【英文】世卫组织报告：全球肿瘤报告（614页）

英文研究报告 2020年06月29日 06:59 管理员

Many gene variants that interact with environmental agents have been identified. However, the assessment of causal evidence is often uncertain, because of the very large sample sizes required to investigate interactions. For each of the key characteristics of carcinogens, genes with inherited variants can be found (Table 3.3.1), but the real impact of these variants in modulating the effect of environmental exposures is largely unknown. Simonds et al. [8] performed a systematic review of published literature from two databases of genetic association studies: the HuGE literature finder and the Cancer GenomeWide Association and Meta Analyses Database (Cancer GAMAdb). Of 3019 articles identified in the searches, only 272 articles met the inclusion criteria.

In both searches, the majority of the publications examined gene– environment interactions in cancers of the colon, rectum, colorectum, breast, or lung. The interactions examined most frequently included environmental factors categorized as energy balance (e.g. indicated by body mass index, diet), exogenous hormonal factors (e.g. oral contraceptives), endogenous hormonal factors (e.g. indicated by menopausal status), particular chemical exposures (e.g. consumption of grilled meats), and lifestyle factors (e.g. smoking, alcohol consumption) (Fig. 3.3.4).

Interestingly, the majority of the interactions examined used loci from candidate gene studies, and none of the studies were genomewide interaction studies (i.e. studies based on genome-wide association studies [GWAS]). The magnitudes of the interactions reported were modest, as is usually the case in the literature on gene–environment interactions in cancer: the risks increased or decreased by 20–50% in carriers of the minor allele compared with wild-type individuals for the same exposure [9] (some examples are given below).