[Overcoming resistance to EGFR-TKI in lung cancer].
Epidermal growth factor receptor(EGFR)tyrosine kinase inhibitor(TKI)as molecular targeted agents has given us an innovative strategy for treatment of patients with advanced non-small cell lung cancer(NSCLC). Patients with activating mutations of the EGFR generally respond to EGFR-TKI very well. HER3 has an essential role to enhance the EGFR signaling pathway, including the downstream pathway of PI3K/Akt pathway. The acquired resistance to EGFRTKI was clinically developed in patients with activating EGFR mutations. Recently, various mechanisms of acquired resistance have been developed, such as T790M, MET amplification, HGF increasing as a ligand of MET. We have to treat patients with NSCLC in the manor of individual medicine strategy today.
Takeda
Koji
K
Department of Clinical Oncology, Osaka City General Hospital, Osaka, Japan.
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D019008:Drug Resistance, Neoplasm / Q000187:drug effects*; D066246:ErbB Receptors / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism*; D017228:Hepatocyte Growth Factor / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000201:enzymology* / Q000235:genetics; D009154:Mutation / Q000235:genetics; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*
D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D017228:Hepatocyte Growth Factor; D066246:ErbB Receptors