Donato Romagnolo, PhD, MSc

Professor of Nutritional and Cancer Biology
Professor, Department of Nutritional Sciences
Professor, College of Agriculture and Life Sciences
Professor, BIO5 Institute
Director of the Mediterranean Diet and Health Study Abroad Program
Associate, Center for Toxicology
Email Address: 
Phone Number: 
(520) 626-9108
FAX: 
(520) 621-9446

UACC Information

UACC Organizational Unit: 
Professional Bio: 

Dr. Romagnolo is a Professor of Nutritional and Cancer Biology and a member of the University of Arizona Cancer Center (UACC), Southwest Environmental Health Sciences Center (SWEHSC), and BIO5 Research Institute. His research interests focus on; (i) role of nuclear receptors in epigenetic regulation of tumor suppressor genes by environmental and dietary xenobiotics; and 2) role of gene x dietary bioactive food component interactions in the etiology and prevention of cancer and inflammation.

As graduate student and postdoctoral fellow, Dr. Romagnolo received training in molecular endocrinology and carcinogenesis. As an independent investigator for the last 15 years, his research has been continuously funded by grants from the National Institutes of Health, U.S. Arhis Department of Defense, Susan G. Komen for the Cure, Arizona Biomedical Research Commission, and American Institute for Cancer Research. Since 2003, he chaired the Research Frontiers in Nutritional Sciences Conference Series at The University of Arizona. This conference series focuses on finding solutions through diet to chronic diseases including cancer.

Dr. Romagnolo has served as a member of study sections for the National Institutes of Health, U.S. Department of Defense, Susan G. Komen Breast Cancer Foundation, and American Institute for Cancer Research. He is currently serving as scientific editor and reviewer for nutrition, cancer, and pharmacology and toxicology journals. He 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.

With this background and experience, Dr. Romagnolo is well suited to be an investigator in Project 1, “Molecular and Metagenomic Characteristics of Early-Onset Colorectal Cancers.”  He has extensive experience in leading epigenetic studies with cell culture and in vivo tumor models.

Formerly, Dr. Romagnolo has been a PI on several federal grants that have focused on impact of dietary exposures to agonists of nuclear receptors on epigenetic regulation of tumor suppressor genes. Recently, in collaboration with other colleagues at the University of Arizona Cancer Center he has developed studies of bile acid regulation in genetic (Apc, Fxr) models of colon cancer. This work was recently selected for outstanding recognition at the 2015 Experimental Biology Meetings in Boston, MA. He is well suited to be a Co-Investigator for the proposed project.

Clinical Information

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Research Information

Research Program: 
Cancer Biology
Member Status: 
Research Member
Summary of Research Activity: 

Some of Dr. Romagnolo's 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.