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

Hiroyasu Kaneda, Takeshi Yoshida, Isamu Okamoto

研究成果: Contribution to journalReview article査読

16 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)91-101
ページ数11
ジャーナルCancer Management and Research
5
1
DOI
出版ステータス出版済み - 5 29 2013

All Science Journal Classification (ASJC) codes

  • Oncology

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