Squamous cell lung cancer (SQCLC) is one of the most prevalent subtypes of lung cancer worldwide, about 400,000 persons die from squamous-cell lung cancer around the world, and its pathogenesis is closely linked with tobacco exposure. Unfortunately, squamous-cell lung cancer patients do not benefit from major advances in the development of targeted therapeutics such as epidermal growth factor receptor (EGFR) inhibitors or anaplastic lymphoma kinase (ALK) inhibitors that show exquisite activity in lung adenocarcinomas with EGFR mutations or echinoderm microtubule associated protein like-4 (EML4)-ALK fusions, respectively. Major efforts have been launched to characterize the genomes of squamous-cell lung cancers. Among the new results emanating from these efforts are amplifications of the fibroblast growth factor receptor 1 (FGFR1) gene, the discoidin domain receptor 2 (DDR2) gene mutation as potential novel targets for the treatment of SQCLCs. Researchers find that there are many specific molecular targeted genes in the genome of squamous-cell lung cancer patients. These changes play a vital role in cell cycle regulation, oxidative stress, cell apoptosis, squamous epithelium differentiation, may be the candidate targeted moleculars in SQCLCs. Here, we provide a review on these discoveries and their implications for clinical trials in squamous-cell lung cancer assessing the value of novel therapeutics addressing these targets.
肺鳞癌（squamous-cell lung cancer, SQCLC）是一种常见的肺癌病理类型，全世界每年约40余万人死于肺鳞癌，发病与吸烟密切相关。然而，研究表明，在肺腺癌中有明显疗效的靶向药物却无法让肺鳞癌患者获益，如人表皮生长因子受体（epidermal growth factor receptor, EGFR）抑制剂、间变性淋巴瘤激酶（anaplastic lymphoma kinase, ALK）抑制剂等。通过大量基因组学研究表明，纤维母细胞生长因子受体1（fibroblast growth factor receptor 1, FGFR1）基因扩增和盘状结构域受体2（the discoidin domain receptor 2, DDR2）基因突变等都可能成为新的用于治疗肺鳞癌的潜在药物分子靶点。此外，肺鳞癌患者基因组中也存在特异性的基因变异位点，这些改变在肺鳞癌细胞周期调控、氧化应激反应、细胞凋亡和鳞状上皮分化过程中发挥了重要作用，也可能为寻找候选分子靶点提供依据。本综述通过回顾近年来肺鳞癌分子靶向治疗的相关研究，分析靶向治疗在肺鳞癌中的研究进展，使肺鳞癌的个体化靶向治疗成为可能。