David E. Fisher, MD, PhD is an internationally known researcher, clinician and academic, who is Chief of the Massachusetts General Hospital Department of Dermatology at Harvard Medical School in Boston, Massachusetts (USA). He also serves as Director of the MGH Cutaneous Biology Research Center and Director of the Melanoma Center at MGH. A Professor of Dermatology and of Pediatrics at Harvard Medical School, Dr. Fisher came to the MGH from the Dana-Farber Cancer Institute, where he previously Directed the Melanoma Program. Dr. Fisher's research has focused on understanding the molecular and genetic events which underlie formation of melanoma as well as skin pigmentation. As a clinician, he has worked to translate these understandings into advances in diagnosis, treatment and prevention of human diseases related to the skin and associated disorders. A graduate of Swarthmore College with a degree in Biology and Chemistry, Dr. Fisher is also an accomplished concert cellist and received a degree from the Curtis Institute of Music in Philadelphia. He received his PhD under Nobel Laureate Gunter Blobel at Rockefeller University and his Medical Degree at Cornell University Medical College under Dr. Henry Kunkel. Dr. Fisher's specialty training in Medicine, Pediatrics, and Oncology were carried out at Harvard Medical School. He recently served for three years as President of the Society for Melanoma Research, the largest international society dedicated to the study of melanoma.
MGH Hotline 5.08.09 Approximately 100 people attended the Friends of the MGH Cancer Center’s annual fundraising forum April 22 in the Bulfinch Tents. This year’s event featured MGH skin cancer experts David Fisher, MD, PhD, chief of the Department of Dermatology and director of the Center for Melanoma, left, and Jennifer Wargo, MD, of the Department of Surgery.
Thinking about heading to an indoor tanning salon this spring? An expert from Mass General’s Department of Dermatology says “think again.”
Browse the latest local and national news articles featuring stories from basic research to innovative breakthroughs in cosmetic dermatology.
MGH Hotline 01.14.11 STRAINS OF SAINT-SAËNS, Bruch and Beethoven filled the Goethe Institut Boston on Dec. 4, as the MGH Department of Dermatology hosted a benefit gala and concert to raise funds for the Vascular Anomalies Center in Vietnam.
In General awards and honors
THOUSANDS OF CHILDREN will have a new lease on life thanks to the $13,000 raised during the MGH Department of Dermatology’s recent benefit concert in support of the Vascular Anomalies Center in Vietnam, which provides free treatment for youth with disfiguring birthmarks.
Nearly $15,000 was raised during the third annual Vietnam Vascular Anomalies Center Benefit Concert, hosted by the MGH Department of Dermatology and the Wellman Center for Photomedicine and held at the Goethe Institut Boston.
Discovery of a molecular switch that turns off the natural process of skin pigmentation may lead to a novel way of protecting the skin – activating the tanning process without exposure to cancer-causing UV radiation.
A major international study has identified a novel gene mutation that appears to increase the risk of both inherited and sporadic cases of malignant melanoma, the most deadly form of skin cancer. The identified mutation occurs in the gene encoding MITF, a transcription factor that induces the production of several important proteins in melanocytes, the cells in which melanoma originates.
A multi-institutional study has revealed that BRAF-positive metastatic malignant melanomas develop resistance to treatment with drugs targeting the BRAF/MEK growth pathway through a major change in metabolism. The findings suggest a strategy to improve the effectiveness of currently available targeted therapies.
A new study from MGH investigators adds important support to the theory that ultraviolet light can actually be addictive, finding that chronic UV exposure raises circulating levels of beta-endorphin in mice and that UV-habituated mice exhibit withdrawal symptoms if beta-endorphin activity is blocked.