scispace - formally typeset
Open AccessJournal ArticleDOI

Activity of crizotinib (PF02341066), a dual mesenchymal-epithelial transition (MET) and anaplastic lymphoma kinase (ALK) inhibitor, in a non-small cell lung cancer patient with de novo MET amplification.

Reads0
Chats0
TLDR
An NSCLC patient with de novo MET amplification but no ALK rearrangement who achieved a rapid and durable response to crizotinib indicating is also a bona fide MET inhibitor.
About
This article is published in Journal of Thoracic Oncology.The article was published on 2011-05-01 and is currently open access. It has received 418 citations till now. The article focuses on the topics: ALK inhibitor & Crizotinib.

read more

Citations
More filters
Journal ArticleDOI

Acquired resistance to TKIs in solid tumours: learning from lung cancer

TL;DR: This Review explores breakthroughs in the understanding and treatment of acquired resistance in NSCLC, focusing on EGFR mutant and ALK rearrangement-positive disease, which may be relevant across multiple different solid malignancies with oncogene-addicted subtypes.
References
More filters
Journal ArticleDOI

MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling

TL;DR: It is proposed that MET amplification may promote drug resistance in other ERBB-driven cancers as well after it was found that amplification of MET causes gefitinib resistance by driving ERBB3 (HER3)–dependent activation of PI3K, a pathway thought to be specific to EGFR/ERBB family receptors.
Journal ArticleDOI

An orally available small-molecule inhibitor of c-met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms

TL;DR: The antitumor activity of PF-2341066 may be mediated by direct effects on tumor cell growth or survival as well as antiangiogenic mechanisms, and the therapeutic potential of targeting c-Met with selective small-molecule inhibitors for the treatment of human cancers is shown.
Related Papers (5)