Role of epidermal growth factor receptor overexpression, K-ras point mutation and c-myc amplification in the carcinogenesis of non-small cell lung cancer

Oncol Rep. Mar-Apr 1998;5(2):351-4.

Abstract

Overexpression of epidermal growth factor receptor (EGF-R), K-ras gene mutations and c-myc gene amplification were studied in tumor and normal lung tissues from 100 patients with non-small cell lung cancer. The mean a standard deviation (SD) of the amount of EGF-R in the tumor (N=97) and the normal (N=82) tissues were 16.0 +/- 3.7 and 10.8 +/- 2.0 fmol/mg, respectively (P=0.015). Overexpression of the receptor was observed in 6 (24.0%) of 25 squamous cell carcinomas, 16 (23.2%) of 69 adenocarcinomas and 23 (23.7%) of a total of 97 tumors. K-ras mutations were observed in nine (9%) of 100 tumors. Of these, five (55.6%) mutations were in codon 12, one (11.1%) was in codon 22, and three (33.3%) were in codon 61. The patterns of the mutations were GC transversions in three (33.3%) tumors, GC transitions in two ( 22.2%) and AT transversions in four (44.4%) tumors. There was no association between EGF-R overexpression and K-ras mutation. c-myc amplification was studied in 23, but was not detected in any tumor (mean number of copies +/- SD = 1.28 +/- 0.24).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics*
  • Adenocarcinoma / metabolism
  • Adult
  • Aged
  • Aged, 80 and over
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology
  • DNA Primers / chemistry
  • DNA, Neoplasm / analysis
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism*
  • Female
  • Gene Amplification
  • Genes, myc / genetics*
  • Genes, ras / genetics*
  • Humans
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology
  • Male
  • Middle Aged
  • Point Mutation*

Substances

  • DNA Primers
  • DNA, Neoplasm
  • ErbB Receptors