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Damon Runyon Cancer Research Foundation grants fellowship awards to 21 top young scientists

New York, NY (July 10, 2012) The Damon Runyon Cancer Research Foundation, a non-profit organization focused on supporting innovative early career researchers, named 21 new Damon Runyon Fellows at its spring 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 for basic scientists, $186,000 each for physician-scientists) to work on innovative projects.

May 2012 Damon Runyon Fellows:

Gira Bhabha, PhD, with her sponsor Ronald D. Vale, PhD, at the University of California, San Francisco, California, is using electron and light microscopy techniques to study the structure and atomic motions of dynein, a molecular motor protein that "walks" along "tracks" in the cell called microtubules. Dynein's crucial role in cellular cargo transport as well as in cell division makes it an important molecule to potentially target for cancer treatment.

Alistair N. Boettiger, PhD, with his sponsor Xiaowei Zhuang, PhD, at Harvard University, Cambridge, Massachusetts, aims to understand the molecular mechanisms of gene silencing through the application of novel super-resolution microscopy techniques. Gene silencing is an important process whereby genes that are not needed in certain tissues are turned off. Loss of silencing can lead to the expression of genes that promote cell proliferation and migration, leading to cancer. The ability to restore and maintain natural patterns of gene silencing may successfully block cancer.

Christopher J. Bohlen, PhD, with his sponsor Ben A. Barres, MD, PhD, at Stanford University School of Medicine, Stanford, California, is studying how cells of the nervous system called microglia communicate to other cell types during nerve injury. He seeks to identify cell-cell signals that contribute to chronic pain induced by tumors. This research will identify potential targets of palliative therapies for cancer patients, and will provide insights into signaling pathways that may become activated or misregulated in brain cancers such as gliomas.

Anne H. Bothmer, PhD [Jake Wetchler Foundation Fellow for Pediatric Innovation] with her sponsor Pier Paolo Pandolfi, MD, PhD, at Beth Israel Deaconess Medical Center, Boston, Massachusetts, is studying how the function of ribosomes, cellular machines responsible for making protein, is changed in cancer cells. She plans to characterize how ribosomes in cancerous cells differ from those in normal cells, and to test whether these differences contribute to the development of diseases such as acute myeloid leukemia (AML). Elucidating how cancer cells differ from normal cells will ultimately contribute to the development of novel therapeutic options for the treatment of cancer.

Angela N. Brooks, PhD, with her sponsor Matthew L. Meyerson, MD, PhD, at Dana-Farber Cancer Institute, Boston, Massachusetts, is analyzing cancer genome sequence data to identify DNA mutations that affect RNA splicing, a form of gene processing and regulation. By characterizing these mutations, her work will provide further understanding of the role of splicing alterations in cancer as well as insight into the functional consequences of cancer mutations.

Gamze . Camdere, PhD, with her sponsor Douglas E. Koshland, PhD, at the University of California, Berkeley, California, is using structural biological analysis and in vitro assays to understand how a protein called cohesion interacts with DNA. Cohesin is required for proper chromosome segregation, DNA repair, gene expression, and overall maintenance of genomic integrity. A better understanding of cohesin will provide important insights into chromosome organization and biology, as well as shed light onto the pathology of cancer.

Steven D. Cappell, PhD, with his sponsor Tobias Meyer, PhD, at Stanford University, Stanford, California, aims to understand the precise molecular events that allow cells to enter the cell cycle (process of cell division), by applying quantitative time-lapse microscopy, live-cell fluorescent reporters and mathematical modeling. The beginning of the cell cycle, the G1/S phase transition, represents the commitment to cell division and is deregulated in nearly all types of cancers. He hopes to identify new regulatory elements controlling the G1/S transition that can be targeted for therapeutic benefit.

Elie J. Diner, PhD, with his sponsor Russell E. Vance, PhD, at the University of California, Berkeley, California, seeks to understand how the innate immune system distinguishes between self- and non-self nucleic acids. This research has a direct application to cancer and tumor biology, as cancerous cells undergo uninhibited cell growth that typically remains undetected by the immune system. Understanding how the immune system recognizes or avoids recognition of specific molecules may lead to the discovery of pathways that can be exploited to direct the immune system to target tumor cells.

Damian C. Ekiert, PhD, with his sponsor Jeffery S. Cox, PhD, at the University of California, San Francisco, California, is exploring the complex network of interactions between the host immune system and Mycobacterium tuberculosis, the pathogen that causes tuberculosis (TB) in humans. In order to survive and replicate inside host cells, M. tuberculosis must evade detection by the immune system and interfere with multiple antimicrobial pathways that would otherwise lead to the destruction of the bacteria. Understanding how pathogens escape immune recognition may shed light on how cancerous cells evade detection by similar tissue surveillance mechanisms.

Mingye Feng, PhD, with his sponsor Irving L. Weissman, MD, at Stanford University, Stanford, California, is studying immunosurveillance in metastasis, which is mediated by cells called macrophages. Cancer cells are confronted with multiple challenges during metastasis, including macrophage-mediated cell removal in the circulation and distant organs. He will focus on defining the mechanisms utilized by metastatic cancer cells to evade cell removal and developing strategies to promote the clearance of metastatic cancer cells by macrophages.

Li He, PhD, with his sponsor Norbert Perrimon, PhD, at Harvard Medical School, Boston, Massachusetts, is studying how organ size and quality are controlled. Cell competition is a phenomenon by which cells possessing unequal "fitness" compete with each other during tissue growth or regeneration. Activation of apoptosis (programmed cell death) in the "loser" cells in turn triggers compensatory proliferation of the "winners." This process can eliminate tumor cells at an early stage; however, it may also be hijacked by cancer cells to invade the healthy tissue. His goal is to generate a comprehensive understanding of signals that govern this process.

Melanie Issigonis, PhD [HHMI Fellow] with her sponsor Phillip A. Newmark, PhD, at the University of Illinois at Urbana-Champaign, Illinois, studies the mechanisms by which somatic stem cells produce germ cells, the cells that give rise to either egg or sperm. Germ cells and cancer cells share several characteristics such as immortalization (transformation) and migration (metastasis). A wide range of cancers arise when germ cell developmental pathways are erroneously activated in somatic cells. Identifying the processes underlying germ cell specification and development will help elucidate the factors that trigger misexpression of germ cell genes in cancer cells.

Shijing Luo, PhD [Miles S. Nadal Fellow] with her sponsor Elaine V. Fuchs, PhD, at The Rockefeller University, New York, New York, aims to discover and characterize genes that control stem cell activation and migration into a wound site upon injury. Chronic injury and aberrant wound healing are correlated with enhanced susceptibility to skin cancer and metastasis. Her goals are to reveal the key missing links of the relationship between wound repair and cancer, and to provide insights into the prevention and treatment of skin cancer and metastasis.

Karl A. Merrick, PhD, with his sponsor Michael B. Yaffe, MD, PhD, at Massachusetts Institute of Technology, Cambridge, Massachusetts, is studying how inflammation affects the development of colorectal cancer and the response of these tumors to chemotherapy. By using animal models and highly quantitative systems-based approaches, he hopes to identify novel therapies and develop methods to predict the efficacy of drug treatment.

Michael E. Pacold, MD, PhD [Sally Gordon Fellow] with his sponsors David M. Sabatini, MD, PhD, and Nathanael S. Gray, PhD, at the Whitehead Institute for Biomedical Research, Cambridge, Massachusetts, studies dehydrogenases, a class of metabolic enzymes that synthesize the building blocks required for the survival and proliferation of cancer cells. His goal is to develop compounds that block the activity of dehydrogenases essential for the growth of treatment-refractory cancers, with a particular focus on certain breast cancers.

Laura Pontano Vaites, PhD, with her sponsor J. Wade Harper, PhD, at Harvard Medical School, Boston, Massachusetts, focuses on the autophagy pathway, a critical regulatory network that allows cells to recycle cellular components to survive nutrient-depleted conditions. Deregulation of autophagy leads to diseases, including cancer. The proposed work will provide detailed insight into the dynamics and organization of complexes required for autophagy and how this organization may be disrupted in cancer.

Lisa R. Racki, PhD [HHMI Fellow] with her sponsor Dianne K. Newman, PhD, at the California Institute of Technology, Pasadena, California, is studying metabolism of compounds called polyphosphates in Pseudomonas aeruginosa, a bacterial pathogen that can lead to lethal infections in immunocompromised cancer patients. Polyphosphates are found from bacteria to mammalian cells. A better understanding of polyphosphate metabolism in a model bacterial pathogen may aid in the design of treatments for cancer-associated pathogens and may also shed light on the poorly understood role of polyphosphates in mammalian cell growth.

Christopher J. Shoemaker, PhD, with his sponsors Vlad Denic, PhD, and Andrew W. Murray, PhD, at Harvard University, Cambridge, Massachusetts, is studying autophagy, a process of cellular housekeeping and energy generation. The activation of autophagy can facilitate cancer drug resistance. By better understanding the processes that govern autophagy, he ultimately seeks to limit the effects of drug resistance during cancer treatment.

Michael J. Smanski, PhD [HHMI Fellow] with his sponsor Christopher A. Voigt, PhD, at Massachusetts Institute of Technology, Cambridge, Massachusetts, is examining magnetic nanoparticles (MNPs), which possess unique physical properties that have led to several clinical applications in cancer diagnosis and therapy. Several species of bacteria have been found to naturally produce MNPs with exquisite control over size and shape that is unmatched by current chemical synthesis methods. He aims to understand how bacterial synthesis of MNPs relies on the coordinated expression of several dozen genes.

Stephanie C. Weber, PhD [HHMI Fellow] with her sponsors Clifford P. Brangwynne, PhD, and Howard A. Stone, PhD, at Princeton University, Princeton, New Jersey, is investigating control of cell size. She aims to understand how the size and activity of the nucleolus, a subnuclear organelle that has been implicated in tumorigenesis, contributes to cell, tissue and body size. Cancer cells are often smaller or larger than normal, suggesting that the mechanisms controlling cell size break down during the course of the disease.

Arun P. Wiita, MD, PhD, with his sponsor James A. Wells, PhD, at the University of California, San Francisco, California, is using a powerful technique called mass spectrometry to isolate and identify proteins degraded during cell death and released into the bloodstream shortly after starting chemotherapy. Chemotherapy is frequently the mainstay of therapy for patients with cancer, yet the current tests available to assess whether chemotherapy is working are typically quite expensive and can only be used weeks to months after the start of therapy. His goal is to identify proteins that can serve as rapid and inexpensive markers of chemotherapeutic efficacy, enabling more effective individualized chemotherapeutic regimens for cancer patients.


Contact: Yung S. Lie, Ph.D.
Damon Runyon Cancer Research Foundation

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