Flat-type colorectal advanced adenomas (laterally spreading tumors) have different genetic and epigenetic alterations from protruded-type advanced adenomas

Mod Pathol. 2007 Jan;20(1):139-47. doi: 10.1038/modpathol.3800722. Epub 2006 Nov 24.

Abstract

Morphologically, colorectal adenomas can be divided into two groups, protruded-type and flat-type. However, the accurate frequencies of genetic and epigenetic alterations in flat-type colorectal advanced adenomas (laterally spreading tumors) have remained largely unknown. In the current study, we investigated genetic and epigenetic alterations in 101 flat-type colorectal advanced adenomas and 68 protruded-type colorectal advanced adenomas by using direct DNA sequencing and quantitative real-time PCR (MethyLight), respectively. KRAS mutation was detected in a significantly higher percentage of flat-type adenomas (35%) than in protruded-type adenomas (13%). When the samples were limited to the tumors in the distal colon, the difference of KRAS mutation was still significant. KRAS mutation in G-to-A transitions at codons 12 and 13 was detected in a significantly higher percentage of flat-type adenomas (26%) than in protruded-type adenomas (9%). BRAF and beta-catenin mutations were detected in 3 and 8% of the 101 flat-type adenomas, respectively. No significant difference was found between frequencies of those mutations in flat-type adenomas and protruded-type adenomas. Methylations of MGMT, CDKN2A (p16) and MLH1 were detected in 28, 33 and 9% of the 101 flat-type adenomas, respectively. CDKN2A methylation was detected in a significantly lower percentage of flat-type adenomas than in protruded-type adenomas (63%). Methylation of at least one gene was detected in a significantly lower percentage of flat-type adenomas (54%) than in protruded-type adenomas (78%). In conclusion, KRAS mutation was frequently detected in flat-type advanced adenomas and the mutational patterns in most of them with KRAS mutations were a transition from G-to-A. Therefore, these genetic alterations seem to play an important role in the development of flat-type advanced adenomas, especially in the distal colon. Epigenetic alterations infrequently occurred in flat-type advanced adenomas, suggesting that they have different genetic and epigenetic alterations from those of protruded-type advanced adenomas.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Adenine
  • Adenoma / chemistry
  • Adenoma / genetics*
  • Adenoma / pathology*
  • Aged
  • Carrier Proteins / genetics
  • Colorectal Neoplasms / chemistry
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / pathology*
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • DNA Methylation*
  • DNA Modification Methylases
  • DNA Mutational Analysis
  • DNA Repair Enzymes
  • Epigenesis, Genetic*
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Guanine
  • Humans
  • Male
  • Middle Aged
  • MutL Protein Homolog 1
  • Mutation
  • Neoplasm Invasiveness
  • Nuclear Proteins / genetics
  • Polymerase Chain Reaction / methods
  • Proto-Oncogene Proteins B-raf / genetics
  • Tumor Suppressor Protein p14ARF / analysis
  • Tumor Suppressor Protein p14ARF / genetics
  • Tumor Suppressor Proteins
  • beta Catenin / genetics
  • ras Proteins / genetics

Substances

  • Adaptor Proteins, Signal Transducing
  • CTNNB1 protein, human
  • Carrier Proteins
  • Cyclin-Dependent Kinase Inhibitor p16
  • MLH1 protein, human
  • Nuclear Proteins
  • Tumor Suppressor Protein p14ARF
  • Tumor Suppressor Proteins
  • beta Catenin
  • Guanine
  • DNA Modification Methylases
  • MGMT protein, human
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf
  • MutL Protein Homolog 1
  • ras Proteins
  • DNA Repair Enzymes
  • Adenine