国际肿瘤学杂志

国际肿瘤学杂志››2012,Vol. 39››Issue (1): 35-37.

• 综述 •上一篇下一篇

EML4-ALK融合基因型非小细胞肺癌抑制剂研究进展

张琪, 曾费天之, 张雷

  1. 410013长沙,中南大学湘雅医学院基础医学院(张琪、 曾费天之); 天津肿瘤医院肺部肿瘤一科(张雷)

  • 出版日期:2012-01-08发布日期:2013-11-11

Progress of EML4-ALK fusion gene non-small cell lung cancer inhibitor

ZHANG Qi, ZENG Fei-Tian-Zhi, ZHANG Lei

  1. College of Preclinical Medicine, Xiangya Medical College of South Central University ,Changsha 410013, China

  • Online:2012-01-08Published:2013-11-11

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摘要：EML4-ALK融合基因是在非小细胞肺癌（NSCLC）中发现的新分子分型，由2号染色体上两个基因片段倒位融合而成，目前发现的9种亚型均具有恶化致癌能力。该融合基因在腺癌、不吸烟或少吸烟和缺少表皮因子生长受体（EGFR）及结直肠癌基因(KRAS)变异的患者中检出率较高。该融合基因能够编码ALK酪氨酸激酶，通过一系列信号转导途径使下游产物异常磷酸化，导致癌变。因此以该融合基因为靶点，使用特异性抑制剂以抑制其表达，可达到治疗效果。目前正在进行临床试验的相关抑制剂为PF02341066和TAE684等。

关键词:肺肿瘤,EML4-ALK融合基因

Abstract:EML4-ALK fusion gene is a new molecular type of non-small cell lung cancer, which is formed by inversion of two gene segments on chromosome 2. Up to now, 9 subtypes have been found and all of them have deteriorated and carcinogenic abilities. The detection rate of this fusion gene is much higher in patients who have adenocarcinoma, never or seldom smoke and lack EGFR/KRAS mutation. This fusion gene codes ALK tyrosine kinase, that abnormally phosphorylates downstream products through signaling pathways, leading to canceration. Therefore, the specific inhibitors which target this fusion gene could inhibit its expression and have good treatment effect. At present, the relevent inhibitors which are undergoing clinical trials are PF02341066 and TAE684.