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Mechanisms of Resistance to Crizotinib in Patients with <i>ALK</i> Gene Rearranged Non–Small Cell Lung Cancer

Clinical Cancer Research · 2012 · Vol. 18(5) · pp. 1472–1482
Robert C. DoebeleAmanda PillingDara L. AisnerTatiana G. KutateladzeAnh T. LeAndrew WeickhardtKimi KondoDerek J. LindermanLynn E. HeasleyWilbur A. FranklinMarileila Varella‐GarciaD. Ross Camidge

Abstract

Crizotinib resistance in ALK(+) NSCLC occurs through somatic kinase domain mutations, ALK gene fusion CNG, and emergence of separate oncogenic drivers.

Lung Cancer Treatments and MutationsLung Cancer Research StudiesPI3K/AKT/mTOR signaling in cancerCrizotinibAnaplastic lymphoma kinaseCancer researchLung cancerALK inhibitorKRASMedicineMutationGene rearrangementFusion gene

MeSH terms

CrizotinibAnaplastic Lymphoma KinaseCarcinoma, Non-Small-Cell LungCell LineHumansLung NeoplasmsModels, MolecularMutationProto-Oncogene ProteinsPyrazolesPyridinesTranslocation, GeneticOncogene Proteins, FusionProto-Oncogene Proteins p21(ras)Protein Structure, Tertiary
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