Public Release: 

Damon Runyon Cancer Research Foundation grants fellowship awards to 16 young scientists

Grants totaling over $3.3 million give early career investigators independence to pursue novel ideas

Damon Runyon Cancer Research Foundation

New York, NY (July 17, 2015) - The Damon Runyon Cancer Research Foundation, a non-profit organization focused on supporting innovative early career researchers, named 16 new Damon Runyon Fellows at its spring Fellowship Award Committee review. The recipients of this prestigious, four-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 ($208,000 each for basic scientists, $248,000 for physician-scientists) to work on innovative projects.

May 2015 Damon Runyon Fellows:

Lacy J. Barton, PhD, with her sponsor Ruth Lehmann, PhD, at the New York University School of Medicine Skirball Institute of Biomolecular Medicine, New York, investigates the regulation of cell migration. Specifically, she aims to understand how spatial information is generated to guide migrating cells and how cell migration is terminated when the target tissue is reached. To gain insights into these processes, she is studying migration of Drosophila germ cells to the gonad during embryogenesis as a model system. Because many features of this model system are similar to tumor cell migration, novel processes she discovers will shed light on the mechanisms of metastasis.

Danfeng Cai, PhD, with her sponsor Jennifer Lippincott-Schwartz, PhD, at the National Institutes of Health, Bethesda, is interested in whether the state of cellular "protein crowdedness" can be used to differentiate healthy normal cells from cancer cells. Having the ability to monitor protein crowding and protein-folding landscapes within cells could provide a valuable "readout" for changes in metabolism and the overall health or dysfunction of cells.

Gina V. Caldas, PhD, with her sponsor Craig C. Mello, PhD, at the University of Massachusetts Medical School, Worcester, is investigating the mechanisms by which RNA interference (RNAi) related pathways, implicated in cancer primarily through their role in regulating gene expression, contribute to the fidelity of cell division. In addition to major changes in gene expression, a hallmark of many cancers is genome instability and chromosome loss, processes highly related to inaccurate cell division. Using C. elegans as a model system, her goal is to identify new aspects of cell division control that can be targeted for cancer therapy.

Qi Hu, PhD, with his sponsor Kevan M. Shokat, PhD, at the University of California, San Francisco, is focusing on developing small molecule inhibitors to regulate the activity of Gαs, a subunit of the stimulatory G protein, which is encoded by the GNAS gene. Activating mutations of GNAS have been revealed to contribute to progression and metastasis of several kinds of cancers. About 64% of these mutations result in a single variant, which keeps Gαs in a constitutively active state. His goal is to design and synthesize small molecules to specifically inhibit the abnormally activated Gαs, which would be promising tools for treatment of cancer.

Bryan C. King, PhD [Berger Foundation Fellow], with his sponsor Craig B. Thompson, MD, at the Memorial Sloan Kettering Cancer Center, New York, is studying mechanisms by which nutrient-deprived cancer cells use extracellular proteins as a source of energy to promote their growth and survival. These mechanisms enable cancer cells to thrive in environments in which normal healthy cells cannot survive. He will investigate a new role for a molecular signaling pathway, called AMPK, in how the cell senses and responds to changes in nutrient availability. These studies may give insights into how cancer cells develop resistance to therapy, as well as be applied to developing new therapeutic approaches.

Allison N. Lau, PhD, with her sponsor Matthew G. Vander Heiden, MD, PhD, at the Massachusetts Institute of Technology, Cambridge, aims to characterize the unique metabolism of pancreatic ductal adenocarcinoma cancer cells. In general, it is known that cancer cells have altered metabolism compared to non-cancerous cells; however, it is unknown how different cell types within a tumor utilize nutrients and how this may contribute to tumor progression and metastasis. This research will provide insight into the metabolic dependencies of different cells found within the pancreatic tumor environment and may potentially be useful for developing novel therapies.

June-Yong Lee, PhD [HHMI Fellow], with his sponsor Dan R. Littman, MD, PhD, at the New York University School of Medicine Skirball Institute of Biomolecular Medicine, New York, studies how the cells and molecules of the immune system within the tumor microenvironment contribute to initiation, tumor progression, and responses to anti-cancer therapy. Of the immune components, cells called interleukin-17-secreting lymphocytes have pivotal pathogenic roles in multiple cancers. He aims to elucidate the regulatory mechanisms by which this pathogenicity is controlled. Ultimately, a better understanding of the pathways may suggest promising targets for therapeutic strategies aimed at reducing the risk of cancer.

Kathrin Leppek, PhD [Layton Family Fellow], with her sponsor Maria Barna, PhD, at Stanford University, Stanford, aims to combine RNA and ribosome biology with developmental biology to investigate how cells regulate protein synthesis through a process called translation. This process requires regulatory mechanisms to fine-tune when and where genes are expressed. Defective expression of certain genes gives rise to uncontrolled growth and metastasis of cancer cells. She will identify and characterize molecular components that play a functional role in mediating translational control during embryogenesis. This will be invaluable for our understanding of how deregulation of accurate gene expression underlies human diseases such as cancer.

Tera C. Levin, PhD [HHMI Fellow], with her sponsor Harmit S. Malik, PhD, at the Fred Hutchinson Cancer Research Center, Seattle, studies how resident microorganisms can manipulate the development of their animal hosts. Through novel genetic approaches, she will explore the mechanisms used by the bacterium Wolbachia pipientis to dramatically disrupt the cell divisions of its host, Drosophila simulans. Because cancerous growth is often driven by the dysregulation of developmental signaling pathways, understanding the mechanistic impacts of resident microbes promises to illuminate both normal and cancer development.

Lyndsay M. Murrow, PhD, with her sponsor Zev J. Gartner, PhD, at the University of California, San Francisco, is using an engineered 3D model of the human mammary gland to determine how stem cells in the breast sense and respond to overall cellular composition. She aims to understand how sparsely distributed stem cells use local cues in the tissue to sense global changes in cell number. Since loss of tissue organization and abnormal stem cell differentiation are two key features underlying breast cancer development, this work will help identify new strategies for breast cancer prevention and treatment.

Vu Quang Nguyen, PhD, with his sponsor Carl Wu, PhD, at the HHMI Janelia Farm Research Campus, Ashburn, uses advanced fluorescence microscopy to visualize how defined structural changes in chromatin, the condensed form of DNA, affect its association with factors required for transcription initiation--an early and essential step in gene expression. Architectural defects in chromatin are found in many cancers and have been linked to aberrant patterns of gene expression. The results of this research will be important in characterizing the connection between chromatin organization and cancer-associated gene misregulation.

Alistair B. Russell, PhD [Merck Fellow], with his sponsor Jesse D. Bloom, PhD, at the Fred Hutchinson Cancer Research Center, Seattle, is investigating the mechanisms by which cells recognize influenza infection. Yearly influenza epidemics present an ongoing medical challenge, and those suffering from cancer are at a potentially increased risk of complication following infection. By identifying both cell-to-cell differences in the response to viral infection and virus-to-virus differences in the capacity to evade the host response, he hopes to develop a better understanding of the kinetics of initial infection and disease progression in individuals.

Joseph D. Schonhoft, PhD [Merck Fellow], with his sponsor Jeffery W. Kelly, PhD, at the Scripps Research Institute, La Jolla, aims to understand how immune cells abnormally proliferate and secrete a pathogenic variety of antibody proteins that cause organ and tissue damage, most notably in the heart and kidneys, during diseases such as amyloidosis and within a subset of multiple myelomas. His research will explain why particular antibody molecules are toxic while others are completely benign. This information may be used to develop new diagnostic probes for the early detection of these molecules, which could greatly improve the effectiveness of current clinical treatments.

Justin L. Sparks, PhD, with his sponsor Johannes C. Walter, PhD, at Harvard Medical School, Boston, focuses on a protein complex called the eukaryotic replisome, which replicates cellular DNA during cell division. He is studying how the replisome handles persistent bulky DNA lesions that block the progression of the replicative helicase enzyme and how cells repair covalent DNA-protein cross-links (DPCs). DPCs are generated by formaldehyde and other environmental mutagens and are almost certainly important for cancer etiology. Genome instability is a hallmark of all cancers, and mechanisms that either prevent or enhance this instability have many implications for cancer biology.

Neil T. Umbreit, PhD [HHMI Fellow], with his sponsor David S. Pellman, MD, at the Dana-Farber Cancer Institute, Boston, studies chromosome segregation, the process by which the genetic information on chromosomes is duplicated and the copies are segregated equally into two new cells. Cancer cell proliferation is marked by frequent errors in chromosome segregation, resulting in abnormal genetic content. He is investigating one type of chromosome segregation error, called a "chromosome bridge," a major mechanism through which genetic information can be amplified and/or rearranged to distort gene function in cancer cells. When these genetic rearrangements include oncogenes and growth factor genes, they can result in acquired drug resistance, unrestrained cell proliferation, and metastasis.

Swathi Yadlapalli, PhD [HHMI Fellow], with her sponsors Orie T. Shafer, PhD, and Edgar Meyhofer, PhD, at the University of Michigan, Ann Arbor, aims to elucidate the neural and molecular mechanisms involved in the regulation of metabolism. Living organisms have evolved neural mechanisms involving circadian clocks to synchronize their physiology, metabolism and behavior with the external environment. Disruption of these clocks is associated with increased incidence of cancer, diabetes, and heart disease. She has developed an ultra-sensitive calorimeter that allows for precise quantification of metabolic activity, which she will use to investigate the circadian regulation of metabolism. These studies will provide novel insights into how networks of circadian clock neurons orchestrate daily changes in metabolism, and may be applied to the development of novel treatments for cancers and metabolic disorders.

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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, Damon Runyon has invested nearly $294 million and funded nearly 3,500 young scientists. This year, it will commit over $14 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.damonrunyon.org

CONTACT

Yung S. Lie, PhD
Deputy Director and Chief Scientific Officer
Damon Runyon Cancer Research Foundation
yung.lie@damonrunyon.org
212.455.0521

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