Lack of somatic mutations in EGFR tyrosine kinase domain in hepatocellular and nasopharyngeal carcinoma

Pharmacogenet Genomics. 2006 Jan;16(1):73-4. doi: 10.1097/01.fpc.0000184959.82903.02.

Abstract

Activating EGFR somatic mutations have been shown to predict treatment response to small molecules targeting the EGFR intracellular tyrosine kinase domain. Recent work on cell-lines and animal models had demonstrated an inhibitory effect of EGFR tyrosine kinase inhibitors in hepatocellular and nasopharyngeal carcinoma, and clinical trials in these tumour types are ongoing. There are few data on the presence or prevalence of EGFR mutations in hepatocellular and nasopharyngeal carcinomas. We studied exons 18-21 of the EGFR gene from 100 hepatocellular and 102 nasopharyngeal carcinomas, and found no exonic mutations of potential significance. Alternative mechanisms may be important for the observed activity of small molecule EGFR tyrosine kinase inhibitors in hepatocellular and nasopharyngeal carcinomas.

MeSH terms

  • Carcinoma, Hepatocellular / drug therapy
  • Carcinoma, Hepatocellular / genetics*
  • DNA Mutational Analysis
  • Exons / genetics
  • Genes, erbB-1 / genetics*
  • Nasopharyngeal Neoplasms / genetics*
  • Protein Structure, Tertiary
  • Protein-Tyrosine Kinases / genetics*

Substances

  • Protein-Tyrosine Kinases