No major difference in K-ras and p53 abnormalities in sporadic and hereditary nonpolyposis colorectal adenomas

Dig Dis Sci. 2000 Nov;45(11):2187-94. doi: 10.1023/a:1026485117125.

Abstract

K-ras and p53 gene mutations are known to occur in high frequencies in sporadic colorectal cancers, but findings are inconsistent in hereditary nonpolyposis colorectal cancer (HNPCC). We compared K-ras codon 12 and 13 gene mutations and p53 protein overexpression in 48 HNPCC (positive for Amsterdam criteria) and 59 sporadic colorectal adenomas, to examine whether they may represent similar or different molecular pathways to cancer. In sporadic adenomas K-ras mutations were detected in 32% and p53 overexpression in 31% of the cases. Similarly, K-ras mutations and p53 overexpression were both found in 25% of HNPCC adenomas. The frequencies of these abnormalities were not significantly different between HNPCC and sporadic adenomas. When taking differences in adenoma size into account, the frequencies were even more similar. In conclusion, these results suggest a similar molecular pathway to adenomas in HNPCC and sporadic carcinogenesis, with respect to involvement of K-ras and p53.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenomatous Polyps / genetics
  • Adult
  • Aged
  • Case-Control Studies
  • Cell Transformation, Neoplastic / genetics
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis
  • Colorectal Neoplasms, Hereditary Nonpolyposis / genetics*
  • DNA Damage / genetics
  • DNA Mutational Analysis
  • Female
  • Gene Expression Regulation, Neoplastic / physiology
  • Genetic Predisposition to Disease / genetics
  • Humans
  • Male
  • Middle Aged
  • Mutation / genetics
  • Proto-Oncogene Proteins p21(ras) / genetics*
  • Tumor Suppressor Protein p53 / genetics*

Substances

  • Tumor Suppressor Protein p53
  • HRAS protein, human
  • Proto-Oncogene Proteins p21(ras)