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Molecularly targeted approaches herald a new era of non-small-cell lung cancer treatment

Authors Kaneda H, Yoshida T, Okamoto I

Received 13 March 2013

Accepted for publication 21 April 2013

Published 7 June 2013 Volume 2013:5 Pages 91—101


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Hiroyasu Kaneda,1 Takeshi Yoshida,1 Isamu Okamoto2

1Department of Medical Oncology, Kinki University, Osakasayama, Japan; 2Center for Clinical and Translational Research, Kyushu University Hospital, Fukuoka, Japan

Abstract: The discovery of activating mutations in the epidermal growth-factor receptor (EGFR) gene in 2004 opened a new era of personalized treatment for non-small-cell lung cancer (NSCLC). EGFR mutations are associated with a high sensitivity to EGFR tyrosine kinase inhibitors, such as gefitinib and erlotinib. Treatment with these agents in EGFR-mutant NSCLC patients results in dramatically high response rates and prolonged progression-free survival compared with conventional standard chemotherapy. Subsequently, echinoderm microtubule-associated protein-like 4 (EML4)–anaplastic lymphoma kinase (ALK), a novel driver oncogene, has been found in 2007. Crizotinib, the first clinically available ALK tyrosine kinase inhibitor, appeared more effective compared with standard chemotherapy in NSCLC patients harboring EML4-ALK. The identification of EGFR mutations and ALK rearrangement in NSCLC has further accelerated the shift to personalized treatment based on the appropriate patient selection according to detailed molecular genetic characterization. This review summarizes these genetic biomarker-based approaches to NSCLC, which allow the instigation of individualized therapy to provide the desired clinical outcome.

Keywords: non-small-cell lung cancer, epidermal growth factor receptor, ALK rearrangement, gefitinib, erlotinib, crizotinib

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