Epigenetics in Cancer Individualizes Environmental and Hereditary Risks
Tuesday, May 17, 2016
You may already know that diet, obesity, exposure to the sun, radiation, and hormones are just a few of the many risk factors associated with cancer diagnoses. But, do you know about other risk factors, especially those playing out through epigenetics, the molecular relationship between the environment and our DNA?
Cancer is one of the leading causes of death around the world. Therefore, the IRP focuses significant effort on research that expands understanding of how to prevent or treat the many causes of cancer. However, we cannot effectively treat varied types of cancers without understanding why and how cancerous cells behave on a molecular level.
One IRP researcher who leads intracellular explorations is Jack Taylor, M.D., Ph.D., head of the Molecular and Genetic Epidemiology Group at the National Institute of Environmental Health Sciences (NIEHS). Dr. Taylor’s team works to understand how environmental exposures interact with human genes to initiate cancer formation.
Their research begins with the idea that exposures to environmental toxins cause genetic alterations that are then associated with cancer risk. In parallel, Dr. Taylor’s group also examines how hereditary genetic alterations influence individuals’ predispositions to developing cancer, with the hypothesis that specific alleles (different forms of a single gene) passed down from parent to child may be more likely to be affected by environmental toxins and, in turn, more likely to cause specific types of cancers.
In this short animation below, Dr. Taylor describes how DNA methylation may increase cancer risk in older people. He, with Zongli Xu, Ph.D., also of the NIEHS Epidemiology Branch, performed the finding’s underlying research and published it in the journal Carcinogenesis.
Many allelic variations that increase susceptibility to further mutation by environmental toxins are located on tumor suppressor genes and proto-oncogenes—the genes responsible for maintaining normal cellular growth cycles. Dr. Taylor and his team have determined that inherited mutations on these genes can negatively affect the capability of cells to repair DNA damage caused by environmental toxins. For example, one of his studies found that a group of cigarette smokers with a specific set of alleles are twice as likely to have bladder cancer as smokers with a different set of alleles, due to an inherited set of failing DNA repair mechanisms.
Using information about specific genetic abnormalities, Dr. Taylor’s team is now working to predict patients’ individualized risk based on their lifestyle choices and environment. Clinicians may then be able to determine which tests to run, what results to look for, and eventually the medical recommendations to make to their patients.
Determining the genetic susceptibilities that increase the risk of cancer might also have positive outcomes on public health programs. Knowing which genes result in increased cancer risk could encourage at-risk populations to be screened for specific genetic alterations, potentially saving many lives through the early detection and diagnosis of cancer.