Squamous Cell Carcinoma of the Lung: Molecular Subtypes and Therapeutic Opportunities

被引：266

作者：

Perez-Moreno, Pablo ^{[1
,2
]}

Brambilla, Elisabeth ^{[3
,4
]}

Thomas, Roman ^{[5
,6
,7
,8
,9
]}

Soria, Jean-Charles ^{[1
,2
]}

机构：

[1] Inst Gustave Roussy, F-94805 Villejuif, France

[2] Univ Paris 11, Dept Med, Unite INSERM U 981, Villejuif, France

[3] Ctr Hosp Univ Albert Michallon, Dept Anat & Cytol Pathol, INSERM, U823, Grenoble, France

[4] Univ Grenoble 1, Inst Albert Bonniot, Grenoble, France

[5] Univ Cologne, Max Planck Inst Neurol Res, D-50931 Cologne, Germany

[6] Univ Cologne, Klaus Joachim Zulch Labs, Max Planck Soc, D-50931 Cologne, Germany

[7] Univ Cologne, Fac Med, D-50931 Cologne, Germany

[8] Univ Cologne, Lab Translat Canc Genom, Ctr Integrated Oncol Koln Bonn, D-50931 Cologne, Germany

[9] Univ Cologne, Dept Internal Med 1, Ctr Integrated Oncol Koln Bonn, D-50931 Cologne, Germany

来源：

CLINICAL CANCER RESEARCH | 2012年 / 18卷 / 09期

关键词：

GENE AMPLIFICATION; SOMATIC MUTATIONS; PROTEIN EXPRESSION; PTEN EXPRESSION; KINASE DOMAIN; COPY NUMBER; PHASE-II; CANCER; GROWTH; MET;

D O I：

10.1158/1078-0432.CCR-11-2370

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Lung cancer is the leading cause of cancer-related deaths worldwide. Next to adenocarcinoma, squamous cell carcinoma (SCC) of the lung is the most frequent histologic subtype in non-small cell lung cancer. Encouraging new treatments (i.e., bevacizumab, EGFR tyrosine kinase inhibitors, and ALK inhibitors) have afforded benefits to patients with adenocarcinoma, but unfortunately the same is not true for SCC. However, many genomic abnormalities are present in SCC, and there is growing evidence of their biologic significance. Thus, in the short term, the molecular characterization of patients with SCC in modern profiling platforms will probably be as important as deciphering the molecular genetics of adenocarcinoma. Patients with SCC of the lung harboring specific molecular defects that are actionable (e.g., fibroblast growth factor receptor 1 amplification, discoidin domain receptor 2 mutation, and phosphoinositide 3-kinase amplification) should be enrolled in prospective clinical trials targeting such molecular defects. Clin Cancer Res; 18(9); 2443-51. (C) 2012 AACR.

引用

页码：2443 / 2451

页数：9

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