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Article

Non-Small Cell Lung Cancer Cells Acquire Resistance to the ALK Inhibitor Alectinib by Activating Alternative Receptor Tyrosine Kinases.

Cancer research - 15 Mar 2016

Isozaki Hideko, Ichihara Eiki, Takigawa Nagio, Ohashi Kadoaki, Ochi Nobuaki, Yasugi Masayuki, Ninomiya Takashi, Yamane Hiromichi, Hotta Katsuyuki, Sakai Katsuya, Matsumoto Kunio, Hosokawa Shinobu, Bessho Akihiro, Sendo Toshiaki, Tanimoto Mitsune, Kiura Katsuyuki

Abstract excerpt

Crizotinib is the standard of care for advanced non-small cell lung cancer (NSCLC) patients harboring the anaplastic lymphoma kinase (ALK) fusion gene, but resistance invariably develops. Unlike crizotinib, alectinib is a selective ALK tyrosine kinase inhibitor (TKI) with more potent antitumor effects and a favorable toxicity profile, even in crizotinib-resistant cases. However, acquired resistance to alectinib,...

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Share to Anaplastic Lymphoma Kinase
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Oncogene Proteins, Fusion

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Source

Identifiers

PMID: 26719536
DOI: 10.1158/0008-5472.CAN-15-1010

Genes

ALK
EML4
HGF
MET

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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