Non-responsiveness to gefitinib in a patient with lung adenocarcinoma having rare EGFR mutations S768I and V769L

Lung Cancer. 2006 Dec;54(3):419-22. doi: 10.1016/j.lungcan.2006.09.005. Epub 2006 Oct 12.

Abstract

Mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) are associated with clinical responsiveness to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung cancers (NSCLCs). However, certain rare EGFR mutations including S768I are reported to confer less in vitro sensitivity to gefitinib, an EGFR-TKI, than major mutations such as exon 19 deletions and L858R and even the wild-type counterpart. Here, we report the first case of adenocarcinoma of the lung in which the patient had rare mutations S768I and V769L and was treated with gefitinib. Disease progressed during 6 weeks of treatment. This case suggests that in vitro sensitivity to gefitinib correlates with distinct clinical responsiveness to gefitinib in various types of EGFR mutations.

Publication types

  • Case Reports

MeSH terms

  • Adenocarcinoma / drug therapy
  • Adenocarcinoma / genetics*
  • Adenocarcinoma / pathology
  • DNA, Neoplasm / analysis
  • Drug Resistance, Neoplasm / genetics*
  • ErbB Receptors / genetics*
  • Gefitinib
  • Humans
  • Isoleucine / chemistry
  • Isoleucine / genetics
  • Leucine / chemistry
  • Leucine / genetics
  • Lung Neoplasms / drug therapy
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / pathology
  • Male
  • Middle Aged
  • Mutation
  • Quinazolines / therapeutic use*
  • Serine / chemistry
  • Serine / genetics
  • Valine / chemistry
  • Valine / genetics

Substances

  • DNA, Neoplasm
  • Quinazolines
  • Isoleucine
  • Serine
  • ErbB Receptors
  • Leucine
  • Valine
  • Gefitinib