2009•PubMedRequires access

[Overcoming resistance to EGFR-TKI in lung cancer].

Koji Takeda

Open publisher page 3 citations

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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What this paper is about

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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OpenAlex reports 3 citations for this work. Citation counts describe recorded attention and do not establish research quality.

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Available 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.

Key concepts: T790M, Epidermal growth factor receptor, Lung cancer, Medicine, Cancer research, Acquired resistance, PI3K/AKT/mTOR pathway, Tyrosine kinase

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