Open AccessMET Alterations Are a Recurring and Actionable Resistance Mechanism in ALK-Positive Lung Cancer
Author(s) -
Ibiayi DagogoJack,
Satoshi Yoda,
Jochen K. Lennerz,
Adam Langenbucher,
Jessica J. Lin,
Marguerite Rooney,
Kylie Prutisto-Chang,
Audris Oh,
Nathaniel A. Adams,
Beow Y. Yeap,
Emily Chin,
Andrew Do,
Hetal D. Marble,
Sara E. Stevens,
Subba R. Digumarthy,
Ashish Saxena,
Rebecca J. Nagy,
Cyril H. Benes,
Christopher G. Azzoli,
Michael S. Lawrence,
Justin F. Gainor,
Alice T. Shaw,
Aaron N. Hata
Publication year - 2020
Publication title -
clinical cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.427
H-Index - 324
eISSN - 1557-3265
pISSN - 1078-0432
DOI - 10.1158/1078-0432.ccr-19-3906
Subject(s) - crizotinib , alk inhibitor , anaplastic lymphoma kinase , lung cancer , cancer research , medicine , acquired resistance , cancer , oncology , malignant pleural effusion
Most ALK -positive lung cancers will develop ALK-independent resistance after treatment with next-generation ALK inhibitors. MET amplification has been described in patients progressing on ALK inhibitors, but frequency of this event has not been comprehensively assessed.