EGFR tyrosine kinase inhibitors: A therapy for a few, for the majority or for all non-small cell lung cancer patients?

Giovanna Finocchiaro, Luca Toschi, Isabella Garassino, Fabio De Vincenzo, Elisabetta Campagnoli, Paolo Zucali, Raffaele Cavina, Giovanni L. Ceresoli, Armando Santoro, Federico Cappuzzo

Research output: Contribution to journalArticlepeer-review

Abstract

The EGF receptor (EGFR) is one of the most important targets for cancer treatment implicated in the control of cell survival, proliferation and metastasis. In the last few years different EGFR molecular antagonists have been evaluated in the clinical setting and some of these drugs have demonstrated clinical efficacy in a subset of non-small cell lung cancer (NSCLC) patients. Gefitinib or erlotinib are a new class of compounds able to inhibit the tyrosine kinase domain of EGFR (EGFR TKI) and, during recent years, clinical and biologic predictors for TKI sensitivity have been identified. Among clinical features, never-smoking history has emerged as the most relevant clinical characteristic predictive of response to TKIs in NSCLC, and EGFR gene mutation or EGFR increased gene copy number represent critical biologic variables associated with an improved outcome for patients exposed to these agents. Unfortunately, cancer cells possess escape mechanisms to overcome inhibition of cell proliferation leading to drug resistance. There are several mechanisms that have been identified as responsible for intrinsic or acquired resistance. The aim of the present review is to analyze available data in order to identify an optimal paradigm for patient selection.

Original languageEnglish
Pages (from-to)183-191
Number of pages9
JournalExpert Opinion on Medical Diagnostics
Volume1
Issue number2
DOIs
Publication statusPublished - Oct 2007

Keywords

  • EGFR
  • erlotinib
  • gefitinib
  • non-small cell lung cancer
  • tyrosine kinase inhibitors

ASJC Scopus subject areas

  • Biomedical Engineering
  • Medicine(all)
  • Biochemistry, medical
  • Molecular Medicine

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