title: Racial disparity in metabolic regulation of cancer.
abstract: 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.
authors.affiliation: Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, 68198, USA.
authors.forename: Kuldeep S
authors.initials: KS
authors.lastname: Attri
authors.affiliation: Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, 68198, USA.
authors.forename: Divya
authors.initials: D
authors.lastname: Murthy
authors.affiliation: Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, 68198, USA, pankaj.singh@unmc.edu.
authors.forename: Pankaj K
authors.initials: PK
authors.lastname: Singh
mesh_terms: D006801:Humans; D055442:Metabolome; D009154:Mutation; D009369:Neoplasms / Q000209:etiology / Q000235:genetics / Q000378:metabolism*; D009857:Oncogenes; D044469:Racial Groups / Q000235:genetics; D012307:Risk Factors; D015398:Signal Transduction; D059016:Tumor Microenvironment