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ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time.

机译:非小细胞肺癌的ALK抑制:从发现到治疗的记录时间。

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摘要

It was only 3 years ago that an acquired translocation of EML4 with ALK leading to the expression of an EML4-ALK oncoprotein in non-small cell lung cancer (NSCLC) was reported. Tumor cells expressing EML4-ALK are "addicted" to its continued function. Now, crizotinib, an oral ALK inhibitor, is demonstrated to provide dramatic clinical benefit with little toxicity in patients having such advanced NSCLC, and a mechanism of clinical resistance to crizotinib is identified. Such therapy "targeted" at oncogenic proteins provides "personalized" medicine and prompts genome-wide mutation analysis of human tumors to find other therapeutic targets.
机译:仅在3年前,据报道,EML4与ALK易位,导致非小细胞肺癌(NSCLC)中EML4-ALK癌蛋白的表达。表达EML4-ALK的肿瘤细胞被“认为”其持续功能。现在,已证明口服ALK抑制剂克唑替尼在具有这种晚期NSCLC的患者中提供了巨大的临床益处,并且几乎没有毒性,并且鉴定了对克唑替尼的临床耐药性机制。这种“靶向”致癌蛋白的疗法提供了“个性化”药物,并促进了人类肿瘤全基因组突变分析,从而找到了其他治疗靶标。

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