生物谷援引：据英国《自然》杂志11日电子版报道，日本自治医科大学间野博行教授领导的一个研究小组发现吸烟者肺癌遗传基因。该研究小组发现，制作细胞骨骼蛋白质的遗传基因“FLM4”与细胞内蛋白质磷酸化的遗传基因“ALK”异常融合后生成的“ELM4－ALK”成为肺癌遗传基因。这是世界上发现的第二例肺癌遗传基因。
研究小组从有吸烟史的肺癌患者标本中提取messegerRNA，从而发现了特定的遗传基因。研究小组对75岁以上包括无吸烟史的日本肺癌患者标本进行分析，结果确认有7%%—10%%的标本中具有“ELM4－ALK”遗传基因。
目前已知的肺癌致病基因是上皮成长因子受容体“FGFR”遗传基因，并已开发出有针对性的治疗药物。但FGFR异常引发的肺癌都发生在非吸烟者身上。
这一发现使科学家有可能研究早期肺癌的诊断方法，以及开发肺癌治疗药物。（科技日报）
原始出处:
Nature advance online publication 11 July 2007 | doi:10.1038/nature05945; Received 15 February 2007; Accepted 17 May 2007; Published online 11 July 2007
Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer
Manabu Soda1,2, Young Lim Choi1, Munehiro Enomoto1,2, Shuji Takada1, Yoshihiro Yamashita1, Shunpei Ishikawa5, Shin-ichiro Fujiwara1, Hideki Watanabe1, Kentaro Kurashina1, Hisashi Hatanaka1, Masashi Bando2, Shoji Ohno2, Yuichi Ishikawa6, Hiroyuki Aburatani5,7, Toshiro Niki3, Yasunori Sohara4, Yukihiko Sugiyama2 & Hiroyuki Mano1,7
Division of Functional Genomics,
Division of Pulmonary Medicine,
Department of Pathology, and,
Division of General Thoracic Surgery, Jichi Medical University, Tochigi 329-0498, Japan
Research Center for Advanced Science and Technology, University of Tokyo, Tokyo 153-8904, Japan
Department of Pathology, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan
Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama 332-0012, Japan
Correspondence to: Hiroyuki Mano1,7 Correspondence and requests for materials should be addressed to H.M. (Email: hmano@jichi.ac.jp).
Improvement in the clinical outcome of lung cancer is likely to be achieved by identification of the molecular events that underlie its pathogenesis. Here we show that a small inversion within chromosome 2p results in the formation of a fusion gene comprising portions of the echinoderm microtubule-associated protein-like 4 (EML4) gene and the anaplastic lymphoma kinase (ALK) gene in non-small-cell lung cancer (NSCLC) cells. Mouse 3T3 fibroblasts forced to express this human fusion tyrosine kinase generated transformed foci in culture and subcutaneous tumours in nude mice. The EML4–ALK fusion transcript was detected in 6.7% (5 out of 75) of NSCLC patients examined; these individuals were distinct from those harbouring mutations in the epidermal growth factor receptor gene. Our data demonstrate that a subset of NSCLC patients may express a transforming fusion kinase that is a promising candidate for a therapeutic target as well as for a diagnostic molecular marker in NSCLC.
