New York, NY (January 13, 2014) - The Damon Runyon Cancer Research Foundation, a non-profit organization focused on supporting innovative early career researchers, named 15 new Damon Runyon Fellows at its fall Fellowship Award Committee review. The recipients of this prestigious, three-year award are outstanding postdoctoral scientists conducting basic and translational cancer research in the laboratories of leading senior investigators across the country. The Fellowship encourages the nation's most promising young scientists to pursue careers in cancer research by providing them with independent funding ($156,000 each) to work on innovative projects.
The Committee also named five new recipients of the Damon Runyon-Dale F. Frey Award for Breakthrough Scientists. This award provides additional funding to scientists completing a prestigious Damon Runyon Fellowship Award who have greatly exceeded the Foundation's highest expectations and are most likely to make paradigm-shifting breakthroughs that transform the way we prevent, diagnose and treat cancer. Each awardee will receive $100,000 to be used toward their research.
Recipients of the Damon Runyon-Dale F. Frey Award for Breakthrough Scientists
David K. Breslow, PhD (Damon Runyon Fellow '11-'14), Stanford University, Stanford, California
Dr. Breslow is studying the primary cilium, a cellular structure that enables cells to sense and respond to specific external cues. While disruptions to primary cilia are known to promote tumor formation and cause developmental defects, how cilia orchestrate these processes remains poorly understood. He is using a combination of genomic, biochemical and cell biology approaches to investigate how specific signaling occurs in the cilia.
Costas A. Lyssiotis, PhD (Damon Runyon Fellow '10-'13), Weill Medical College of Cornell University, New York, New York
Dr. Lyssiotis focuses on how oncogenes affect cellular metabolism in pancreatic cancer. In particular, he is interested in understanding how mutations in the oncogene Kras alter cellular metabolism in pancreatic ductal adenocarcinoma to facilitate cell growth. He will determine if distinct components of Kras-mediated signaling can be targeted for therapeutic gain. Ultimately, this work aims to translate our understanding of pancreatic cancer cell metabolism into therapies for this devastating disease.
Raymond E. Moellering, PhD (Damon Runyon Fellow '11-'13), The Scripps Research Institute, La Jolla, California
Dr. Moellering is interested in understanding the link between alteration of metabolic pathways and corresponding protein modifications that occur in cancer cells. In addition, he is investigating whether cancer cells use small molecule signaling, known as quorum-sensing, to communicate and thus control tumor initiation, growth and metastasis. His goal is to provide insights into many aspects of tumor progression and to potentially identify new opportunities for therapeutic intervention.
Nathan D. Thomsen, PhD (Damon Runyon Fellow '11-'13), University of California, San Francisco, California
Dr. Thomsen is studying the molecular interactions that are required for specific signaling pathways in the cell. In cancer cells, these signaling pathways are often disrupted or misregulated. Using sophisticated new techniques he has developed, he will "capture and trap" proteins in real time, as they are signaling--similar to a video freeze-frame. He plans to then engineer antibodies that will specifically target and inhibit these pathways, which can be used to learn more about the molecular mechanisms underlying signaling and may eventually be developed into therapeutics for cancer and other diseases.
Cole Trapnell, PhD (Damon Runyon Fellow '11-'14), Harvard University, Cambridge, Massachusetts
Dr. Trapnell studies the vast complexity underlying cell identity and fate. He will use genomic and computational biology approaches to analyze individual tumor cells and understand how a variety of genetic mutations give rise to aggressive tumor cell behavior. He aims to map the key pathways controlling cell fate, ultimately leading to information that may aid the development of more effective targeted therapies.
November 2013 Damon Runyon Fellows
Brittany Adamson, PhD [HHMI Fellow] with her sponsor Jonathan S. Weissman, PhD, at University of California, San Francisco, California, is using large-scale genetic approaches to map the regulatory networks responsible for maintaining molecular equilibria inside human cells. An important question in cancer research is how cancer cells adapt to abnormal growth environments and proliferate under stress. Systematic characterization of the processes that maintain these equilibria will be critical for better understanding cancer formation and growth.
Ryan D. Baldridge, PhD, with his sponsor Thomas A. Rapaport, PhD, at Harvard Medical School, Boston, Massachusetts, focuses on a cellular process called endoplasmic reticulum associated degradation (ERAD), a system involved in recognition, transport and degradation of regulated and misfolded proteins. ERAD plays a role in cancer processes, in some instances by regulating the levels of proteins involved in tumor growth and metastasis. His goal is to understand the mechanism and specificity of the ERAD system.
Liron Bar-Peled, PhD, with his sponsor Benjamin F. Cravatt, PhD, at The Scripps Research Institute, La Jolla, California, is exploring how the protease Caspase-8 regulates T cell activation, which represents a critical step in the adaptive immune response to cancer. While Caspase-8 is known to be essential for T cell activation, the molecular mechanisms underlying its role in this process remain poorly understood. His work will focus on identifying and characterizing the proteins cleaved by Caspase-8, which may provide additional therapeutic avenues to activate T cells to target malignant cells in cancer patients.
Ankur Jain, PhD, with his sponsor Ronald D. Vale, PhD, at University of California, San Francisco, California, focuses on understanding how the level of mRNA species in the cell is regulated. Disruption of these regulatory processes can lead to cancer initiation and progression. These processes are carried out at discrete cytoplasmic non-membrane bound organelles called processing bodies (P-bodies). He aims to develop a molecular understanding of P-body architecture, assembly rules, and their role in gene regulation.
Matthew P. Miller, PhD [HHMI Fellow] with his sponsor Susan Biggins, PhD, at Fred Hutchinson Cancer Research Center, Seattle, Washington, is investigating how cells ensure the correct partitioning of genetic material during cell division. Errors in this process occur in nearly all tumor cells and are the leading cause of miscarriages and congenital birth defects in humans. He is using novel techniques to isolate and examine the physical binding properties of the molecules that mediate this process. The goal of his work is to determine the molecular mechanisms that direct genome partitioning during cell division and understand how this process becomes error-prone during tumorigenesis.
Antoine Molaro, PhD, with his sponsor Harmit S. Malik, PhD, at Fred Hutchinson Cancer Research Center, Seattle, Washington, studies how an ancient "evolutionary arms race" between Krab-Zinc-Finger genes (KZNFs) and DNA sequence elements called retrotransposons has shaped transcriptional networks of stem cells and pluripotency. Because many cancers dedifferentiate to a stem cell-like state, refined knowledge about how KZNFs act may prove essential for the development of new cancer drugs.
Gabriela C. Monsalve, PhD [Robert Black Fellow] with her sponsor Keith R. Yamamoto, PhD, at University of California, San Francisco, California, is studying glucocorticoids (GCs), naturally occurring steroid hormones that can be used therapeutically to kill certain tumor cells. Aggressive blood cancers like lymphomas and leukemias are commonly treated with chemotherapy drugs, including GCs. Unfortunately, some patients do not respond to GCs. To improve the treatment of patients with GC-resistant cancers, and to better understand how GCs destroy cancerous cells, she aims to understand how and where they are absorbed in the body.
Shruti Naik, PhD, with her sponsor Elaine V. Fuchs, PhD, at The Rockefeller University, New York, New York, is studying the interactions between immune cells and adult skin tissue stem cells in an effort to understand the how this crosstalk drives epithelial disorders, including chronic inflammation and cancer. Because adult tissue stem cells are long-lived cells that continually replenish tissues throughout an organism's lifetime, they represent ideal points of therapeutic intervention. Identification of inflammation-induced molecular changes in skin stem cells that drive epithelial dysfunction will facilitate the development of therapies for various epithelial inflammatory diseases and cancer.
Hanjing Peng, PhD, with her sponsor Jun O. Liu, PhD, at The Johns Hopkins University School of Medicine, Baltimore, Maryland, seeks to identify compounds that inhibit the proteasome, the protein degradation machinery in the cell that maintains the balance of cell growth and death. Inhibitors that regulate proteasome function are potential anticancer drugs. She has designed and constructed a synthetic library of compounds in search of potent proteasome inhibitors. She hopes to discover new anticancer drug candidates with lower toxicity or side effects than current drugs.
Erin F. Simonds, PhD, with his sponsor William A. Weiss, MD, PhD, at University of California, San Francisco, California, is investigating tumor-initiating cells in pediatric glioblastoma, a type of brain tumor. This rare subpopulation of cells has the unique capacity to re-establish the tumor after therapy, and is therefore a critical therapeutic target. He is using a technique called mass cytometry to determine how these cells respond to communication signals from their environment. The goal of this work is to identify drugs that specifically kill tumor-initiating cells by blocking the signaling networks that sustain their survival.
Alexey A. Soshnev, MD, PhD [HHMI Fellow] with his sponsor C. David Allis, PhD, at The Rockefeller University, New York, New York, studies how genetic information is packaged in the nucleus and how such packaging is interpreted by the cellular machinery. Changes in nuclear architecture may simultaneously affect the function of thousands of genes and are a hallmark of cancer. This research focuses on a family of small nuclear proteins termed "linker histones," which are thought to orchestrate higher-order folding of DNA in the nucleus. Understanding the molecular connection between the nuclear architecture and gene regulation will shed new light on the processes underlying oncogenic transformation.
Rohith K. Srivas, PhD, with his sponsor Michael P. Snyder, PhD, at Stanford University, Stanford, California, is studying the changes in the composition and function of bacteria inhabiting the human gut (microbiome). The microbiome plays an extensive role in modulating host metabolism and inflammation, which when disrupted can lead to diseases such as cancer. By tracking changes in the gut microbiome of patients undergoing drastic weight loss, this research will map the dynamics of host-microbiome connections, potentially highlighting strategies for modifying the microbiome to treat metabolic disorders and reduce the risk of gastric and colon cancers.
Chenxi Tian, PhD, [Sherry and Alan Leventhal Family Fellow] with her sponsor Richard O. Hynes, PhD, at Massachusetts Institute of Technology, Cambridge, Massachusetts, studies pancreatic ductal adenocarcinoma (PDAC). PDAC is characterized by an extremely stiff texture, which is caused by accumulation of excessive extracellular matrix (ECM). The compositions of ECM, known to have major effects on tumor progression, are not well understood in PDAC disease. She aims to identify global ECM changes during PDAC progression by proteomic approaches, and to investigate how these changes impact cancer progression. This research will provide novel insights into diagnosis, prognosis and treatments of this very difficult disease.
Thomas S. Vierbuchen, PhD [HHMI Fellow] with his sponsor Michael E. Greenberg, PhD, at Harvard Medical School, Boston, Massachusetts, aims to understand how neurons adapt to experience by modifying the complement of genes they express. He is using high-throughput sequencing-based approaches to identify and characterize the function of genomic regulatory elements that control neuronal activity-regulated gene transcription.
Eric M. Woerly, PhD, with his sponsor Eric N. Jacobsen, PhD, at Harvard University, Cambridge, Massachusetts, aims to develop new chemical synthetic methods for the preparation of cancer therapeutics. The introduction of fluorine into pharmaceutical targets is an important element of drug design. The controlled, selective synthesis of fluorinated compounds, however, can be a great synthetic challenge. He plans to enable access to such targets by developing a method for the asymmetric synthesis of fluorinated small molecules, potentially leading to improved cancer therapies.
Damon Runyon Cancer Research 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 $270 million and funded more than 3,400 young scientists. This year, it will commit over $12 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.
For more information visit http://www.
Yung S. Lie, PhD Chief Scientific Officer Damon Runyon Cancer Research Foundation firstname.lastname@example.org 212.455.0521