Damon Runyon Cancer Research Foundation announces five new Physician-Scientist Training Awards

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New York, NY (May 16, 2018) – 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 2018 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.

2018 Damon Runyon Physician-Scientist Training Award Recipients:

Nicholas C. DeVito, MD, with mentor Brent A. Hanks, MD, PhD, at Duke University Medical Center, Durham

Immunotherapy has resulted in positive outcomes for patients with melanoma, lung cancer, and other malignancies; however, most patients do not have meaningful responses to this treatment strategy. Tumors that fail to respond to immunotherapy have effectively hidden themselves from detection by the host immune system. Understanding how cancers create an immune-excluded environment promises to lead to the development of more highly effective immunotherapies. Dendritic cells (DCs) play a central role in orchestrating the immune response to cancers by enabling T cells to "see" and destroy cancerous cells. Previous work has shown that melanomas secrete a protein called Wnt5a that potently suppresses DC function and ultimately contributes to the development of immunotherapy resistance. Dr. DeVito will examine certain tumor signaling pathways that have been implicated in driving Wnt5a production and facilitating cancer spreading by suppressing DC function within nearby draining lymph node tissues, which are critical for generating immune responses capable of destroying developing cancers. These studies will further investigate the ability of Wnt5a inhibition to sensitize cancers that are typically resistant to immunotherapy strategies. In addition, he is conducting a clinical trial to determine if the activation of these pathways correlates with immunotherapy failure in melanoma patients. He anticipates that this research will lead to the discovery of novel, more effective immunotherapy strategies, and may identify biomarkers that will improve selection of tailored immunotherapies for specific cancer patients.

John R. Ferrarone, MD, with mentor Harold E. Varmus, MD, at Joan & Sanford I. Weill Medical College of Cornell University, New York

Adenocarcinoma is the most common type of lung cancer. Approximately 10% of patients with lung adenocarcinoma will have a tumor that simultaneously carries mutations in genes called KRAS and LKB1. Patients that have a lung cancer harboring both these mutations develop resistance to chemotherapy more rapidly, are more likely to develop brain metastases, and have a worse overall prognosis. Currently, there are no targeted therapies available for patients with this type of lung cancer. Mutations in genes like KRAS and LKB1 lead to a rewiring of normal cellular processes that results in cancer. Importantly, this rewiring also makes tumors more dependent on certain cellular functions, which can be targeted to disrupt tumor growth. In order to identify these vulnerabilities in lung cancers with mutations in both KRAS and LKB1, Dr. Ferrarone is utilizing the CRISPR/Cas9 DNA editing technology on a genome-wide scale. Using CRISPR, he will introduce gene "knockouts" in lung cancer cells carrying both KRAS and LKB1 mutations to see which genetic disruptions are most lethal to the cancer. Identification of the most significant tumor vulnerabilities may lead to the development of new targeted therapies to treat this type of lung cancer.

Lillian M. Guenther, MD, with mentor Kimberly Stegmaier, MD, at Dana-Farber Cancer Institute, Boston

Ewing sarcoma is an aggressive bone tumor that occurs in children and young adults. Cure rates, particularly when disease has spread, are low with currently available treatments. Dr. Guenther aims to identify critical genes on which Ewing sarcoma cells are dependent for survival, with the goal of discovering weaknesses in these cancer cells that may be exploited to stop cancer growth. CITED2 is of particular interest as a Ewing sarcoma-specific dependency gene based on a genome-wide screen in hundreds of cancer cell lines. In some other cancers, CITED2 is described as important for helping cells repair damage and survive stress, such as when they are exposed to chemotherapy. She has found that CITED2 is present in higher levels in Ewing sarcoma cells than in other types of cancer, and when its function is turned off in Ewing sarcoma cells, they grow more slowly. She aims to first confirm that CITED2 is critical for Ewing sarcoma survival. Additionally, she wants to understand CITED2's function in Ewing sarcoma cells, including any role for CITED2 in the repair of damage to DNA after chemotherapy or stress. The goal of this work is to develop new directed cancer therapies for patients with this devastating disease. She hopes that these studies will have an additional impact on the treatment of other cancers where CITED2 has been shown to play a role, including acute myeloid leukemia.

David Liu, MD, with mentors Eliezer Van Allen, MD, and Keith Flaherty, MD, at Dana-Farber Cancer Institute, Boston

The treatment of metastatic melanoma has been transformed over the past decade with the development of (1) targeted therapies that target a very common gene mutation (BRAF mutations in 50-60% of tumors) in melanoma and (2) two different types of immune therapies that induce the immune system to attack the cancer (CTLA-4 and PD-1 inhibition). However, not all patients respond to either targeted or immune therapy, and there is evidence suggesting that patients who quickly develop resistance on the initial therapy (whether targeted or immune) have worse outcomes. Thus, being able to predict which patients will respond to targeted and immune therapies is critically important to personalize therapy and improve patient outcomes. Dr. Liu proposes to address this issue by analyzing large cohorts of melanoma patients treated with targeted and immunotherapy with deep genetic sequencing and molecular characterization of their tumors, developing algorithms to identify molecular features that predict differential response or resistance to therapy. Importantly, he will apply approaches from machine learning to develop and validate a predictive model integrating genetic and clinical tumor characteristics to predict response to therapy in individual patients. His findings will shed light on the biological mechanisms that underpin response and resistance to therapy, identifying novel therapeutic targets and potential synergistic therapy combinations. Taken together, the success of this proposal will have important biological and clinical implications, informing future drug and combination therapy development as well as impacting clinical care.

Harshabad Singh, MBBS, with mentor Ramesh A. Shivdasani, MD, PhD, at Dana-Farber Cancer Institute, Boston

Cancers involving the lower esophagus (esophageal adenocarcinomas) have dramatically increased in number over the last several decades. The reason for rise in the incidence of this cancer is not completely understood. However, long before these esophageal cancers arise, the normal esophageal multilayered squamous lining (or epithelium) is replaced by a single layered columnar epithelium which has features similar to the lining of the intestine and is known as Barrett's esophagus. Dr. Singh proposes to investigate the origins and factors governing the genesis of Barrett's esophagus and understand its specific vulnerability to progress to cancer. This work will yield insights into disease mechanisms and reveal novel preventive strategies for esophageal adenocarcinomas.

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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 $340 million and funded over 3,650 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
[email protected]
212.455.0521

Media Contact

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

https://www.damonrunyon.org/

https://www.damonrunyon.org/latest-news/entries/4136

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