RAYMOND E BOISSY, PH.D.



Dr. Boissy is Professor of Dermatology & Cell Biology and Director of Basic Science Research at the University of Cincinnati College of Medicine (UCCOM). The research programs at the UCCOM focus on many aspects of pigment cell biology including regulation of skin pigmentation, melanoma biology, and pathophysiology of pigmentary diseases.

Dr. Boissy received his Ph.D. in Veterinary Sciences from the University of Massachusetts, where his thesis research focused on the loss of pigmentation in the avian model for vitiligo, the Smyth chicken. Dr. Boissy subsequently trained in Dermatology Research at the Yale University School of Medicine under the tutelage of Dr. Aaron Lerner, where he began to investigate the melanocyte pathophysiology of vitiligo. In 1986, Dr. Boissy joined the faculty of the Departments of Dermatology and Cell Biology at the University of Cincinnati College of Medicine where he continued his investigation of vitiligo with Dr. James Nordlund. For the past two decades, Dr. Boissy has also investigated the cellular/molecular biology underlying pigment granule formation, melanosome transfer to keratinocytes, Albinism, Hermansky-Pudlak Syndrome, Chediak-Higashi Syndrome, and Neurofibromatosis.

Dr. Boissy has published over 100 scientific papers, 30 review articles and book chapters, and has helped edit a book entitled The Pigmentary System: Physiology and Pathophysiology. Dr. Boissy has lectured throughout the world and has recently received the Literature Award from the Society for Cosmetic Chemistry for his publications on pigment cell biology and the 2009 Career Achievement Award from the American Skin Association. Dr. Boissy is the past Secretary/Treasurer of the PanAmerican Society for Pigment Cell Research and is currently Chairman of the National Vitiligo Foundation.

RESEARCH BACKGROUND AND FOCUS AREA

Vitiligo is an acquired cutaneous disease in which the melanocyte component of the skin is destroyed, resulting in amelanotic lesions of variable size and extent. The cause of vitiligo consists of multiple factors including genetic, cytotoxic, and autoimmune components. The current prevailing hypothesis is that some inducing agent triggers the genetically susceptible vitiligo melanocytes into an autolytic process. Subsequently, an auto immune response develops in the patient that appears to exacerbate the disease. We are currently characterizing the etiology of this disease that affects 1% of the human population worldwide. The main focus in our research lab is to understand why the vitiligo melanocyte is susceptible to cell death, and what the process of cell death is, so that appropriate therapies can be developed to prevent melanocyte death in vitiligo.

Dr. Boissy can be contacted at boissyre@ucmail.uc.edu.

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