Kathryn Hughes Barry, PhD, MPH

• B.S., Biology and Community Health (cum laude), Tufts University, Medford, MA, 2003
• M.P.H., Chronic Disease Epidemiology, Yale University, New Haven, CT, 2005
• CDC/Council of State and Territorial Epidemiologists (CSTE) Applied Epidemiology Fellowship, Washington State Department of Health, Tumwater, WA, 2005-2007
• M.Phil., Chronic Disease Epidemiology, Yale University, New Haven, CT, 2009
• Ph.D., Chronic Disease Epidemiology, Yale University, New Haven, CT, 2011
• Pre-Doctoral Fellowship, Occupational and Environmental Epidemiology and Cancer Epidemiology, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, 2009-2011
• Post-Doctoral Fellowship, Occupational and Environmental Epidemiology and Cancer Epidemiology, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, 2011-2016

Dr. Barry conducted her undergraduate studies at Tufts University and her graduate work at Yale. Prior to beginning her doctoral program at Yale, she spent two years as a CDC/CSTE Applied Epidemiology Fellow at the Washington State Department of Health. In this role, she evaluated patterns of cancer incidence/mortality and screening in Washington State and conducted cluster investigations of non-infectious conditions, including various cancers.

Dr. Barry joined the University of Maryland School of Medicine (UMSOM) in 2016 after spending more than 7 years at the National Cancer Institute (Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics) as a pre-doctoral then post-doctoral fellow. For her doctoral dissertation as part of the Yale/NCI Partnership T32 Doctoral Training Program in Cancer Epidemiology, Dr. Barry investigated the risk of cancer associated with pesticide exposures and the modifying role of inherited genetic variation in DNA repair genes (i.e. gene-environment interactions) in the U.S. Agricultural Health Study (AHS). During her post-doctoral fellowship at the NCI, she continued to study occupational and environmental risk factors for cancer and the role of genetic susceptibility in the AHS and other studies. Dr. Barry also led molecular epidemiology studies focused on identifying DNA methylation markers of prostate cancer risk (both global DNA methylation and targeted studies of DNA methylation in particular genomic regions) within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.

At the UMSOM, Dr. Barry uses classical and molecular epidemiology studies to investigate occupational, environmental, and lifestyle risk factors for cancer, underlying biological pathways, and biomarkers of cancer risk and prognosis. She has continued to investigate cancer risk associated with chemical exposures such as pesticides, PFAS (also known as “forever chemicals”), and drinking water nitrate. More recently, she has also studied the relationship of residential neighborhood disadvantage with the development of aggressive tumors, stress-related biomarkers, adverse cancer outcomes, and cancer health disparities. Her current research largely focuses on identifying risk factors and biomarkers related to aggressive prostate cancer, which is more likely to be fatal and disproportionately affects African American men. She also leads and collaborates on projects related to cancer disparities for head and neck cancer, among other cancers. The long-term goal of these lines of research is to inform population-based interventions and precision medicine approaches (e.g., tailoring screening for prostate cancer to high-risk groups) that will reduce the burden of aggressive disease, improve outcomes, and reduce disparities.

cancer epidemiology, molecular epidemiology, cancer disparities, biomarkers of cancer risk and prognosis, gene-environment interactions, epigenomics, DNA methylation, transcriptomics, prostate cancer, head and neck cancer, colorectal cancer, colorectal adenoma, non-Hodgkin lymphoma (NHL), occupational and environmental risk factors for cancer, neighborhood disadvantage, pesticides, per- and polyfluoroalkyl substances (PFAS), lifestyle factors, quality of life

Barry KH, Koutros S, Berndt SI, Andreotti G, Hoppin JA, Sandler DP, Burdette LA, Yeager M, Beane Freeman LE, Lubin JH, Ma X, Zheng T, Alavanja MC. Genetic variation in base excision repair pathway genes, pesticide exposure and prostate cancer risk. Environ Health Perspect 2011;119(12):1726-1732. PMCID: 3261977.

Barry KH, Moore LE, Sampson J, Koutros S, Yan L, Meyer A, Reddy M, Oler A, Cook MB, Fraumeni J, Jr., Yeager M, Amundadottir L, Berndt SI. Prospective study of DNA methylation at chromosome 8q24 in peripheral blood and prostate cancer risk. Br J Cancer 2017; 116(11):1470-1479. PMCID: 5520085.

He S, Berndt SI, Kunzmann AT, Kitahara CM, Huang WY, Barry KH. Weight change and incident distal colorectal adenoma risk in the PLCO Cancer Screening Trial. JNCI Cancer Spectrum 2022;6(1):pkab098, doi: 10.1093/jncics/pkab098. PMCID: 8804223.*

Boyle J, Yau J, Slade JL, Butts DA, Zhang Y, Legesse TB, Cellini A, Clark K, Park JY, Wimbush J, Ambulos N, Jr, Yin J, Hussain A, Onukwugha E, Knott CL, Wheeler DC (shared senior authorship), Barry KH. Neighborhood disadvantage and prostate tumor RNA expression of stress-related genes among African American and European American men. JAMA Network Open 2024;7(7):e2421903. doi: 10.1001/jamanetworkopen.2024.21903. PMCID: 11245728.

Boyle J, Yau J, Slade JL, Butts DA, Wimbush J, Park JY, Hussain A, Onukwugha E, Knott CL, Wheeler DC (shared senior authorship), Barry KH. Neighborhood disadvantage and prostate tumor aggressiveness among African American and European American men. Cancer Epidemiol Biomark Prev 2024;33(10):1318-1326. doi: 10.1158/1055-9965.EPI-240450. PMCID: 11614192.

*student-led paper