The role of epigenetic modifications in mediating cancer health disparities.

The dysregulation of tumorigenesis at the epigenetic level entails erratic gene expression, in which changes do not rely on alterations to the genetic sequence. Such changes are often orchestrated by mechanisms that involve modifying DNA or the histones that package it, as well as interrupting or suppressing microRNAs. For instance, tumor suppressor genes may be turned off, oncogenes can be turned on, or the genes affecting cellular genetic stability may be damaged recognizably, i.e., with certain patterns of expression, such as the hypermethylation of the BRCA1 gene in some types of breast cancer or such as the hypermethylation of the BRCA1 gene in some types of breast cancer or the combination of promoter-specific hypermethylation and global hypomethylation that characterizes many colorectal cancers. The so-called "social determinants of health (SDOH)," which also have been shown to include aspects of physical and social environments such as exposure to pollution, food insecurity, and the compounding of health-threatening factors due to chronic stress, are one of the key players in the story of the epigenome and cancer. The review aims to address how these cancer-causing factors alter the epigenome, particularly in the context of social determinants of health. If we wish to prevent and treat cancer among the socially disadvantaged, we must reshape research and policy in a global way. For the prevention and treatment of cancer, an advanced understanding of epigenetic analysis is needed.