EGFR-mutated oncogene-addicted non-small cell lung cancer: Current trends and future prospects

被引:112
作者
Soria, Jean-Charles [1 ,2 ]
Mok, Tony S. [3 ]
Cappuzzo, Federico [4 ]
Jaenne, Pasi A. [5 ]
机构
[1] Inst Gustave Roussy, INSERM, Serv Innovat Therapeut Precoces, U981, F-94805 Villejuif, France
[2] Univ Paris 11, F-94805 Villejuif, France
[3] Chinese Univ Hong Kong, State Key Lab Oncol S China, Sir YK Pao Ctr Canc, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China
[4] Osped Civile Livorno, Ist Toscano Tumori, I-57100 Livorno, Italy
[5] Dana Farber Canc Inst, Boston, MA 02215 USA
关键词
Biological markers; Carcinoma; Non-small cell lung; Receptor; Epidermal growth factor; Erlotinib; Gefitinib; Mutation; Oncogenes; GROWTH-FACTOR-RECEPTOR; GENE COPY NUMBER; PHASE-III TRIAL; TYROSINE KINASE INHIBITOR; IN-SITU HYBRIDIZATION; CLINICAL-PRACTICE GUIDELINES; EML4-ALK FUSION GENE; ACQUIRED-RESISTANCE; DOUBLE-BLIND; ACTIVATING MUTATIONS;
D O I
10.1016/j.ctrv.2011.10.003
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Non-small cell lung cancer (NSCLC) tumours with certain mutations in the epidermal growth factor receptor (EGFR) tyrosine kinase have been termed 'oncogene addicted' to reflect their dependence on EGFR-mediated pro-survival signalling and their high susceptibility to apoptosis induced by EGFR tyrosine kinase inhibitors (EGFR-TKIs, e.g. gefitinib and erlotinib). The most common mutations (L858R and exon 19 deletions) predict an improved clinical response to first-line oral EGFR-TKIs compared with standard platinum-based chemotherapy in patients with advanced NSCLC. Moreover, these mutations are also prognostic of a relatively indolent course of disease, regardless of treatment, as compared with classical NSCLC. Treatment strategies for oncogene-addicted NSCLC are therefore distinct from those for non-oncogene addicted NSCLC, and will depend on the specific genetic mutation present. (C) 2011 Published by Elsevier Ltd.
引用
收藏
页码:416 / 430
页数:15
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