Donato Romagnolo
Associate, Center for Toxicology
Professor, Animal and Comparative Biomedical Sciences
Professor, BIO5 Institute
Professor, Nutritional Sciences
Professor, Cancer Biology - GIDP
Primary Department
Department Affiliations
(520) 626-9108
Research Interest
Donato Romagnolo, MSc, PhD, has served as a member of study sections for the National Institutes of Health, the U.S. Department of Defense, the Susan G. Komen Breast Cancer Foundation, and as a scientific reviewer for nutritional, cancer, and pharmacology and toxicology scientific journals. Dr. Romagnolo is a member of the Training Grant in Cancer Biology at the University of Arizona. Dr. Romagnolo's research focuses on: 1) mechanisms of epigenetic silencing of tumor suppressor genes by environmental and dietary xenobiotics, and 2) role of dietary bioactive food components in the etiology and prevention of cancer and inflammation. For the last 14 years, Dr. Romagnolo's research has been funded by grants from the National Institutes of Health, the U.S. Army Department of Defense, the Susan G. Komen for the Cure and the Arizona Biomedical Research Commission.Some of his research reveals humans are exposed to a complex mixture of ligands of the aromatic hydrocarbon receptor (AhR). Prototypical AhR agonists include the polycyclic aromatic hydrocarbon (PAH) benzo[a]pyrene (B[a]P), and the dioxin-like compound 2,3,7,8 tetrachlorodibenzene(p)dioxin (TCDD). Increased incidence of breast cancer is documented in human populations of industrialized areas where high levels of dioxins are found in the air, soil, drinking water, and cow milk. Unlike PAH, TCDD is not metabolized and it promotes tumor development. Population studies reported the presence of TCDD in breast milk, suggesting this agent may accumulate in breast tissue and be a potential risk factor in mammary neoplasia. The in-utero activation of the AhR with TCDD increased the susceptibility to mammary carcinogens in rat female offspring. The activation of the AhR pathway may increase the susceptibility to breast cancer through epigenetic silencing of tumor suppressor genes, including p16 and p53, while inducing transcription of the proinflammatory COX-2 gene.