
Anaplastic lymphoma tyrosine kinase oncogene in human cancer: gene aberrations, methods of detection and therapeutic potential
Author(s) -
Rosalaura Sabetta,
Monica Gargiulo,
Marina Accardo,
Federica Zito Marino,
Renato Franco
Publication year - 2017
Publication title -
translational medicine reports
Language(s) - English
Resource type - Journals
ISSN - 2532-1250
DOI - 10.4081/tmr.6803
Subject(s) - crizotinib , anaplastic lymphoma kinase , cancer research , lung cancer , tyrosine kinase , receptor tyrosine kinase , anaplastic large cell lymphoma , lymphoma , alk inhibitor , acquired resistance , receptor protein tyrosine kinases , tyrosine kinase inhibitor , oncogene , gene , cancer , biology , medicine , kinase , signal transduction , oncology , immunology , cell cycle , genetics , malignant pleural effusion
Anaplastic lymphoma tyrosine kinase (ALK) gene could be an attractive oncotarget in human cancers, since it is involved in several genetic alterations resulting in an aberrant activity of the receptor. To date, ALK-rearrangement represents a molecular target for the treatment of ALK-rearranged Non Small Cell Lung Cancer patients, who are highly sensitive to crizotinib, a specific inhibitor. ALK-rearranged patients treated with crizotinib show relevant clinical implications, however several different resistance mechanisms have been identified. Here we review various critical issues related to ALK-targeting therapy, including ALK gene aberrations, methods of detection, mechanism of acquired resistance and second-generation ALK inhibitors.