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 two new recipients of the 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 Dale F. Frey Award for Breakthrough Scientists:
Adam de la Zerda, PhD (Damon Runyon Fellow '11-'12), Stanford University, Stanford, California
Dr. de la Zerda is building tools that would allow scientists, for the first time, to look inside a tumor and directly visualize the signaling that takes place between cancer cells in a tumor. Learning about this signaling is essential to our understanding of cancer growth, spread and response to treatment. Such new understanding will ultimately translate to better diagnostic and therapeutic approaches.
Gabriel C. Lander, PhD (Damon Runyon Fellow '10-'13), The Scripps Research Institute, La Jolla, California
Dr. Lander will use high-resolution cryo-electron microscopy to characterize the structural organization of the large protein complexes that make up "molecular machines" in cells. By determining the molecular architecture of these machines, he aims to gain a more comprehensive understanding of the mechanisms that underlie important biological processes such as cell cycle regulation and cell division. His research will potentially reveal novel approaches to detect and suppress the onset of tumorigenesis in a wide variety of cancers.
November 2012 Damon Runyon Fellows:
Nicholas Arpaia, PhD [Robert Black Fellow] with his sponsor Alexander Rudensky, PhD, at Memorial Sloan-Kettering Cancer Center, New York, New York, focuses on how the immune system distinguishes between beneficial gut bacteria versus those that may be pathogenic and cause disease. Changes in the levels of these microbes are correlated with cancer-associated intestinal inflammatory disorders like Crohn's disease and ulcerative colitis. His research may aid in the development of new therapeutics aimed at treating aberrant inflammation that can lead to cancer.
Christine R. Beck, PhD [HHMI Fellow] with her sponsor James R. Lupski, MD, PhD, at Baylor College of Medicine, Houston, Texas, is investigating the mechanisms that are involved in complex genomic rearrangements, such as gene duplications and triplications. Studying the mechanisms by which copy number changes occur may elucidate fundamental processes that lead to cancer in humans.
Alba Diz Mu-oz, PhD, with her sponsors Orion D. Weiner, PhD, at University of California, San Francisco, California, and Daniel A. Fletcher, PhD, at University of California, Berkeley, California, aims to develop a precise understanding of how cells migrate and decipher the differences between cell migration in a physiological context (such as immune cells) and that of a cancer cell. She will determine how physical forces affect specific molecular components of the signaling pathway that directs motility.
Lydia Finley, PhD, with her sponsor Craig B. Thompson, MD, at Memorial Sloan-Kettering Cancer Center, New York, New York, examines how cells sense their nutritional status to regulate cell growth. Cancer cells rewire their metabolic pathways to support rapid growth, often subverting the normal checks and balances that guard against uncontrolled proliferation. Her research will provide insight into the metabolic alterations that cancer cells may adopt to support tumorigenesis.
Ari J. Firestone, PhD, with his sponsor Kevin M. Shannon, MD, at the University of California, San Francisco, California, is exploring novel strategies for inhibiting the cancer-causing activity of the N-Ras oncoprotein, which plays an important role in promoting cellular growth and survival. Ras mutations lead to uncontrolled proliferation in many types of cancer. Using mouse models of leukemia, he aims to determine whether disrupting the subcellular localization of Ras could be an effective therapeutic intervention.
Junjie U. Guo, PhD, with his sponsor David P. Bartel, PhD, at the Whitehead Institute for Biomedical Research, Cambridge, Massachusetts, is investigating how regulatory RNAs function by interacting with their target RNAs. Misregulation of these interactions has been shown to contribute to tumorigenesis. He aims to develop a high-throughput experimental strategy that can identify these interactions within each RNA and between different RNAs.
Itamar Harel, PhD, with his sponsor Anne Brunet, PhD, at the Stanford University School of Medicine, Stanford, California, is studying the basic molecular components that characterize "young" and "aged" cellular states. Aging is associated with an increased onset of cancer. Ultimately, he hopes to design strategies to directly convert "old" cells from a patient into "young" ones, eventually developing more effective cancer therapies and prevention methods.
Serkan Kir, PhD, with his sponsor Bruce M. Spiegelman, PhD, at Dana-Farber Cancer Institute, Boston, Massachusetts, is studying the signaling mechanisms that mediate cancer cachexia, a wasting disorder of adipose fat tissue and skeletal muscle that leads to profound weight loss. Up to 50% of cancer patients suffer from cachexia, which reduces quality of life, limits treatment options and shortens survival time. Identification of tumor-derived factors that regulate this process could lead to new therapeutic strategies to prevent cancer cachexia.