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ID 52785
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Author
Shien, Kazuhiko
Toyooka, Shinichi
Abstract
Non-small cell lung cancer (NSCLC) harboring an activating mutation within the epidermal growth factor receptor (EGFR) was defined as a clinically distinct molecular group. These lesions show oncogene addiction to EGFR and dramatic responses to the EGFR tyrosine kinase inhibitors (TKIs). Several large Phase III trials have shown that EGFR-TKIs improved the progression-free survival of patients with EGFR mutant NSCLC compared to conventional chemotherapy. However, the long-term effectiveness of EGFR-TKIs is usually limited because of acquired drug resistance. To overcome this resistance to EGFR-TKIs, it will be essential to identify the specific mechanisms underlying the resistance. Many investigators have attempted to identify the mechanisms using preclinical models and drug-resistant clinical samples. As a result, several mechanisms have been showed to be responsible for the resistance, but not all of the relevant mechanisms have been uncovered. In this review, we provide an overview of mechanisms underlying drug-resistance to EGFR-TKIs, focusing on results obtained with preclinical models, and we present some possible strategies to overcome the EGFR-TKI resistance.
Keywords
non-small cell lung cancer
EGFR mutation
tyrosine-kinase inhibitor
drug resistance
cancer stem cell
Amo Type
Review
Published Date
2014-08
Publication Title
Acta Medica Okayama
Volume
volume68
Issue
issue4
Publisher
Okayama University Medical School
Start Page
191
End Page
200
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
英語
Copyright Holders
CopyrightⒸ 2014 by Okayama University Medical School
File Version
publisher
Refereed
True
PubMed ID
Web of Sience KeyUT