Public Release: 

Damon Runyon Cancer Research Foundation announces new physician-scientist training awards

Grants totaling over $1.8 million give four physician-scientists resources to pursue cancer research

Damon Runyon Cancer Research Foundation

New York, NY (June 30, 2017) - 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 four scientists with novel approaches to fighting cancer have been named the 2017 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.

2017 Damon Runyon Physician-Scientist Training Award Recipients:

Jennifer Caswell-Jin, MD, with Mentors Christina N. Curtis, PhD, and Allison W. Kurian, MD, MSc, at Stanford University, Stanford, California

The development of HER2-targeted therapies over the past two decades has had tremendous positive impact on the lives of HER2-positive breast cancer patients. However, tumor resistance to these therapies remains a significant challenge: a sizable portion of patients with early-stage HER2-positive breast cancer develop recurrence, and the vast majority of patients with metastatic HER2-positive breast cancer eventually progress through treatment. Jennifer proposes to construct a model of HER2-positive breast cancer evolution that will reveal how the cancer changes over time when treated with HER2-targeted therapy. She will examine each tumor at multiple time points in the course of its treatment: at diagnosis, during initial treatment (with HER2-targeted therapy and/or chemotherapy), after completion of initial treatment, and at one or more sites of metastasis. To create this model, she will analyze multiple regions within each tumor and also test circulating DNA that the tumor sometimes sheds into the blood. She will also examine the specific changes present in the cells that develop resistance to HER2-targeted therapy. A deeper understanding of how tumors evolve under the pressure of treatment will open new avenues to optimizing treatment delivery. Markers of treatment resistance may further allow us to personalize therapy choices, delivering extra therapy to those patients who need it and sparing others unnecessary toxicity.

Christopher J. Gibson, MD, with Mentor Benjamin L. Ebert, MD, DPhil, at Dana-Farber Cancer Institute, Boston, Massachusetts

Christopher's research centers on the earliest steps whereby normal cells transform into abnormal cells with the potential to become cancer. He will focus on better understanding the first steps of the process by which normal blood cells become lymphomas, cancers that are generally thought to arise from blood cells that have already committed to becoming lymphocytes, an important component of the immune system. He hypothesizes, however, that some lymphomas actually arise from earlier hematopoietic stem cells (HSCs). He will interrogate this hypothesis by studying a cohort of lymphoma patients who also have detectable genetic mutations in HSCs that are known to be associated with blood cancers - a condition known as clonal hematopoiesis of indeterminate potential, or CHIP - to determine whether the mutations in the HSCs were the earliest events in the development of the patients' lymphomas. Having a better understanding of lymphomas' cellular basis will hopefully allow new insights into their clinical behavior and therapeutic vulnerabilities.

Melody Smith, MD, with Mentor Marcel R.M. Van Den Brink, MD, PhD, at Memorial Sloan Kettering Cancer Center, New York, New York

Bone marrow transplant (BMT) is a treatment approach where cells from a healthy donor are given to a patient with blood cancer who has not responded to other treatments. Unfortunately, there are risks to this procedure such as graft-versus-host disease (GVHD), which occurs if the cells from the donor attack the "foreign" patient tissue; this can cause serious organ damage and is life-threatening. Melody is investigating an approach to decrease GVHD while also maintaining the benefits of BMT, specifically graft versus tumor (GVT). She utilizes T immune cells from the donor and enables them to express a B cell marker, CD19; these cells can induce complete remissions in patients with CD19-positive leukemia and lymphoma. Administration of these cells following BMT mediates persistent GVT and decreased GVHD. Given that donor T cells are the culprits that cause GVHD, the finding of decreased GVHD in her model was paradoxical. She will now translate these pre-clinical findings to a clinical trial in order to benefit patients.

Sakiko Suzuki, MD, with Mentor Glen Raffel, MD, PhD, at University of Massachusetts Medical School, Worcester, Massachusetts

Despite many recent advances, today's treatment of leukemia still relies on medications that have very toxic side effects and can cause death. Therefore, it is crucial to search for new types of therapies that directly target leukemia without harming the normal cells of the body. A gene called MPL encodes a protein found to be important for the growth and survival of a significant proportion of Acute Myeloid Leukemias (AMLs) and other blood diseases including Essential Thrombocythemia (ET), a malignancy affecting the platelet-producing cells of the bone marrow. Sakiko has been focusing on the function of a truncated variant of MPL produced by splicing out a section of the MPL RNA message used to make the protein. This variant, MPL-TR, opposes the function of MPL in cells; she believes that increasing MPL-TR in leukemia cells will suppress their growth. Anti-sense oligonucleotides (AONs) are very short segments of RNA or DNA that can be constructed to bind specifically to RNA messages in the cell, so no other genes are affected. By targeting AONs to the regions in MPL RNA important for splicing, she proposes that leukemia cells will make more MPL-TR, thus inhibiting their growth and survival. She will test a series of AONs targeting human MPL splicing, designed to enhance levels of MPL-TR. These experiments will provide the foundation for establishing a clinical trial with the novel, targeted AON. The principles founded by this project would also be broadly applicable for targeting splicing in other genes essential for multiple forms of leukemia and lymphoma.

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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 $327 million and funded over 3,600 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.

CONTACT

Yung S. Lie, PhD
Deputy Director and Chief Scientific Officer
Damon Runyon Cancer Research Foundation
yung.lie@damonrunyon.org
212.455.0521

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