Managing Resistance to EFGR- and ALK-Targeted Therapies

Christine M. Lovly, Puneeth Iyengar, Justin F. Gainor

Research output: Contribution to journalReview article

8 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)607-618
Number of pages12
JournalAmerican Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting
Volume37
DOIs
StatePublished - Jan 1 2017

ASJC Scopus subject areas

  • Medicine(all)

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