生物谷援引：據(jù)英國《自然》雜志11日電子版報道,，日本自治醫(yī)科大學間野博行教授領導的一個研究小組發(fā)現(xiàn)吸煙者肺癌遺傳基因,。該研究小組發(fā)現(xiàn)，制作細胞骨骼蛋白質的遺傳基因“FLM4”與細胞內蛋白質磷酸化的遺傳基因“ALK”異常融合后生成的“ELM4－ALK”成為肺癌遺傳基因,。這是世界上發(fā)現(xiàn)的第二例肺癌遺傳基因。
研究小組從有吸煙史的肺癌患者標本中提取messegerRNA，從而發(fā)現(xiàn)了特定的遺傳基因,。研究小組對75歲以上包括無吸煙史的日本肺癌患者標本進行分析,，結果確認有7%%—10%%的標本中具有“ELM4－ALK”遺傳基因。
目前已知的肺癌致病基因是上皮成長因子受容體“FGFR”遺傳基因,，并已開發(fā)出有針對性的治療藥物。但FGFR異常引發(fā)的肺癌都發(fā)生在非吸煙者身上,。
這一發(fā)現(xiàn)使科學家有可能研究早期肺癌的診斷方法,，以及開發(fā)肺癌治療藥物,。（科技日報）
原始出處:
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: [email protected]).
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.
