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Damon Runyon Cancer Research Foundation grants prestigious awards to 17 young scientists
Date:1/28/2013

New York, NY (January 28, 2013) 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 Muoz, 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.

Chih-Yung Lee, PhD [HHMI Fellow] with his sponsor Geraldine Seydoux, PhD, at Johns Hopkins University, Baltimore, Maryland, is studying how the first germ cell is specified during embryonic development. Several characteristics of germ cells are reminiscent of cancer cells, including rapid proliferation and immortality; proteins expressed specifically in the germline are often misexpressed in tumors. Identifying new genes and pathways required for germ cell development will provide insights into how re-activation of germ cell fate is triggered during tumorigenesis.

Wenyu Luo, PhD, with her sponsor Yuh-Nung Jan, PhD, at the University of California, San Francisco, California, is exploring the neuronal and genetic basis of stress-induced depression-like behavior in Drosophila. Loss of resilience to stress leads to depression and other mental disorders, which may increase the risk of other severe diseases including liver and lung cancers. This research may develop new stress intervention approaches to improve quality of life in cancer patients.

Maria Mihaylova, PhD [Robert Black Fellow] with her sponsor David M. Sabatini, MD, PhD, at the Whitehead Institute for Biomedical Research, Cambridge, Massachusetts, aims to understand how aberrant nutrient sensing can lead to metabolic reprogramming and transformation. Utilizing a mouse model, she will examine the re-wiring of cellular metabolism in intestinal stem cells in response to dietary changes. She hopes that these studies will lead to insights about how nutrient sensing affects stem cell maintenance and tumorigenesis.

Evgenia N. Nikolova, PhD [Robert Black Fellow] with her sponsor Peter E. Wright, PhD, at The Scripps Research Institute, La Jolla, California, aims to elucidate the molecular mechanism of gene silencing mediated by the protein Kaiso. Previous studies suggest that Kaiso acts as a tumor suppressor gene that can block cells from progressing to cancer; irregular Kaiso function is linked to cancer cell proliferation in a number of human cancers including colon, prostate, breast and lung cancers, as well as leukemia.

Summer B. Thyme, PhD [HHMI Fellow] with her sponsor Alexander F. Schier, PhD, at Harvard University, Cambridge, Massachusetts, is engineering protein tools to alter epigenetic modifications in important developmental pathways in a zebrafish model. Epigenetic misregulation, particularly of key regulators of cell fate specification, underlies a vast number of cancers. These tools could be applied to reprogram cell fate, as a means of treating epigenetically mediated diseases such as cancer.

Ozlem Yildirim, PhD [HHMI Fellow] with her sponsor Robert E. Kingston, PhD, at Massachusetts General Hospital, Boston, Massachusetts, aims to identify factors that maintain cellular identity during mammalian cell proliferation. This will shed light on how cells remember which cell type they were and should become after division. A mechanistic understanding of this process will yield new insights into the many cell fate changes cancer cells display during their abnormal growth.

Dmitriy Zamarin, MD, PhD [Dr. Bart A. Kamen Morphotek Fellow] with his sponsor Jedd D. Wolchok, MD, PhD, at Memorial Sloan-Kettering Cancer Center, New York, New York, is studying oncolytic viruses, a class of promising emerging cancer therapeutics. Oncolytic viruses can efficiently and specifically lyse cancer cells; they also induce important tumor-specific immune responses. He is exploring different immunotherapeutic strategies to make oncolytic virus-based immunotherapy applicable to all cancer types.


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Contact: Yung S. Lie, PhD
yung.lie@damonrunyon.org
212-455-0521
Damon Runyon Cancer Research Foundation
Source:Eurekalert

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