O6-methylguanine-DNA methyltransferase promoter hypermethylation in colorectal carcinogenesis

Oncol Rep. 2007 Jun;17(6):1421-7.

Abstract

Epigenetic alterations have been reported in colorectal neoplasia which can either complement or in some cases be predisposed to genetic alterations such as K-ras mutations. We examined the promoter methylation status of the CDKN2A and O6-methylguanine-DNA methyltransferase (MGMT) genes, after sodium bisulfite conversion and DNA amplification with methylation specific PCR. Moreover, we searched for G to A transitions in codons 12 and 13 of the K-ras oncogene in normal colorectal mucosae, aberrant crypt foci (ACF, early premalignant lesions) and carcinomas. CDKN2A hypermethylation was an infrequent event in ACF (2 of 26, 7.7%). On the contrary, MGMT hypermethylation was found in the normal mucosae (3 of the 12 samples, 25%), in 14 of the 26 ACF (53.8%) and in 7 of the 9 (77.8%) carcinomas examined. K-ras mutations were evident in 6 ACF (23%) and in 3 carcinomas (33.3%), mostly associated with MGMT promoter hypermethylation. These findings strongly support the hypothesis that epigenetic mechanisms play an important role in the early steps of colorectal carcinogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Carcinoma / genetics
  • Cell Transformation, Neoplastic / genetics*
  • Colorectal Neoplasms / genetics*
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • DNA Methylation
  • Epigenesis, Genetic*
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Genes, ras / genetics
  • Humans
  • Intestinal Mucosa / metabolism
  • Male
  • Middle Aged
  • Mutation
  • O(6)-Methylguanine-DNA Methyltransferase / genetics*
  • Promoter Regions, Genetic
  • Sequence Analysis, DNA
  • Sulfites / chemistry

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • Sulfites
  • O(6)-Methylguanine-DNA Methyltransferase
  • sodium bisulfite