Low incidence of point mutation of c-Ki-ras and N-ras oncogenes in human hepatocellular carcinoma

Jpn J Cancer Res. 1989 Mar;80(3):196-9. doi: 10.1111/j.1349-7006.1989.tb02290.x.

Abstract

We examined the incidence of point mutation in codons 12, 13 and 61 of c-Ki-ras and N-ras genes in human hepatocellular carcinoma (HCC) using the polymerase chain reaction and oligonucleotide hybridization techniques. Among 34 tissues specimens surgically resected from 30 patients and 5 cell lines of human HCC, only two had ras point mutations; in one case, codon 12 of c-Ki-ras was altered from GGT, coding glycine, to GTT, coding valine; in the other case, codon 61 of N-ras was altered from CAA, coding glutamine, to AAA, coding lysine. Thus, point-mutational activation of ras oncogenes is an uncommon event in human HCC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Hepatocellular / genetics*
  • Codon
  • DNA / genetics
  • Humans
  • Liver Neoplasms / genetics*
  • Membrane Proteins
  • Mutation*
  • Nucleic Acid Hybridization
  • Oligonucleotide Probes
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins p21(ras)
  • Proto-Oncogenes*
  • Tumor Cells, Cultured

Substances

  • Codon
  • Membrane Proteins
  • Oligonucleotide Probes
  • Proto-Oncogene Proteins
  • DNA
  • HRAS protein, human
  • Proto-Oncogene Proteins p21(ras)