Established in honor of Nobel laureate Szent-Gyorgyi, co-founder of the NFCR, the prize recognizes outstanding scientific achievement in the war against cancer and celebrates leading researchers who have made extraordinary contributions in the field of cancer research.
In 1983, Dvorak and his colleagues were the first to demonstrate that tumor cells secreted vascular endothelial growth factor (VEGF), known at the time as vascular permeability factor or VPF.
"Dr. Dvorak's seminal discoveries in basic science have led to significant clinical benefits for cancer patients, perfectly fitting the unique criteria of the Albert Szent-Gyorgyi Prize for Progress in Cancer Research," notes NFCR Chief Scientific Officer Sujuan Ba, PhD, co-chair of the prize committee. "Dr. Dvorak's key VPF/VEGF discovery paved the way for researchers to better understand the mechanisms involved in tumor angiogenesis. His work is now being utilized in very real practical applications, offering hope for angiogenesis-centered treatments to halt, and even reverse, tumor growth."
Adds prize committee chairman Daniel Von Hoff, vice president of the Translational Genomics Research Institute in Phoenix, Arizona, "Without Dr. Dvorak's fundamental discovery we would probably not have had the therapeutic agent bevacizumab, which has had a tremendous impact on improving survival for patients with advanced colorectal cancer, breast cancer, non-cell lung cancer and renal cell carcinoma. In addition, other small molecules which inhibit VEGF have also shown outstanding clinical antitumor activity with dramatic therapeutic effects for patients worldwide."
Dvorak's original findings, published in the journal Science, demonstrated that tumors secreted VPF/VEGF. This discovery provided the molecular basis for the field of angiogenesis. Today, agents that work by inhibiting angiogenesis are considered among the most promising of cancer therapies under investigation.
Three years later, Dvorak made the critically important observation that tumors behave like "wounds that fail to heal," recognizing that just as a wound forms a clot to begin the process of healing, tumors "turn on" this same mechanism to enable blood vessels to grow. While in both cases, it is the VEGF molecule that produces the clotting agent, he discovered that tumors differ from wounds in a very important respect: Once a wound has healed, VEGF production abruptly stops while in the case of tumors, VEGF production continues, thereby keeping the "healing mechanism" in an on position and causing cancerous tumors to grow and spread.
"Hal Dvorak's contributions to the field of cancer research are legendary," notes Jeffrey S. Flier, MD, chief academic officer of BIDMC. "His initial discovery helped to take cancer investigations in a whole new direction, an endeavor he continues to this day. BIDMC is extremely honored to have Hal as a member of our research faculty."
A graduate of Princeton University and Harvard Medical School, Dvorak completed medical residency training in pathology at Massachusetts General Hospital and did postdoctoral research training at the National Institutes of Health. He joined the former Beth Israel Hospital (now Beth Israel Deaconess Medical Center) in 1967, from which he retired as chief of the division of pathology in July 2005. He is the Mallinkrodt Professor of Pathology Emeritus at Harvard Medical School and is a fellow of the American Association for the Advancement of Science and of the National Foundation for Cancer Research. A past president of the American Society for Investigative Pathology, he is the author of more than 220 original scientific articles.
Beth Israel Deaconess Medical Center is a patient care, research and teaching affiliate of Harvard Medical School and ranks fourth in National Institute of Health funding among independent hospitals nationwide. BIDMC is clinically affiliated with the Joslin Diabetes Center and is a research partner of Dana-Farber/Harvard Cancer Center. BIDMC is the official hospital of the Boston Red Sox. For more information, visit www.bidmc.harvard.edu.