Nat Genet :与肠癌相关两个罕见基因突变

2013-01-09 Nat Genet 互联网

英国科学家的一项最新研究发现了两个新的基因。这一研究成果可用来解释,为什么有些家庭非常容易患上肠癌。 科学家发现的这两个基因由父亲或母亲传递给后代,可极大地提高肿瘤形成风险。这项研究发表在新一期的Nature Genetics上,对20位具有家族肠癌史的的20人的DNA进行了分析。 研究成果奖可用来开发新的判断肠癌风险的检测方法。 参与这项实验的一位叫Joe Wiegand的志愿者在28岁的

英国科学家的一项最新研究发现了两个新的基因。这一研究成果可用来解释,为什么有些家庭非常容易患上肠癌。

科学家发现的这两个基因由父亲或母亲传递给后代,可极大地提高肿瘤形成风险。这项研究发表在新一期的Nature Genetics上,对20位具有家族肠癌史的的20人的DNA进行了分析。

研究成果奖可用来开发新的判断肠癌风险的检测方法。

参与这项实验的一位叫Joe Wiegand的志愿者在28岁的时候被诊断出患有肠癌。他的大部分结肠已经被切除。

Joe Wiegand说:“我的家族有肠癌史,我奶奶和姑姑都患了肠癌,我爸爸在43岁被诊断出肠癌,我的几个表兄弟也患有肠癌和脑癌。很明显,我们家族中有些什么不对劲。”

研究者对20位参与研究的志愿者的DNA进行分析后,在两个基因中发现了错误,这些错误会增加他们患癌的几率。

这项研究的作者—牛津大学Ian Tomlinson教授说:“在一些家族中,有很多的成员会患肠癌,但是却没有携带那些已知的的显着提高发病风险的遗传错误。”

“新发现的两个遗传错误非常罕见,但是一旦携带则患肠癌风险会非常高。”

Ian Tomlinson教授表示,从短期来看,这些研究发现可以用来筛查具有肠癌高风险的人群,也可用来在癌症高发家族中筛查哪些人具有高风险以及需要进一步的定期筛查。

他也表示,非常确信在将来会有特定的疗法用于克服这些突变。

该研究被评论为近年来有关肠癌基因研究领域最重要的发现。英国癌症研究院的Julie Sharp博士表示,这些研究意味着医生们可以利用这一发现帮助那些具有肠癌疾病史的家庭预防癌症发生,或者是提早对肠癌做出诊断从而挽救更多人的生命。

doi:10.1038/ng.2503
PMC:
PMID:

Germline mutations affecting the proofreading domains of POLE and POLD1 predispose to colorectal adenomas and carcinomas

Claire Palles1, 18 Jean-Baptiste Cazier2, 18 Kimberley M Howarth1 Enric Domingo1 Angela M Jones1 Peter Broderick3 Zoe Kemp1 Sarah L Spain1 Estrella Guarino Almeida4 Israel Salguero4 Amy Sherborne3 Daniel Chubb3 Luis G Carvajal-Carmona1 Yusanne Ma3 Kulvinder Kaur5 Sara Dobbins3 Ella Barclay1 Maggie Gorman1 Lynn Martin1 Michal B Kovac1, 6 Sean Humphray7 The CORGI Consortium The WGS500 Consortium Anneke Lucassen9 Christopher C Holmes10 David Bentley7 Peter Donnelly2, 10 Jenny Taylor5 Christos Petridis11 Rebecca Roylance12 Elinor J Sawyer11 David J Kerr13 Susan Clark14 Jonathan Grimes15, 16 Stephen E Kearsey4 Huw J W Thomas17 Gilean McVean2 Richard S Houlston3 Ian Tomlinson1, 5

Many individuals with multiple or large colorectal adenomas or early-onset colorectal cancer (CRC) have no detectable germline mutations in the known cancer predisposition genes. Using whole-genome sequencing, supplemented by linkage and association analysis, we identified specific heterozygous POLE or POLD1 germline variants in several multiple-adenoma and/or CRC cases but in no controls. The variants associated with susceptibility, POLE p.Leu424Val and POLD1 p.Ser478Asn, have high penetrance, and POLD1 mutation was also associated with endometrial cancer predisposition. The mutations map to equivalent sites in the proofreading (exonuclease) domain of DNA polymerases ε and δ and are predicted to cause a defect in the correction of mispaired bases inserted during DNA replication. In agreement with this prediction, the tumors from mutation carriers were microsatellite stable but tended to acquire base substitution mutations, as confirmed by yeast functional assays. Further analysis of published data showed that the recently described group of hypermutant, microsatellite-stable CRCs is likely to be caused by somatic POLEmutations affecting the exonuclease domain.

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    2013-09-17 canlab
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    2013-05-02 cy0324
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    2013-07-11 liye789132251
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    2013-01-11 syscxl

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