Mutations in both KRAS and BRAF may contribute to the methylator phenotype in colon cancer.

ABSTRACT:

Background & aims

Colorectal cancers (CRCs) with the CpG island methylator phenotype (CIMP) often associate with epigenetic silencing of hMLH1 and an activating mutation in the BRAF gene. However, the current CIMP criteria are ambiguous and often result in an underestimation of CIMP frequencies in CRCs. Because BRAF and KRAS belong to same signaling pathway, we hypothesized that not only mutations in BRAF but mutant KRAS may also associate with CIMP in CRC.

Methods

We determined the methylation status in a panel of 14 markers (7 canonical CIMP-related loci and 7 new loci), microsatellite instability status, and BRAF/KRAS mutations in a collection of 487 colorectal tissues that included both sporadic and Lynch syndrome patients.

Results

Methylation analysis of 7 CIMP-r

SUBMITTER: Nagasaka T 

PROVIDER: S-EPMC2543132 | biostudies-literature | 2008 Jun

REPOSITORIES: biostudies-literature