Damon Runyon Cancer Research Foundation Awards Fellowships to 15 Young Scientists

New York, NY (July 23, 2019) – The Damon Runyon Foundation for Cancer Research, a non-profit organization dedicated to supporting innovative early career researchers, has named 15 new members Damon Runyon. The recipients of this prestigious four-year award are outstanding postdoctoral researchers who conduct fundamental and translational research on cancer in the labs of leading researchers across the country. The scholarship encourages the country's most promising young scientists to pursue careers in cancer research by providing them with independent funding ($ 231,000 in total) to work on high-risk creative projects.

Damon Runyon Fellows of Spring 2019:

Liudmila Andreeva, Ph.D., with her godfather, Hao Wu, PhD, at the Boston Children's Hospital, studies the role of a molecule called NLRP3 in the badembly of complex inflammatomes, multiprotein that form in response to a cellular infection or stress. NLRP3 acts as a sensor inside the cell that detects danger signals and activates the inflammasome complex in order to trigger inflammation and cell death. Dr. Andreeva seeks to discover the step-by-step mechanism of NLRP3 activation and regulation to understand how to prevent "false alarms" that cause disease. This research could contribute to the development of drugs that specifically deactivate the NLRP3 inflammasome and treat various inflammatory disorders, from osteoarthritis to Alzheimer's disease and cancer.

Caroline Bartman, PhD [Mark Foundation for Cancer Research Fellow], with sponsor Joshua Rabinowitz, MD, PhD, at Princeton University, Princeton, is studying the unique nutritional needs of cancer cells versus healthy tissue. Dr. Bartman will use labeled nutrient mbad spectrometry measurements and computer modeling to quantify the metabolic fluctuations of pancreatic cancer cells and healthy organs in mice. Since alteration of metabolism is a hallmark of cancer cells, systematic mapping of these metabolic changes can guide the development of drugs to rationally target cancer while sparing healthy cells.

Kunitoshi Chiba, Ph.D., with his sponsor, Stephen Elledge, Ph.D., at Brigham and Women's Hospital, Boston, is studying how cancer cells escape the immune system of a patient . Although blocking treatments at checkpoints have expanded the options available to cancer patients, only a fraction of those treated actually benefit from the emergence of immune resistance. Dr. Chiba will use molecular and genetic approaches to dissect the ways in which cancer-badociated mutations modify the tumor environment to avoid immune surveillance. The goal of this research is to improve the effectiveness of cancer immunotherapy so that many other patients benefit.

Hokyung Kay Chung, PhD, with her sponsor Susan Kaech, PhD, at the Salk Institute in La Jolla, is developing a new technical approach to creating smart, tenacious T cells with sustainable antitumor activity. Its goal is to create improved T cells that will infiltrate tumors, kill cancer cells and persist in the long term to prevent recurrence. Dr. Chung will use cutting-edge multidisciplinary approaches, including bioinformatics, protein engineering and genetic engineering, and tumor immunology, to design a synthetic T-cell differentiation pathway. This T cell reprogramming platform has the potential to turn cellular immunotherapies (such as CAR T) into "smarter" cells that target cancer with persistence and increased potency.

Christina L. Hueschen, PhD, with her sponsor Alex Dunn, Ph.D., of Stanford University, studies the motility of Apicomplexan parasites, which cause malaria, food-borne illness (toxoplasmosis), and infections in immunocompromised patients. These parasites move in the human body using a mechanism called "sliding" to migrate to the host cells and through the surrounding extracellular matrix. Dr. Hueschen's goal is to understand how the molecules inside the parasite are organized, coordinated, and regulated to produce forces that direct movement. This research could help develop therapies to prevent opportunistic infections.

Grace E. Kenney, PhD [Merck Fellow]with her mentor Emily P. Balskus, Ph.D., at Harvard University in Cambridge, is studying how microbes make natural products, a major source of new drug candidates for chemotherapy. Dr. Kenney identifies the chemical reactions used by microbes in nature to synthesize compounds that may act as chemotherapeutic drugs. Once the biological synthesis of these compounds is understood, this information can be used to identify, study and ultimately rearrange new families of natural products whose potential can be evaluated as a new drug.

Thomas R. LaBar, Ph.D., with his sponsor, Andrew W. Murray, Ph.D., of Harvard University, Cambridge, uses budding yeast and computer modeling to study the fundamental processes that determine how cancer cell populations evolve according to their environment. Dr. LaBar seeks to understand how the number of cells in a tumor can result in the evolution of cancer cells based on their contribution to new mutations. His research could potentially highlight specific mutations occurring in certain cancers, alterations allowing abnormal growth of cancer cell populations, as well as strategies for predicting the evolution of cancer cell populations and the prognosis of patients.

Jasper E. Neggers, PhD, along with his sponsors, Andrew J. Aguirre, MD and Ph.D., and Todd R. Golub, MD, of the Dana-Farber Cancer Institute, in Boston, are focusing on the validation of a new target drug for pancreatic cancer. With the help of a large-scale genetic screening, Dr. Neggers discovered that a subset of cancers, including more than 50% of pancreatic cancers, selectively require proliferation and growth. of the VPS4A gene. When VPS4A is disabled, the cells stop dividing and die. He will investigate this vulnerability in patient-derived pancreatic cancer models and clinically relevant mouse models to understand how it works. His research could help confirm whether this gene should be pursued as a significant drug target.

Esteban Orellana Vinueza, Ph.D., with her godfather, Richard I. Gregory, of the Boston Children's Hospital, is investigating whether changes that alter the form, stability, and function of transfer RNAs (tRNAs) play a role. role in cancer development. The tRNA molecules participate in the process of translating messenger RNA into a protein. Dr. Orellana Vinueza is interested in the complex tRNA methyltransferase that works poorly in glioblastomas and liposarcomas. It will evaluate how alterations in the activity of this enzyme affect the overall patterns of methylation in normal and human cancer cells. Methylation is the process that controls the timing and amount of protein produced in cells. Understanding the decomposition of this process can help decipher the mechanisms behind cancer and guide the development of new treatments.

Janice M. Reimer, PhD [Merck Fellow]with his sponsor Andres Leschziner, PhD, at the University of California at San Diego, is studying the molecular mechanisms that regulate the family of SWI / SNF chromatin remodelers, mutated in more than 20% of cancers. The condensed DNA is stored in the nucleus as chromatin, which it is impossible to access for protein transcription. Chromatin remodelers are complex protein machines that alter the accessibility of DNA. Function gain mutations lead to functional complexes with abnormal activities and are potential therapeutic targets. Dr. Reimer will use cryo-electron microscopy to understand how oncogenic mutations can disrupt the normal regulation and behavior of SWI / SNF remodelers.

Jose Reyes, PhD, with his mentors Scott Lowe, PhD, and Dana Pe, PhD, at Memorial Sloan Kettering, NY, focuses on karyotype-complex acute myelogenous leukemia (CK-AML), a form aggressive LMA with prognosis and limited therapeutic options. Dr. Reyes uses mouse models and unicellular technologies to track the parallel evolution of cancer cells from the onset of the disease to its terminal stage. This approach can predict the evolution of heterogeneous cancer cell populations in order to identify targets involved in the ability of a cancer cell to adapt and reproduce after treatment.

Tyler Starr, Ph.D., with mentors Jesse D. Bloom, PhD, and Frederick Matsen, PhD, at Seattle's Fred Hutchinson Cancer Research Center, focus on the process the immune system uses to produce antibodies that specifically recognize pathogen antigens and bind to them. and cancer cells. Dr. Starr combines computer badyzes of antibody sequences with experimental methods to test the effects of possible mutations on antibody function. This iterative process, similar to what the body does naturally, will help identify the best antibodies for an infection. The results of this research could lead to HIV treatments that can reduce the incidence of AIDS-related cancers and improve the development of antibody-based anti-cancer immunotherapies.

Sophia Tintori, PhD, with her sponsor Matt Rockman, Ph.D., at New York University, is studying nematode worms from Chernobyl, Ukraine, to study the biological effects of a continuous exposure to radiation. It is known that ionizing radiation can cause cancer, but little is known about levels that increase health risks or how animals adapt to environments that are highly exposed to radiation. Dr. Tintori compares Chernobyl worms, the region where the highest background levels are known on the planet, with similar animals that have not been exposed. This research could shed light on specific challenges posed by radiation and possible biomolecular defenses.

Lexy von Diezmann, PhD [Mark Foundation for Cancer Research Fellow], with its sponsors, Ofer Rog, PhD, and Erik Jorgensen, PhD, from the University of Utah in Salt Lake City, are studying how cells control the pathways used to repair DNA. DNA repair errors contribute to the development of many cancers, such as bad, ovarian and pancreatic cancers. Dr. von Diezmann will explore the basic principles governing DNA damage response by examining the functioning of a specific subtype of homologous repair enzymes in the reproductive cells of the body. model organism C. elegans. His project will provide mechanistic information on how alterations in the organization of proteins in liquid form at the DNA damage sites regulate repair, supporting the development of novel chemotherapies modulating response. to the damage of the DNA.

John C. Zinder, PhD [Lorraine W. Egan Fellow], with its sponsor Titia de Lange, PhD, at Rockefeller University in New York, is studying the telomeres that cover the ends of chromosomes and their role in the development of cancer. Telomeres usually shorten each time a cell divides until they become so short that cell division stops. Dr. Zinder focuses on Shelterin, a multiprotein complex that binds to telomeres to protect them from damaged DNA. Mutations in Shelin's components are found in both cancer and premature aging diseases. By purifying this complex and visualizing it in atomic detail, it seeks to better understand how telomeres are protected and how their length is controlled in normal cells and cancer.

###

To accelerate breakthroughs, the Damon Runyon Cancer Research Foundation provides the best young scientists of the day with the means to pursue innovative research. The Foundation has gained worldwide recognition in cancer research by identifying outstanding researchers and physician-researchers. Twelve scientists supported by the Foundation have received the Nobel Prize and others are leading cancer centers and renowned research programs. Each of its reward programs is extremely competitive, with less than 10% of applications funded. Since its founding in 1946, the Foundation has invested nearly $ 375 million and funded more than 3,750 young scientists. This year, he will devote over $ 19 million in new awards to bright young researchers.

100% of all donations to the Foundation are used to support scientific research. Its administrative and fundraising costs are covered by its ticket service and Damon Runyon Broadway staffing.

For more information, visit damonrunyon.org.