Damon Runyon Foundation selects new recipients of Physician-Scientist Training Award

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New York, NY (May 23, 2016) – Physician-scientists are crucial to moving scientific discoveries from the lab to patients, but their numbers have been dwindling just when they are needed most, particularly in cancer research, as the number of cancer cases is projected to increase by 45 percent in the next fifteen years and elevate cancer to the leading cause of death in America.

"Physician-scientists have the unique capacity to blend their insights from treating patients and working in the laboratory in a way that enables and accelerates medical advances," said Yung S. Lie, PhD, Deputy Director and Chief Scientific Officer of the Damon Runyon Cancer Research Foundation. "If the present shortage of physician-scientists continues, we risk a situation in which some major laboratory research discoveries may not reach patients at all, and that would represent a true crisis in cancer research."

To help increase the number of physician-scientists, the Damon Runyon Cancer Research Foundation (Damon Runyon) created the Damon Runyon Physician-Scientist Training Award, which provides physicians who have earned an MD degree and completed clinical specialty fellowship training the opportunity to gain the research skills and experience they need to become leaders in translational and clinical research. The program was launched in 2015.

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. It will also retire up to $100,000 of any medical school debt still owed by an award recipient. (The average medical school debt is now more than $150,000.)

Damon Runyon announced that five scientists with novel approaches to fighting cancer have been named the 2016 recipients of the Damon Runyon Physician-Scientist Training Award. The awardees were selected through a highly competitive and rigorous process by a scientific committee comprised of leading cancer researchers who are themselves physician-scientists. Only those scientists showing exceptional promise and a passion for finding new cures for cancer were selected to receive the award.

"Too often, medical students and recent graduates discover their passion for research when it is too late to join an MD-PhD program or otherwise acquire the experience they need to pursue a research career," said Lorraine W. Egan, President and CEO of Damon Runyon. "Physicians are essential to cancer research but often lack the opportunity and grant support needed to become researchers. We felt it was important to create that opportunity and hope that other organizations will use this award as a model."

The Physician-Scientist Training Award was established thanks to the generosity of Damon Runyon Board members Leon Cooperman and Michael Gordon.

2016 Damon Runyon Physician-Scientist Training Award Recipients:

Giada Bianchi, MD [Damon Runyon-Celgene Physician-Scientist], with Mentor Kenneth C. Anderson, MD, at Dana-Farber Cancer Institute, Boston, Massachusetts
Multiple myeloma (MM) is an incurable cancer of blood cells. It evolves from monoclonal gammopathy of undetermined significance (MGUS), a pre-malignant condition affecting 3-5% of individuals older than 50 years. MGUS patients progress to MM at a rate of 1% per year and the mechanisms underlying such transformation are unknown. No genetic driver mutations have been identified in MM to date, thus limiting our therapeutic options. Signaling through the transmembrane receptor Roundabout1 (ROBO1) is important in solid tumors, particularly gastrointestinal cancer. In MM, ROBO1 expression level was found to correlate with adverse survival in newly diagnosed patients, and ROBO1 mutations have been recently identified in patient-derived MM cells. Dr. Bianchi aims to investigate whether ROBO1 is sufficient to promote disease pathogenesis and to identify the downstream signaling molecules responsible for its function. She anticipates that her results will provide new insights into disease biology and the basis for development of biomarkers and novel therapies against MM and/or precursor conditions, allowing for rapid bench-to-bedside translation.

Kristopher R. Bosse, MD, with Mentor John M. Maris, MD, at Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
Neuroblastoma is a cancer of the nervous system that occurs in young children and is often lethal. An improved understanding of neuroblastoma tumorigenesis is urgently needed to catalyze development of innovative and effective therapies. Recent immunotherapy advances have provided optimism for the use of this treatment type in children with neuroblastoma. However, there is a desperate need for new molecules that can be safely and specifically targeted with immune-based therapeutic approaches. Recent work showed that a protein called glypican-2 (GPC2) is abundant on neuroblastoma cells, but not found on normal cells, and that GPC2 helps neuroblastomas grow aggressively. Thus, GPC2 may be an ideal cell surface molecule to target with immune-based therapies. Dr. Bosse seeks to validate GPC2 as a candidate for engineered targeted immune cells in high-risk neuroblastoma. This research will also define how GPC2 promotes cancer growth, thus providing additional critical knowledge for the therapeutic exploitation of an important tumor-sustaining pathway. Finally, this work will help establish a robust pipeline for the identification of novel tumor-specific molecules for immunotherapeutic targeting in pediatric cancer. This blueprint will allow for the rapid translation of prioritized molecules to a clinically available targeted immunotherapeutic, with an aim to make meaningful differences in the clinical care of children with high-risk pediatric malignancies.

Julia C. Carnevale, MD, with Mentor Alan Ashworth, PhD, at University of California, San Francisco, California
Pancreatic cancer may soon become the second leading cause of cancer deaths in the nation. While many cancers have mutations that can be targeted with specific drugs, historically no such targets had been recognized in pancreatic cancer. This changed recently with the discovery that approximately one of every four pancreatic cancers has a defect in the machinery that repairs DNA damage. For example, some have been found to have mutations in the BRCA genes as well as other similar genes involved in repairing double-strand breaks in DNA. Because BRCA-mutant cancers have impaired DNA damage repair, they rely on backup DNA repair systems to survive. Other tumors with BRCA mutations are particularly vulnerable to certain drugs: having such a mutation is an Achilles' heel for the tumor. If the relevant backup systems in these cells can be identified, we can potentially use these dependencies against the tumors. One example of a backup system, the PARP DNA repair system, is currently being targeted in clinical trials in BRCA-mutant pancreatic cancer. Dr. Carnevale aims to uncover multiple vulnerabilities in these cancers that can be targeted with higher efficacy than PARP inhibitors. There may also be candidates for PARP inhibitor combination therapies to more potently eradicate these tumors and/or avoid the development of resistance.

Michael W. Drazer, MD, with Mentor Lucy Godley, MD, at The University of Chicago, Chicago, Illinois
Leukemia is, for some patients, an inherited disease that may affect multiple individuals within a single family. Similar to other diseases such as inherited breast cancer, we now understand that specific genes may increase an individual's risk for developing leukemia over the course of his or her lifetime. While an increasing number of genes involved in inherited leukemia have been identified, the underlying molecular mechanisms that contribute to the development of leukemia and other blood cancers are less well understood. Some individuals with inherited blood cancers develop abnormal blood conditions years before actually developing overt leukemia. Dr. Drazer aims to better understand the molecular mechanisms that cause these abnormal blood conditions to transition into leukemia. The goal of this work is to apply these findings to inform future therapies for patients with blood cancers.

David M. Kurtz, MD, with Mentor Ash Alizadeh, MD, PhD, at Stanford University, Stanford, California
Despite improved outcomes for patients with non-Hodgkin lymphoma over the last two decades, a significant number of patients – about 40% in the most common type of lymphoma – will ultimately die from their disease. One of the major reasons for this is a lack of response to chemotherapy. Predicting how an individual patient will respond to treatment remains a major challenge. Current methods rely on risk factors measured prior to therapy; however, cancer is a dynamic process with dramatic changes throughout therapy. Dr. Kurtz aims to develop methods that use emerging blood-based biomarkers to measure changes in cancer patients over time. This technology allows the creation of tools for precise prediction of outcomes to therapy from a simple blood test. Ultimately, this technology could help doctors make personalized treatment decisions and tailor therapy to individual patients.

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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 over $300 million and funded over 3,500 young scientists. This year it will commit over $16 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.

CONTACT
Yung S. Lie, PhD
Deputy Director and Chief Scientific Officer
Damon Runyon Cancer Research Foundation
[email protected]
212.455.0521

Media Contact

Yung S. Lie, Ph.D.
[email protected]
212-455-0521

https://www.damonrunyon.org/

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