Abstract
The fusion gene between echinoderm microtubule-associated protein-like 4 (EML4) and anaplastic lymphoma kinase (ALK) has recently been identified as a new molecular target of non-small cell lung cancers (NSCLC). Stage Ⅰ and stage Ⅱ clinical trials have observed remarkably clinical efficacy of ALK inhibitors in NSCLC patients harboring EML4-ALK translocations, with response rates exceeding ＞ 80%. Investigation of EML4-ALK's biological functions and its correlation with clinical characteristics may shed some light on a new treatment strategy for NSCLC. Key words: Carcinoma,Non-small-cell lung; Echinoderm microtubule-associated protein-like 4
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