-ras mutations were present in 18% of the patients independent of recurrent disease. No B-raf mutations were found. RASSF1A methylation was demonstrated in 85% of endometrial carcinomas, independent of recurrence. The presence of K-ras mutations and RASSF1A promoter methylation were not related, either directly or inversely. Analysis in premenopausal endometrial carcinomas demonstrated K-ras mutations in 40%, no B-raf mutations, and RASSF1A promoter methylation in 70% of the cases. RASSF1A methylation was also observed in samples of cyclic (n = 14), hyperplastic (n = 8), and atrophic (n = 13) endometrial tissues in 21%, 50% and 38%, respectively. Conclusions: RASSF1A methylation was observed in a high frequency in endometrioid endometrial carcinoma whereas K-ras and B-raf mutations were observed in a low frequency. No association was observed with the development of recurrent disease. High-frequency RASSF1A methylation in premenopausal carcinomas and an increased frequency in endometrial hyperplasia indicate that this may be an early event in endometrial carcinogenesis.
Original language | English (US) |
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Pages (from-to) | 491-497 |
Number of pages | 7 |
Journal | Annals of Oncology |
Volume | 18 |
Issue number | 3 |
DOIs | |
State | Published - Mar 2007 |
Keywords
- B-raf
- Endometrial carcinoma
- K-ras
- Mutation
- RASSF1A
ASJC Scopus subject areas
- Oncology
- Cancer Research