Jeffrey Sosman, M.D., professor of Medicine, Ingram Chair for Cancer Research and director of the Vanderbilt Melanoma Program, was named one of the Hottest Scientific Researchers of the last year by Thomson Reuters Science Watch.
The annual ranking recognizes researchers whose published papers recorded notably higher levels of citations during the previous year.
Sosman is among nearly two dozen researchers cited by Thomson Reuters, a news and information company that specializes in business information across a wide range of industries.
He has been the lead author or co-author on several recent papers on melanoma, the most deadly form of skin cancer.
In addition to his leadership of the Vanderbilt Melanoma Program, Sosman is the first Mary Hendrickson-Johnson ACS Melanoma Professor for his efforts to bring translational medicine to melanoma therapy. He is also co-leader of the Cell Proliferation and Signal Transduction Program at Vanderbilt-Ingram Cancer Center (VICC). He has directed numerous clinical research trials studying non-chemotherapy based treatment of cancer. The trials include a strong translational component frequently centered on immunotherapy, and more recently, targeted therapy aimed at mutated or overexpressed oncogenes.
At VICC, Sosman directs one of the first programs in the nation to offer melanoma patients routine genotyping of their tumors to help identify and offer treatments based on their genetic mutations. More recently his efforts have turned to personalized therapy of melanoma with well-defined targets (BRAFv600, NRAS mutations, CKIT mutations).
“We are finally seeing a paradigm shift in the treatment of melanoma and we are beginning to understand what is happening in the tumors at the molecular level,” Sosman said. “It is very exciting to finally be able to offer our patients new therapies that may extend their lives, even as we try to understand what the melanoma does to prevent these therapies from providing a cure.”
To further this approach he has played a role in studies of secondary resistance to BRAF inhibitors, as well as efforts to define other “druggable” targets for the many patients with NRAS mutations and those whose tumors do not have a defined mutation.
