Mechanisms of resistance to EGFR tyrosine kinase inhibitors gefitinib/erlotinib and to ALK inhibitor crizotinib

Alfredo Tartarone, Chiara Lazzari, Rosa Lerose, Vincenza Conteduca, Giuseppina Improta, Angela Zupa, Alessandra Bulotta, Michele Aieta, Vanesa Gregorc

Research output: Contribution to journalArticlepeer-review

Abstract

The discovery of several molecular alterations that underlie non-small cell lung cancer (NSCLC) pathogenesis has led to the development of targeted therapies. In particular, gefitinib and erlotinib have become the standard of care in patients harboring epidermal growth factor receptor mutations, while crizotinib showed an impressive efficacy in patients with ALK-positive NSCLC. Nevertheless, the occurrence of clinical resistance limits the long term results of these novel agents. The identification of the molecular mechanisms responsible for acquired resistance to targeted therapy is crucial in order to pursue the creation of rational strategies to overcome resistance. In the current review, we will focus on the acquired resistance mechanisms to EGFR-TKIs and crizotinib and the therapeutic strategies currently under study to overcome resistance.

Original languageEnglish
Pages (from-to)328-336
Number of pages9
JournalLung Cancer
Volume81
Issue number3
DOIs
Publication statusPublished - Sep 2013

Keywords

  • ALK translocation
  • Epidermal growth factor receptor
  • Non small cell lung cancer
  • Primary and acquired resistance to EGFR-TKIs
  • Resistance to crizotinib
  • Targeted therapy

ASJC Scopus subject areas

  • Oncology
  • Pulmonary and Respiratory Medicine
  • Cancer Research

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