New York, NY (July 6, 2018) - The Damon Runyon Cancer Research Foundation named six new Damon Runyon Clinical Investigators at its spring 2018 Clinical Investigator Award Committee review. The recipients of this prestigious three-year award are outstanding early career physician-scientists conducting patient-oriented cancer research at major research centers under the mentorship of the nation’s leading scientists and clinicians. Each will receive $450,000 to support the development of his/her cancer research program.
The Foundation also awarded Continuation Grants to three Damon Runyon Clinical Investigators. Each award will provide an additional two years of funding totaling $300,000. The Continuation Grant is designed to support Clinical Investigators who are approaching the end of their original awards and need extra time and funding to complete a promising avenue of research or initiate/continue a clinical trial. This program is possible through the generous support of the William K. Bowes, Jr. Foundation.
“The quality of research proposed by our new Clinical Investigators is exceptionally strong, and we are thrilled to be able to continue our proud tradition of funding outstanding early career physician-scientists conducting patient-oriented cancer research,” said Yung S. Lie, PhD, Deputy Director and Chief Scientific Officer at Damon Runyon. “We are helping to launch the careers of tomorrow’s brightest cancer researchers.”
The Clinical Investigator Award program is specifically intended to help address the shortage of physicians capable of translating scientific discovery into new breakthroughs for cancer patients. Through partnerships with industry sponsors and its Accelerating Cancer Cures initiative, the Damon Runyon Cancer Research Foundation has committed nearly $63 million to support the careers of 99 physician-scientists across the United States since 2000.
2018 Damon Runyon Clinical Investigators
Collin M. Blakely, MD, PhD [Doris Duke-Damon Runyon Clinical Investigator]
Non-small cell lung cancers are frequently driven by specific genetic alterations that can be targeted by precision medicine therapies. However, these therapies often result in only partial responses to treatment, allowing some cancer cells to survive and become fully resistant to therapy. This ultimately limits patients’ long-term survival. Dr. Blakely focuses on a particular type of lung cancer that is driven by mutations in the EGFR gene and frequently develops in younger patients who are non-smokers. Treatment of this disease with the targeted therapy osimertinib results in partial (incomplete) responses in the vast majority of cases. His goal is to understand why responses to this treatment are almost always incomplete, and to identify new targets for therapies to be used in combination with osimertinib. Ultimately, the goal of this research is to identify novel combination therapy strategies that can improve the depth and duration of response to targeted therapies, allowing patients to live longer. Dr. Blakely works under the mentorship of Trever Bivona, MD, PhD, at University of California, San Francisco. He will be co-funded through a partnership with the Doris Duke Charitable Foundation through its 2018 Clinical Scientist Development Awards.
Brian C. Capell, MD, PhD
Squamous cell carcinoma (SCC) can occur on a number of epithelial surface tissues ranging from the skin and lung to the esophagus and oropharynx, and collectively, are the most common form of cancer in the world. Recent sequencing studies have found that mutations in epigenetic regulators that control gene expression frequently occur in all forms of SCC. Dr. Capell aims to harness the great accessibility of human skin to understand how altered epigenetics promotes cutaneous SCC. Given that epigenetic changes are inherently reversible and numerous epigenetic drugs are currently in development, he hopes that by understanding these mechanisms he will identify better therapies for these incredibly common and potentially deadly cancers. Dr. Capell works under the mentorship of Shelley L. Berger, PhD, at University of Pennsylvania, Philadelphia.
Matthew D. Hellmann, MD
The recent discovery that the immune system can be used to treat cancers has revolutionized treatment and given new hope for long-term response and survival to patients with lung cancer. Research so far has demonstrated that there are some predictors of response to immunotherapy, such as tumor mutation burden which is increased in patients most likely to benefit from immunotherapy. Dr. Hellmann will focus on gaining a deeper understanding of how responses are initiated, why they can remain so durable, and what are the features that characterize resistance when it occurs. He aims to use this information to build better immunotherapy strategies in the future for patients with lung cancer – to broaden the number of patients who can benefit, to improve the depth and durability of response, and have rational strategies for overcoming resistance if it occurs. Dr. Hellmann works under the mentorship of Charles M. Rudin, MD, PhD, and Jedd D. Wolchok, MD, PhD, at Memorial Sloan Kettering Cancer Center, New York.
Andrew M. Intlekofer, MD, PhD
New drugs that target metabolic pathways have shown promise for the treatment of cancer, but the benefits of these drugs have been restricted to rare patients whose cancers have mutations in specific metabolic enzymes. Dr. Intlekofer identified a metabolic pathway whereby subpopulations of genetically identical cancer cells produce a metabolite called L-2-hydroxyglutarate (L-2HG) that induces stem cell-like properties associated with resistance to anti-cancer therapies. He is investigating the mechanisms by which L-2HG regulates the identity and function of cancer stem cells in order to determine whether targeting the L-2HG pathway represents a broadly applicable strategy for treating cancer. Dr. Intlekofer works under the mentorship of Ross L. Levine, MD, at Memorial Sloan Kettering Cancer Center, New York.
Christopher A. Klebanoff, MD
A form of cancer immunotherapy termed adoptive T cell transfer (ACT) can induce long-lasting remissions in patients with advanced blood cancers. In this approach, T white blood cells specific for proteins found on the surface of cancer cells (antigens) are activated and expanded outside the immunosuppressive environment of a cancer patient’s body before re-infusion as a therapy. Thus far, this promising form of cancer immunotherapy has failed to work in most patients with cancers arising from solid organs, the leading cause of cancer-related deaths in adults. Two critical gaps in knowledge limit the ability of ACT to be successfully applied to solid cancers: 1) understanding which antigens on the surface of cancer cells can be targeted by T cells that do not have the potential to cross-react and injure normal tissues, and 2) insight into what factor(s) limit the ability of transferred T cells to expand and persist following re-infusion into a patient. Dr. Klebanoff seeks to use a genetic engineering approach to simultaneously address both these issues. Success of these efforts would be a decisive step forward toward extending the ability of ACT to deliver potentially curative responses in patients with common cancers, including those arising from the breast, uterus, cervix and colon. Dr. Klebanoff works under the mentorship of Michel Sadelain, MD, PhD, and Larry Norton, MD, at Memorial Sloan Kettering Cancer Center, New York.
Catherine C. Smith, MD
Acute myeloid leukemia (AML) is one of the deadliest blood cancers. Mutations in the FLT3 gene are the most common of all mutations in AML and are associated with poor outcomes in both adult and pediatric patients. Despite the importance of FLT3 mutations in AML, we still do not understand the way in which FLT3 is regulated and the functional impact of novel FLT3 mutations identified in recent large AML sequencing studies. Drugs targeting FLT3 have been successful in achieving remissions in AML patients but are limited by the rapid development of drug resistance, particularly due to reactivation of abnormal cancer signaling through the oncogene RAS. Dr. Smith proposes studies to better understand how mutations found in AML patients cause dysregulation of FLT3 function and how activation of RAS signaling contributes to drug resistance and AML development. Her goal is to cultivate novel treatment strategies to target FLT3 in patients that will optimize response rates and prevent disease relapse. Dr. Smith works under the mentorship of Neil P. Shah, MD, PhD, at University of California, San Francisco.
2018 Clinical Investigator Continuation Grants
Priscilla K. Brastianos, MD
Massachusetts General Hospital, Boston
"Investigation of novel targeted therapeutic approaches for brain metastases” with Keith T. Flaherty, MD, and Tracy Batchelor, MD
Aude G. Chapuis, MD
Fred Hutchinson Cancer Research Center, Seattle
“Multifaceted transgenic TCR approach to high-risk AML” with Philip D. Greenberg, MD
Eliezer M. Van Allen, MD
Dana-Farber Cancer Institute, Boston
“Dissecting response to conventional and emerging DNA damage and repair therapies” with Geoffrey I. Shapiro, MD, PhD
About the 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. Twelve 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, the Foundation has invested nearly $355 million and funded nearly 3,700 young scientists. This year it will commit over $17 million in new awards to brilliant young investigators.
100% of all donations to the Foundation are used to support scientific research. Its administrative and fundraising costs are paid from its Damon Runyon Broadway Tickets Service and endowment.
