Three exceptional young clinicians with novel approaches to fighting cancer have been named the 2025 recipients of the Damon Runyon Physician-Scientist Training Award. This award, established to help bolster the ranks of this vital cohort of cancer researchers, provides physicians who have completed clinical specialty fellowship training with the opportunity to become leaders in translational and clinical research. The awardees are selected through a highly competitive and rigorous process by a committee of leading cancer researchers who are themselves physician-scientists.
Physician-scientists are uniquely positioned to conduct research that has the potential to be translated into therapies that improve and prolong the lives of their patients. However, the pipeline of physician-scientists is dwindling. Damon Runyon seeks to address the financial disincentives that often deter physicians from pursuing a research career by providing considerably higher funding than most research fellowships—$100,000 in the first year, with increases of $10,000 per year over the next three years ($460,000 total over four years). It will also retire up to $100,000 of any medical school debt still owed by an award recipient. (The average medical school debt now exceeds $250,000.)
Since its launch in 2015, the program has funded 46 new physician-scientists from across a range of disciplines. Their research has not only brought forth insights into how cancer develops and spreads but also led to the development of new therapies, including several in clinical trials.
The Physician-Scientist Training Award was established thanks to the generosity of Damon Runyon Board members Leon Cooperman and Michael Gordon.
2025 Physician-Scientists
Alexandra E. Rojek, MD, with mentor Justin P. Kline, MD, at The University of Chicago, Chicago
Dr. Rojek’s research aims to identify why cellular therapies, such as CAR T cells and tumor-infiltrating lymphocytes (TILs), confer long-lasting responses for some cancer patients while others only experience transient clinical benefit. CAR T therapies have transformed the treatment landscape for patients with blood cancers, and TILs have entered wider clinical practice to treat melanoma patients. Dr. Rojek aims to identify the genetic and epigenetic differences in CAR T cells and TILs that are associated with long-lasting versus transient responses. She is also investigating how to promote “memory” formation in CAR T cells, with the goal of translating these findings to early phase trials of cellular therapies for patients with lymphoma or melanoma.
Charles S. Dai, MD, with mentors Daniel A. Haber, MD, PhD, and Shyamala Maheswaran, PhD, at Massachusetts General Hospital, Boston
Some breast cancers and most prostate cancers express high levels of androgen receptors. Curiously, both activation and inhibition of androgen receptor signaling can result in tumor shrinkage, and the molecular mechanisms driving these opposing effects remain unclear. By studying circulating tumor cells from the blood, Dr. Dai and his colleagues found that this paradoxical effect is mainly caused by abnormal binding of androgen receptors to DNA, changing its three-dimensional structure and resulting in the shutdown of a key cancer gene called MYC. Dr. Dai may have discovered a way to therapeutically target MYC, which has long been a challenging drug target, by overactivating androgen receptors to disrupt the DNA structure required to keep MYC turned on. This could be a promising new strategy to treat certain breast and prostate cancers. He is now investigating why this effect occurs, and how many cancers could be treated this way. Dr. Dai’s research could lead to a new approach to cancer treatment: activating androgen receptors to disrupt the genes that cancers rely on to grow.
Annabelle J. Anandappa, MD, with mentors Daniel T. Starczynowski, PhD, and Linde A. Miles, PhD, at Cincinnati Children's Hospital Medical Center, Cincinnati
Acute myeloid leukemia (AML) is an aggressive blood cancer, diagnosed in about 20,000 people in the U.S. each year. New targeted therapies have greatly expanded treatment options, particularly for older adults who cannot tolerate chemotherapy, but despite these advances, most patients with AML will experience relapse. Research has identified that mutations in the RAS signaling pathway are associated with relapse after targeted therapies. Dr. Anandappa aims to establish a role for RAS inhibitors in treating AML and elucidate the role of inflammation in RAS-mutated AML. She will use CRISPR to study over 300 genes involved in inflammatory signaling and determine if blocking them will increase response to treatment with a RAS inhibitor. The outcomes of this project will ultimately guide the design of combination regimens for the treatment of RAS-mutated AML.
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Damon Runyon Cancer Research Foundation
To accelerate breakthroughs, the Damon Runyon Cancer Research Foundation provides today's best young scientists with funding to pursue innovative research. The Foundation has gained worldwide prominence in cancer research by identifying outstanding researchers and physician-scientists. Thirteen scientists supported by the Foundation have received the Nobel Prize, and others are heads of cancer centers and leaders of renowned research programs. Each of its award programs is extremely competitive, with less than 10% of applications funded. Since its founding in 1946, in partnership with donors across the nation, the Damon Runyon Cancer Research Foundation has invested over $470 million and funded more than 4,000 scientists.