Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, 68198, USA.
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, 68198, USA,
Front Biosci (Landmark Ed). 2017 Mar 1;22(8):1221-1246. doi: 10.2741/4543.
Genetic mutations and metabolic reprogramming are two key hallmarks of cancer, required for proliferation, invasion, and metastasis of the disease. While genetic mutations, whether inherited or acquired, are critical for the initiation of tumor development, metabolic reprogramming is an effector mechanism imperative for adaptational transition during the progression of cancer. Recent findings in the literature emphasize the significance of molecular cross-talk between these two cellular processes in regulating signaling and differentiation of cancer cells. Genome-wide sequencing analyses of cancer genomes have highlighted the association of various genic mutations in predicting cancer risk and survival. Oncogenic mutational frequency is heterogeneously distributed among various cancer types in different populations, resulting in varying susceptibility to cancer risk. In this review, we explore and discuss the role of genetic mutations in metabolic enzymes and metabolic oncoregulators to stratify cancer risk in persons of different racial backgrounds.
遗传突变和代谢重编程是癌症的两个关键标志,是疾病增殖、侵袭和转移所必需的。虽然遗传突变(无论是遗传的还是获得的)对肿瘤发展的启动至关重要,但代谢重编程是癌症进展过程中适应性转变所必需的效应机制。文献中的最新发现强调了这两个细胞过程之间分子串扰在调节癌细胞信号转导和分化中的重要性。对癌症基因组的全基因组测序分析强调了各种基因突变与预测癌症风险和生存的关联。致癌突变频率在不同人群的不同癌症类型中呈异质性分布,导致对癌症风险的易感性不同。在这篇综述中,我们探讨和讨论了遗传突变在代谢酶和代谢共调节因子中的作用,以对不同种族背景的人进行癌症风险分层。