Acquired MET Exon 14 Alteration Drives Secondary Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor in EGFR-Mutated Lung Cancer-Reference-Cited by-同舟云学术

Acquired MET Exon 14 Alteration Drives Secondary Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor in EGFR-Mutated Lung Cancer

Published:2019-12 Issue:3 Volume: Page:1-8
ISSN:2473-4284
Container-title:JCO Precision Oncology
language:en
Short-container-title:JCO Precision Oncology

Author:

Suzawa Ken¹,Offin Michael¹,Schoenfeld Adam J.¹,Plodkowski Andrew J.¹,Odintsov Igor¹,Lu Daniel²,Lockwood William W.²,Arcila Maria E.¹,Rudin Charles M.¹,Drilon Alexander¹,Yu Helena A.¹,Riely Gregory J.¹,Somwar Romel¹,Ladanyi Marc¹

Affiliation:

1. Memorial Sloan Kettering Cancer Center, New York, NY

2. University of British Columbia, Vancouver, British Columbia, Canada

Publisher

American Society of Clinical Oncology (ASCO)

Subject

Cancer Research,Oncology

Link

https://ascopubs.org/doi/pdfdirect/10.1200/PO.19.00011

Reference16 articles.

1. Concurrent Alterations in EGFR-Mutant Lung Cancers Associated with Resistance to EGFR Kinase Inhibitors and Characterization of MTOR as a Mediator of Resistance

2. Assessment of Resistance Mechanisms and Clinical Implications in Patients WithEGFRT790M–Positive Lung Cancer and Acquired Resistance to Osimertinib

3. MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

4. Activation of MET by Gene Amplification or by Splice Mutations Deleting the Juxtamembrane Domain in Primary Resected Lung Cancers

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