Chief, Division of Infectious Disease
Department of Medicine
Associate Member, Dept. of Immunology
Roswell Park Cancer Institute

Associate Professor of Medicine
School of Medicine & Biomedical Sciences
University at Buffalo

Current Program

• Study NADPH oxidase as a critical regulator of host defense and inflammation
• Pathogenesis of invasive aspergillosis
• Evaluate the role of NADPH oxidase in tumor immunology

Profile
Dr. Brahm H. Segal joined the staff of Roswell Park Cancer Institute (RPCI) in 1999, as Consultant, Division of Infectious Disease, Department of Medicine, and was appointed Chief of the Division in 2000. He earned his medical degree from the Albert Einstein College of Medicine, Bronx, NY, in 1992, and completed residency training in Internal Medicine at New England Medical Center, Boston, MA, in 1995. He completed a fellowship in Infectious Diseases at the National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, in 1999. He is currently Associate Professor of Medicine with tenure at the University at Buffalo School of Medicine & Biomedical Sciences and Associate Professor of Oncology (Department of Medicine) and Associate Member (Dept. of Immunology) at RPCI.

Dr. Segal has authored or co-authored more than 70 peer-reviewed publications as well as numerous book chapters.  He is Chair of the NCCN panel, “Prevention and treatment of cancer-related infections”, and has served on guideline panels for the CDC and Infectious Diseases Society of America.

Laboratory Research
The major interest of our lab is to study NADPH oxidase as a critical regulator of inflammation and host defense. NADPH oxidase is an emergency host defense pathway that is rapidly activated in response to certain microbial products, and converts molecular oxygen to superoxide anion and downstream reactive oxidant intermediates (ROIs). Chronic granulomatous disease is an inherited disorder of the NADPH oxidase characterized by severe bacterial and fungal infections (e.g., invasive aspergillosis) and by excessive inflammation. In addition to its critical host defense role, our lab, in collaboration with colleagues from Vanderbilt University (Drs. Tim Blackwell and Michael Freeman) found that NADPH oxidase also functions to restrain inflammation by modulating redox-sensitive innate immune pathways.NADPH oxidase also affects T-cell responses, including the balance between Tn17 and regulatory T-cells. We have an NIH grant to further elucidate mechanisms by which NADPH oxidase regulates inflammation.

We believe that our work has broad relevance to human diseases associated with inflammation, such as autoimmunity and tumor immunology. Indeed, several of the pathways that NADPH oxidase regulates are important in tumorigenesis and the tumor microenvironment (e.g., NF-kB, Nrf2, IL-17, Tregs), and are potential therapeutic targets. In collaboration with colleagues, we are examining how NADPH oxidase influences tumor immunity.