[Overcoming resistance to EGFR-TKI in lung cancer].
Koji Takeda
Abstract
Koji Takeda
Abstract
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.
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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.
Key concepts: T790M, Epidermal growth factor receptor, Lung cancer, Medicine, Cancer research, Acquired resistance, PI3K/AKT/mTOR pathway, Tyrosine kinase