论文部分内容阅读
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 def iciencies 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 collabor ations, 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.
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. However, many of the causal genes in sporadic CRC have hitherto proved elusive. The power of large international collabor ations, coupled with genome-wide association studies, has implicated a major functional role of the tumor growth factor-β pathway in CRC susceptibility. Nutrient regulation of gene expression may be particularly important here. 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.