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- W4230723433 endingPage "618" @default.
- W4230723433 startingPage "607" @default.
- W4230723433 abstract "Targeted therapies have transformed the management of non-small cell lung cancer (NSCLC) and placed an increased emphasis on stratifying patients on the basis of genetic alterations in oncogenic drivers. To date, the best characterized molecular targets in NSCLC are the epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK). Despite steady advances in targeted therapies within these molecular subsets, however, acquired resistance to therapy is near universal. Recent preclinical models and translational efforts have provided critical insights into the molecular mechanisms of resistance to EGFR and ALK inhibitors. In this review, we present a framework for understanding resistance to targeted therapies. We also provide overviews of the molecular mechanisms of resistance and strategies to overcome resistance among EGFR-mutant and ALK-rearranged lung cancers. To date, these strategies have centered on the development of novel next-generation inhibitors, rationale combinations, and use of local ablative therapies, such as radiotherapy." @default.
- W4230723433 created "2022-05-11" @default.
- W4230723433 creator A5025135477 @default.
- W4230723433 creator A5074068244 @default.
- W4230723433 creator A5081227348 @default.
- W4230723433 date "2017-05-01" @default.
- W4230723433 modified "2023-09-24" @default.
- W4230723433 title "Managing Resistance to EFGR- and ALK-Targeted Therapies" @default.
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