Thornburg Todd, Turner Aubrey R, Chen Yong Q, Vitolins Mara, Chang Baoli, Xu Jianfeng
Comprehensive Cancer Center, Wake Forest University Health Sciences, Winston-Salem, NC 27157, USA.
Future Oncol. 2006 Apr;2(2):213-23. doi: 10.2217/14796694.2.2.213.
The growing body of knowledge in cancer prevention demonstrates that for many cancers, risk must be defined in terms of both environmental and genetic factors. In prostate cancer, there is increasing evidence linking risk with polymorphisms in the alpha-methylacyl-CoA racemase (AMACR) gene and branched-chain fatty acids derived from specific sources of dietary fats. We are now at the point where we can begin to conceptualize possible inter-relationships between dietary and genetic risk as applied to prostate cancer, with the goal of generating testable hypotheses amenable to coordinated examinations. A greater understanding of such relationships should provide better ways to establish overall risk, to screen for the disease and perhaps to offer specific opportunities for prevention and treatment.
癌症预防领域不断增长的知识表明,对于许多癌症而言,必须从环境和遗传因素两方面来界定风险。在前列腺癌方面,越来越多的证据表明,风险与α-甲基酰基辅酶A消旋酶(AMACR)基因的多态性以及源自特定膳食脂肪来源的支链脂肪酸有关。我们现在已经到了这样一个阶段,即可以开始构思饮食风险与遗传风险在前列腺癌中的可能相互关系,目标是生成适合进行协同研究的可检验假设。对这种关系的更深入理解应该能提供更好的方法来确定总体风险、筛查疾病,或许还能提供预防和治疗的具体机会。