Abstract
Anaplastic lymphoma kinase (ALK) encodes a receptor tyrosine kinase, and ALK gene rearrangement (ALK+) is implicated in the oncogenesis of non-small cell lung carcinomas (NSCLCs), especially adenocarcinomas. The ALK inhibitor crizotinib was approved in August 2011 by the US Food and Drug Administration (FDA) for treating late-stage NSCLCs that are ALK+, with a companion fluorescent in situ hybridization (FISH) test using the Vysis ALK Break Apart FISH Probe Kit. This review covers pertinent issues in ALK testing, including approaches to select target patients for the test, pros and cons of different detection methods, and mechanisms as well as monitoring of acquired crizotinib resistance in ALK+ NSCLCs.
MeSH terms
-
Anaplastic Lymphoma Kinase
-
Antineoplastic Agents / pharmacology
-
Antineoplastic Agents / therapeutic use
-
Carcinoma, Non-Small-Cell Lung / drug therapy*
-
Carcinoma, Non-Small-Cell Lung / genetics*
-
Carcinoma, Non-Small-Cell Lung / pathology
-
Crizotinib
-
Drug Resistance, Neoplasm
-
Gene Rearrangement*
-
Genetic Testing*
-
Humans
-
Immunohistochemistry
-
In Situ Hybridization, Fluorescence
-
Lung Neoplasms / drug therapy
-
Lung Neoplasms / genetics
-
Lung Neoplasms / pathology
-
Protein Kinase Inhibitors / pharmacology
-
Protein Kinase Inhibitors / therapeutic use
-
Pyrazoles / pharmacology
-
Pyrazoles / therapeutic use
-
Pyridines / pharmacology
-
Pyridines / therapeutic use
-
Receptor Protein-Tyrosine Kinases / antagonists & inhibitors*
-
Receptor Protein-Tyrosine Kinases / genetics*
Substances
-
Antineoplastic Agents
-
Protein Kinase Inhibitors
-
Pyrazoles
-
Pyridines
-
Crizotinib
-
ALK protein, human
-
Anaplastic Lymphoma Kinase
-
Receptor Protein-Tyrosine Kinases