RASSF1A methylation and K-ras and B-raf mutations and recurrent endometrial cancer

J. M A Pijnenborg, G. C. Dam-de Veen, N. Kisters, B. Delvoux, M. van Engeland, J. G. Herman, P. G. Groothuis

Research output: Contribution to journalArticlepeer-review


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 languageEnglish (US)
Pages (from-to)491-497
Number of pages7
JournalAnnals of Oncology
Issue number3
StatePublished - Mar 2007


  • B-raf
  • Endometrial carcinoma
  • K-ras
  • Mutation

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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