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Recent advances in understanding of interactions between genes and diet in the etiology of colorectal cancer

机译:结直肠癌病因中基因与饮食相互作用的最新研究进展

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摘要

At an international level, colorectal cancer (CRC) is a major cause of morbidity and mortality. Diet plays a major etiologic role, and a range of putative dietary carcinogens have been identified. The probability with which these lead to mutations, and thereby cause cancer, is strongly impacted by variants in genes coding for xenobiotic metabolizing or DNA repair enzymes. Nutrient deficiencies also play a role, which will be exacerbated by variants in metabolic genes. However, many of the causal genes in sporadic CRC have hitherto proved elusive. The power of large international collaborations, coupled with genome-wide association studies, has implicated a major functional role of the tumour growth factor-β pathway in CRC susceptibility. Nutrient regulation of gene expression may be especially important here. Future large collaborative studies must consider gene-gene and gene-diet interactions, coupled with high throughput genomic technologies, in order to uncover the relative roles of genetic variants, mutagenic xenobiotics, nutrient imbalance and gene expression in the etiology of CRC.
机译:在国际上,结直肠癌(CRC)是发病率和死亡率的主要原因。饮食起着主要的病因作用,并且已经确定了一系列推测的饮食致癌物。这些导致突变并因此导致癌症的可能性,受到编码异种生物代谢或DNA修复酶的基因变异的强烈影响。营养不足也会发挥作用,新陈代谢基因的变异会加剧营养不足。然而,迄今为止,散发性CRC中的许多致病基因已被证明难以捉摸。大型国际合作的力量,加上全基因组关联研究,已经暗示了肿瘤生长因子-β途径在CRC易感性中的重要功能。基因表达的营养调节在这里尤其重要。未来的大型合作研究必须考虑基因-基因和基因-饮食之间的相互作用,以及高通量基因组技术,以揭示遗传变异,诱变的异种生物,营养失衡和基因表达在CRC病因学中的相对作用。

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