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Mary Beth Terry, PhD
Professor, Department of Epidemiology
Mailman School of Public Health
New York, New York
- Seeking to improve breast cancer risk models for high-risk families.
- Studies are ongoing to measure exposure to chemical pollutants and non-genetic changes to DNA to enhance cancer risk prediction models.
- This work will lead to better risk prediction models in high-risk individuals by incorporating biomarkers of environmental exposures, genetic susceptibility and non-genetic alterations to DNA.
Breast cancers that occur frequently in families can be due to both genetic and environmental factors. A person’s genetic background can affect how his/her body responds to a range of environmental influences; from diet to common chemicals. Drs. Santella and Terry are conducting studies to understand the impact of environmental exposures in young girls from high-risk families to develop better risk prediction models and preventive strategies.
Full Research Summary
Drs. Santella and Terry are pursuing multiple approaches to better understand how environmental factors influence breast cancer risk in high-risk families. One way they measure environmental impact is by looking at DNA methylation, which is a reversible chemical modification of DNA. Changes in DNA methylation can affect gene expression, including genes implicated in cancer.
They are studying women and young girls participating in two studies: Breast Cancer Family Registry (BCFR), a cohort of families at high risk for breast and ovarian cancer, and LEGACY, a cohort of 1040 young girls ages 6-13 years old from these high-risk families as well as from average-risk families.
Current studies are focused on polycyclic aromatic hydrocarbons (PAHs), common environmental pollutants. Exposures to PAHs is widespread from diet, smoking and air pollution. In an analysis of women in the BCFR study group, investigation showed that women who already have a high risk of breast cancer may have an even greater risk of breast cancer development when exposed to PAHs.
The researchers suspect that the increased risk from PAH exposure is due to differences in DNA methylation. This year, they will use data from the LEGACY study to examine the effects of PAH exposure on age at full breast development and breast tissue composition in adolescents and young women and breast cancer risk in young women.
Ultimately, their goal is to improve risk prediction and modification by incorporating biomarker data and genetic susceptibility into current risk models.
Mary Beth Terry, PhD, is a Professor of Epidemiology at Columbia University’s Mailman School of Public Health. She focuses her research on breast cancer and in the molecular epidemiology and life-course methods of the disease, in particular. She is a cancer epidemiologist with over 15 years of leading studies of breast cancer etiology specifically focused on the role genetics, epigenetics, and other biomarkers play in modifying the effects of environmental exposures. Dr. Terry currently leads four NIH grants through the National Cancer Institute and the National Institute for Environmental Health Sciences that focus on following cancer risk within family-based cohorts. Her more recent work studying biomarkers, which can be modified throughout life, supports the assertion that selected markers of DNA methylation and other biomarkers are associated with breast cancer risk even within high risk families. Understanding whether biomarkers can help explain risk in higher risk women is important, as only a minority of women with a family history of cancer carry the BRCA1 or BRCA2 mutation. Her work also focuses on measuring risk factors for mammographic density, a strong intermediate marker of breast cancer. In addition to her doctorate in epidemiology from Columbia University, Dr. Terry has a Master's degree in economics and previously worked as an econometrician and program evaluator for a number of government-sponsored programs. Dr. Terry teaches introductory and advanced epidemiologic methods at the Mailman School of Public Health.