Daley Denise, Lewis Susan, Platzer Petra, MacMillen Melissa, Willis Joseph, Elston Robert C, Markowitz Sanford D, Wiesner Georgia L
Department of Epidemiology and Biostatistics, University Hospitals of Cleveland/Case Western Reserve University, Cleveland, OH 44106, USA.
Am J Hum Genet. 2008 Mar;82(3):723-36. doi: 10.1016/j.ajhg.2008.01.007. Epub 2008 Feb 28.
Colorectal cancer (CRC) is the third most commonly diagnosed cancer in Americans and is the second leading cause of cancer mortality. Only a minority ( approximately 5%) of familial CRC can be explained by known genetic variants. To identify susceptibility genes for familial colorectal neoplasia, the colon neoplasia sibling study conducted a comprehensive, genome-wide linkage scan of 194 kindreds. Clinical information (histopathology, size and number of polyps, and other primary cancers) was used in conjunction with age at onset and family history for classification of the families into five phenotypic subgroups (severe histopathology, oligopolyposis, young, colon/breast, and multiple cancer) prior to analysis. By expanding the traditional affected-sib-pair design to include unaffected and discordant sib pairs, analytical power and robustness to type I error were increased. Sib-pair linkage statistics and Haseman-Elston regression identified 19 linkage peaks, with interesting results for chromosomes 1p31.1, 15q14-q22, 17p13.3, and 21. At marker D1S1665 (1p31.1), there was strong evidence for linkage in the multiple-cancer subgroup (p = 0.00007). For chromosome 15q14-q22, a linkage peak was identified in the full-sample (p = 0.018), oligopolyposis (p = 0.003), and young (p = 0.0009) phenotypes. This region includes the HMPS/CRAC1 locus associated with hereditary mixed polyposis syndrome (HMPS) in families of Ashkenazi descent. We provide compelling evidence linking this region in families of European descent with oligopolyposis and/or young age at onset (<or=51) phenotypes. We found linkage to BRCA2 in the colon/breast phenotypic subgroup and identified a second locus in the region of D21S1437 segregating with, but distinct from, BRCA2. Linkage to 17p13.3 at marker D17S1308 in the breast/colon subgroup identified HIC1 as a candidate gene. We demonstrated that using clinical information, unaffected siblings, and family history can increase the analytical power of a linkage study.
结直肠癌(CRC)是美国人中第三大最常被诊断出的癌症,也是癌症死亡的第二大主要原因。只有少数(约5%)的家族性CRC可由已知的基因变异来解释。为了确定家族性结直肠肿瘤的易感基因,结肠肿瘤同胞研究对194个家族进行了全面的全基因组连锁扫描。在分析之前,临床信息(组织病理学、息肉大小和数量以及其他原发性癌症)与发病年龄和家族史一起被用于将这些家族分类为五个表型亚组(严重组织病理学、寡息肉病、年轻、结肠/乳腺癌和多种癌症)。通过将传统的患病同胞对设计扩展到包括未患病和不一致的同胞对,分析能力以及对I型错误的稳健性都得到了提高。同胞对连锁统计和哈斯曼-埃尔斯顿回归确定了19个连锁峰,其中1p31.1、15q14-q22、17p13.3和21号染色体的结果很有趣。在标记D1S1665(1p31.)处,有强有力的证据表明在多种癌症亚组中存在连锁(p = 0.00007)。对于15q14-q22染色体,在全样本(p = 0.018)、寡息肉病(p = 0.003)和年轻(p = 0.0009)表型中确定了一个连锁峰。该区域包括与阿什肯纳兹血统家族中的遗传性混合息肉病综合征(HMPS)相关的HMPS/CRAC1基因座。我们提供了令人信服的证据,将欧洲血统家族中的这个区域与寡息肉病和/或发病年龄较小(≤51岁)的表型联系起来。我们在结肠/乳腺癌表型亚组中发现了与BRCA2的连锁,并在D21S1437区域确定了第二个基因座,它与BRCA2分离但不同。在乳腺/结肠亚组中标记D17S1308处与17p13.3的连锁确定HIC1为候选基因。我们证明,使用临床信息、未患病的同胞和家族史可以提高连锁研究的分析能力。