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发表于 2010-5-28 21:40:58
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来自： 中国湖北宜昌
原帖由 步行者 于 2010-5-20 19:18 发表 
对于非小细胞肺癌（NSCLC），针对特定的靶点开展个体化治疗已成为现实，例如通过检测表皮生长因子受体（EGFR）基因突变，筛选适合EGFR酪氨酸激酶抑制剂（EGFR-TKI）治疗的患者亚群。近日，美国麻省总医院研究人员发表 ...
步行者，好像不太可能，有EML4-ALK突变的病人是不会有EGFR突变的，只是目标人群吻合而已。
the EML4-ALK fusion gene was identified in 2007 by a group of Japanese investigators headed by Dr. Hiroyuki Mano, who identifed a novel fusion gene from a surgical specimen of a patient with lung adenocarcinoma. The EML4 gene and the ALK gene, which are normally separate from each other but both on chromosome 2, had become fused together in this patient’s cancer. This fusion results in increased activity of ALK, which was already known to be implicated in a certain type of lymphoma. The authors subsequently found that this fusion gene was present in the tumors of other patients. When they put this gene into cells and then put the cells into mice, the mice developed tumors. In the lab, they tested an inhibitor of ALK against cancer cells with this fusion gene and found that it dramatically inhibited their growth. Subsequent studies have identified that patients with the EML4-ALK fusion gene tend to be younger than the average lung cancer patient, are more likely to be light or never smokers, and have adenocarcinomas. While these clinical characteristics are also shared by patients with EGFR mutations, patients with EML4-ALK do not have EGFR mutations.
EML4-ALK混合基因在2007年被一个日本研究团队发现，研究者从一个肺腺癌患者的病理样本中发现一种新型的混合基因，EML4基因和ALK基因，正常情况下是分开的但都存在于2号染色体上，在这个患者身上基因融合在一起。融合导致了ALK的激增活动，之前已经发现可以导致某种淋巴癌。作者逐渐发现混合基因存在于其他病人的肿瘤种。当他们把基因片段植入小鼠，小鼠迅速生长肿瘤。实验中，他们实验了一种ALK的抑制剂发现大幅抑制了肿瘤的生长。随后的研究他们界定出EML4-ALK基因突变的病人倾向于比平均病患年龄年轻，不吸烟或少量吸烟的腺癌患者。虽然他们和EGFR的目标人群临床特性吻合，但是有EML4-ALK基因变异的患者没有EGFR基因变异 |
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