[Small-molecule tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR)].
Five years have passed since the activating mutation of the epidermal growth factor receptor (EGFR) gene was discovered. Patients with lung cancer harboring EGFR mutation respond remarkably well to small molecules, such as gefitinib or erlotinib, that specifically inhibit tyrosine kinase of the EGFR. Furthermore, recent evidence leads strong support to the idea that EGFR-tyrosine kinase inhibitors prolong survival of lung cancer patients with EGFR mutation. It has been also shown that secondary mutation of the EGFR gene and amplification of the MET gene are responsible for acquired resistance that emerges in virtually all cases treated with EGFR-TKI. Strategies to circumvent this resistance is currently in development. It is possible to personalize lung cancer therapy using the genetic information.
Mitsudomi
Tetsuya
T
Department of Thoracic Surgery, Aichi Cancer Center Hospital, Chikusa-ku, Nagoya, Japan.
D066246:ErbB Receptors / Q000037:antagonists & inhibitors*; D005260:Female; D018773:Genes, erbB-1 / Q000235:genetics; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy*; D008297:Male; D009154:Mutation; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors*
D066246:ErbB Receptors; D011505:Protein-Tyrosine Kinases