Kantor Elizabeth D, Giovannucci Edward L
Department of Epidemiology, Harvard School of Public Health, Boston, MA, 02115.
Department of Epidemiology, Harvard School of Public Health, Boston, MA, 02115 ; Department of Nutrition, Harvard School of Public Health, Boston, MA, 02115.
Curr Nutr Rep. 2015 Mar;4(1):13-21. doi: 10.1007/s13668-014-0114-2.
A number of studies have evaluated the role of gene-diet interaction in the etiology of colorectal cancer (CRC). Historically, these studies focused on established dietary risk factors and genes involved in their metabolism. However, results from these candidate gene studies were inconsistent, possibly due to multiple testing and publication bias. In recent years, genome-wide association studies have identified a number of CRC susceptibility loci, and subsequent meta-analyses have observed limited evidence that diet may modify the risk associated with these susceptibility loci. Statistical techniques have been recently developed to evaluate the presence of interaction across the entire genome; results from these genome-wide studies have demonstrated limited evidence of interaction and have failed to replicate results from candidate gene studies and those using established susceptibility loci. However, larger sample sizes are likely needed to elucidate modest or weak interaction in genome-wide studies of gene-diet interaction.
许多研究评估了基因 - 饮食相互作用在结直肠癌(CRC)病因学中的作用。从历史上看,这些研究集中在既定的饮食风险因素以及参与其代谢的基因上。然而,这些候选基因研究的结果并不一致,可能是由于多重检验和发表偏倚。近年来,全基因组关联研究已经确定了一些结直肠癌易感位点,随后的荟萃分析发现,饮食可能改变与这些易感位点相关风险的证据有限。最近开发了统计技术来评估整个基因组中相互作用的存在;这些全基因组研究的结果表明相互作用的证据有限,并且未能重复候选基因研究以及那些使用既定易感位点的研究结果。然而,在基因 - 饮食相互作用的全基因组研究中,可能需要更大的样本量来阐明适度或微弱的相互作用。