Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka, Japan.
Cancer Sci. 2011 Aug;102(8):1602-4. doi: 10.1111/j.1349-7006.2011.01970.x.
The echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) is a recently identified fusion-type oncoprotein that exists in approximately 5% of non-small cell lung cancer (NSCLC). It has been demonstrated that NSCLC driven by EML4-ALK is strongly addicted to this fusion-type oncokinase. A clinical trial of crizotinib (PF-02341066) sponsored by Pfizer has proven this oncogene addiction in humans by demonstrating a high response rate to inhibition of ALK kinase activity. In the present study, we report on three cases harboring EML4-ALK rearrangement who were enrolled in the trial (A8081001, NCT00585195). All three patients showed favorable responses to the ALK-specific tyrosine kinase inhibitor.
棘皮动物微管相关蛋白样 4（EML4）-间变性淋巴瘤激酶（ALK）是一种最近发现的融合型癌蛋白，存在于约 5%的非小细胞肺癌（NSCLC）中。已经证明，由 EML4-ALK 驱动的 NSCLC 强烈依赖于这种融合型癌激酶。辉瑞公司赞助的克唑替尼（PF-02341066）的临床试验通过证明对 ALK 激酶活性的抑制具有很高的反应率，证明了人类对这种致癌基因的依赖性。在本研究中，我们报告了 3 例接受试验（A8081001，NCT00585195）的 EML4-ALK 重排患者。所有 3 名患者对 ALK 特异性酪氨酸激酶抑制剂均有良好的反应。
