de Jong Mirjam M, Nolte Ilja M, te Meerman Gerard J, van der Graaf Winette T A, de Vries Elisabeth G E, Sijmons Rolf H, Hofstra Robert M W, Kleibeuker Jan H
Department of Gastroenterology, University Hospital Groningen, The Netherlands.
Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1332-52.
This report focuses on low-penetrance genes that are associated with colorectal adenoma and/or cancer or that are in strong linkage disequilibrium with colorectal adenoma and/or cancer causing variants. A pooled analysis was performed for 30 polymorphisms in 20 different genes that have been reported in more than one colorectal adenoma or cancer study. An association with colorectal cancer was found for seven polymorphisms in seven genes reported in more than one study; no associations were found with colorectal adenoma. Four of the polymorphisms exhibited an increased colorectal cancer risk [GSTT1, NAT2 (phenotype), HRAS1, and ALDH2]. Two others [MTHFR, Tp53 (intron 3)] exhibited a decreased risk. For the tumor necrosis factor (TNF)a polymorphism of the TNF-alpha gene, one allele was associated with an increased risk (a2 allele) and two other TNFa alleles with decreased risks (a5 and a13 allele). No association with colorectal adenoma and/or cancer was detected for 23 other polymorphisms in 15 genes. However, of all 30 polymorphisms, only three pooled analyses had sufficiently large samples to confirm (MTHFR) or to exclude (GSTM1 and NAT2 genotype) the association with a P < 0.0026 and a power of 90%. Eighteen polymorphisms in 15 genes were each described in only one study, all with very small sample sizes. For 11 polymorphisms in 10 of these genes, an association with colorectal adenoma and/or cancer was found. Only simultaneous genotyping and combined analysis of different polymorphisms in large numbers of patients and controls, stratified by ethnicity, gender, and tumor localization and taking relevant dietary and lifestyle habits into account, will make it possible to describe the exact relations between polymorphisms and colorectal cancer susceptibility with an adequate power.
本报告聚焦于与结直肠腺瘤和/或癌症相关的低 penetrance 基因,或与导致结直肠腺瘤和/或癌症的变异处于强连锁不平衡状态的基因。对 20 个不同基因中的 30 个多态性进行了汇总分析,这些基因已在不止一项结直肠腺瘤或癌症研究中被报道。在不止一项研究中报道的 7 个基因中的 7 个多态性与结直肠癌存在关联;未发现与结直肠腺瘤有关联。其中 4 个多态性显示结直肠癌风险增加[谷胱甘肽 S-转移酶 T1(GSTT1)、N-乙酰转移酶 2(NAT2,表型)、哈-柔二氏肉瘤病毒癌基因同源物 1(HRAS1)和乙醛脱氢酶 2(ALDH2)]。另外两个[亚甲基四氢叶酸还原酶(MTHFR)、肿瘤蛋白 p53(Tp53,内含子 3)]显示风险降低。对于肿瘤坏死因子(TNF)α基因的 TNF-α多态性,一个等位基因与风险增加相关(a2 等位基因),另外两个 TNFα等位基因与风险降低相关(a5 和 a13 等位基因)。在 15 个基因中的其他 23 个多态性未检测到与结直肠腺瘤和/或癌症有关联。然而,在所有 30 个多态性中,只有三项汇总分析有足够大的样本量来确认(MTHFR)或排除(谷胱甘肽 S-转移酶 M1(GSTM1)和 NAT2 基因型)与 P < 0.0026 和 90%检验效能的关联。15 个基因中的 18 个多态性仅在一项研究中被描述,所有研究样本量都非常小。在这些基因中的 10 个基因的 11 个多态性中,发现与结直肠腺瘤和/或癌症有关联。只有在大量患者和对照中同时进行基因分型并对不同多态性进行联合分析,按种族、性别和肿瘤定位分层,并考虑相关饮食和生活习惯,才有可能以足够的检验效能描述多态性与结直肠癌易感性之间的确切关系。