Nat Genet:新的胃癌致病基因ARID1A被发现

2012-01-06 MedSci原创 MedSci原创

近日,国际著名杂志《自然-遗传学》Nature Genetics刊登了来自香港大学李嘉诚医学院和辉瑞制药公司等机构的研究人员的最新研究成果“Exome sequencing identifies frequent mutation of ARID1A in molecular subtypes of gastric cancer。”,研究人员利用先进的基因组技术,揭示了胃癌的所有基因突变,并发现了

近日,国际著名杂志《自然-遗传学》Nature Genetics刊登了来自香港大学李嘉诚医学院和辉瑞制药公司等机构的研究人员的最新研究成果“Exome sequencing identifies frequent mutation of ARID1A in molecular subtypes of gastric cancer。”,研究人员利用先进的基因组技术,揭示了胃癌的所有基因突变,并发现了20个胃癌驱动基因,并证实一种名为ARID1A的肿瘤驱动基因在某种类型的胃癌中突变率高达70%-80%。

胃癌是香港第六位最常见的癌症,是所有癌症中死亡率最高的第四位,每年新发病例逾***,有600多人死于此病。胃癌由基因突变引发,但医学界并不知道一个胃癌会有多少个突变基因。最近香港大学李嘉诚医学院病理学系进行一项研究,利用先进的基因组技术,揭示胃癌的所有基因突变,并发现20个胃癌驱动基因,而其中一种名为ARID1A的肿瘤驱动基因,在某种类型的胃癌中突变率高达70%到80%。发现及鉴定这些致癌的基因突变有助开发全新药物或试用现有的标靶药物,专门针对杀灭带有基因突变的癌细胞,而不影响正常细胞,此发现对发展胃癌治疗带来了新方向。

关于胃癌

胃癌是人类健康的重大威胁,全球肿瘤中8%的发病率和10%死亡率由其引起。仅就2008年而言,全球有接近100万新诊断病例,死于此病者近74 万人。早期胃癌无明显症状,大多数患者就诊时已到中晚期,没有有效治疗方法。胃癌由基因突变引发,因幽门螺杆菌的细菌感染、进食过多腌肉及泡菜等腌制食品、或吸烟、令致癌物于胃部形成,破坏DNA而导致,发病率于老年人尤其高。

研究背景

从前医学界并不知道一个胃癌会有多少个突变基因,而医学界相信,发现及鉴定这些致癌的基因突变有助开发毒副作用较少的标靶药物,专门针对杀灭带有基因突变的癌细胞,而不影响正常细胞。

人类基因组含有逾3万个基因,由30亿个基因密码组成,在这浩如烟海的基因组中,要逐一检测去寻找导致胃癌的基因突变有如大海捞针,不仅困难而且进度缓慢。所以,过去数十年来,只有大约十几个胃癌相关的基因突变被发现和证实。绝大多数致癌的基因突变发生于‘外显子'区域,这一区域约占整个基因组的 2%,是负责制造蛋白质这一人体的重要组件。最近DNA测序技术突飞猛进,利用外显子测序技术选择性地捕获所有外显子区域DNA作下一代DNA测序,可在两周内完成一个胃癌组织所有基因外显子的测序,找出当中的所有突变基因。

研究方法与成果

为寻找新的胃癌治疗方法,确定胃癌的致癌基因突变,港大研究人员与制药企业辉瑞公司展开合作研究。研究测序22个香港胃癌患者的肿瘤组织和相应的瘤旁正常组织的16万个基因外显子,「一网打尽」所有的癌基因突变。研究小组发现每个胃癌患者人平均约有62个导致蛋白序列改变的基因突变、最高的可以有过千。有些基因的突变,虽发生于很少数胃癌患者身上,但现已有标靶药物于临床试验阶段,有助发展个人化治疗。

研究小组又发现,有些突变的基因在多个胃癌患者的肿瘤组织中频繁出现,可能对肿瘤发展至关重要,被称为肿瘤驱动基因。研究小组发现了20个胃癌驱动基因,许多前所未知。其中,名为ARID1A的肿瘤驱动基因,被发现在某种类型的胃癌中突变率高达70%到80%。这个基因属于染色质修饰基因家族成员,通过改变细胞的染色质结构行使功能。我们的DNA是一个构造精致的柔软链式结构,由染色质作为支架。染色质的架构很大程度上决定某些基因的功能。染色质修饰基因家族许多成员被发现为肿瘤驱动基因,许多制药公司趋之若鹜,研发与之相应的药物。一些通过改变染色质结构以治疗其他疾病的新药已在研发中。由于我们发现胃癌中染色质修饰基因突变频繁,这些药物很可能也能用于治疗胃癌。

此研究之重要性

此项研究揭示了胃癌中所有的基因突变,加深我们对胃癌发展的理解,有助于推进早期诊断技术及实行个人化治疗。另外,研究发现的多个肿瘤驱动基因,为胃癌的新药开发提供了新的靶标,包括ARID1A在内的染色质修饰基因的频发突变,使通过改变染色质结构以治疗胃癌变成可行的疗法。

关于研究小组

这项研究由香港大学李嘉诚医学院病理学系临床教授梁雪儿教授及辉瑞公司徐江春博士领导,其他主要研究人员包括香港大学博士后研究生阚君锁、袁兆灿教授、朱建民教授、罗英杰教授,及辉瑞公司王凯博士和茅矛博士。

生物谷Bioon.com)

Exome sequencing identifies frequent mutation of ARID1A in molecular subtypes of gastric cancer

Kai Wang,1, 7 Junsuo Kan,2, 7 Siu Tsan Yuen,2 Stephanie T Shi,3 Kent Man Chu,4 Simon Law,4 Tsun Leung Chan,2 Zhengyan Kan,1 Annie S Y Chan,2 Wai Yin Tsui,2 Siu Po Lee,2 Siu Lun Ho,2 Anthony K W Chan,2 Grace H W Cheng,2 Peter C Roberts,5 Paul A Rejto,1 Neil W Gibson,1, 6 David J Pocalyko,1 Mao Mao,1 Jiangchun Xu1 & Suet Yi Leung2

Gastric cancer is a heterogeneous disease with multiple environmental etiologies and alternative pathways of carcinogenesis1, 2. Beyond mutations in TP53, alterations in other genes or pathways account for only small subsets of the disease. We performed exome sequencing of 22 gastric cancer samples and identified previously unreported mutated genes and pathway alterations; in particular, we found genes involved in chromatin modification to be commonly mutated. A downstream validation study confirmed frequent inactivating mutations or protein deficiency of ARID1A, which encodes a member of the SWI-SNF chromatin remodeling family, in 83% of gastric cancers with microsatellite instability (MSI), 73% of those with Epstein-Barr virus (EBV) infection and 11% of those that were not infected with EBV and microsatellite stable (MSS). The mutation spectrum for ARID1A differs between molecular subtypes of gastric cancer, and mutation prevalence is negatively associated with mutations in TP53. Clinically, ARID1A alterations were associated with better prognosis in a stage-independent manner. These results reveal the genomic landscape, and highlight the importance of chromatin remodeling, in the molecular taxonomy of gastric cancer.

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    2012-03-20 liye789132251
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    2012-10-01 canlab
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    2012-11-07 cy0324
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