Public Release: 

Damon Runyon Cancer Research Foundation grants fellowship, Breakthrough Scientist awards

Grants totaling $3.76 million give early career investigators independence to pursue novel ideas

Damon Runyon Cancer Research Foundation

New York, NY (January 30, 2015) - 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, 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.

The Committee also named six 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:

Angela N. Brooks, PhD (Damon Runyon Fellow '12-'15)
Dana-Farber Cancer Institute, Boston

Dr. Brooks is developing computational and experimental approaches to study genomic changes that give rise to cancer. She designed a powerful new computational tool that she used to analyze data from The Cancer Genome Atlas; she identified and characterized specific genetic alterations in lung adenocarcinoma tumors that disrupt a process called splicing. Her goal for the future is to expand her computational analysis to build a database of splicing alterations in many different cancers and to apply these genomic studies to understudied human populations.

Sidi Chen, PhD (Damon Runyon Fellow '12-'15)
Massachusetts Institute of Technology, Cambridge

Dr. Chen aims to understand the relationship between small RNAs (microRNAs) and cancer. Small RNAs are important regulators of genetic networks inside the cell; perturbation of these networks can lead to malignant cell growth. He is studying the role of microRNAs in tumor metastasis, or spread, in models of lung and liver cancers and will validate his findings using clinical and genomic data from human patients. His goal is to accelerate the development of more effective diagnostics and therapeutics for cancer by targeting microRNAs.

Robert K. McGinty, MD, PhD (Damon Runyon Fellow '12-'16)
Pennsylvania State University, University Park

Dr. McGinty is examining the structure and function of enzymes called methyltransferases. His structural biology approach has already revealed unexpected roles for certain of these enzymes. As these enzymes are commonly misregulated in human leukemias, an understanding of their normal function may provide insight into novel platforms for drug development.

Michael J. Smanski, PhD (Damon Runyon Fellow '12-'14)
University of Minnesota, Saint Paul

Dr. Smanski seeks to develop a new platform for accelerating the discovery of anticancer agents from natural sources. He will use "gene cluster" sequence information from microbes to produce anticancer agents in the laboratory. His ultimate goal is to demonstrate that this technique can be used to rapidly produce drug-like molecules in a highly efficient manner.

Angela J. Waanders, MD, MPH (Damon Runyon-Sohn Pediatric Cancer Fellow '12-'15)
Children's Hospital of Philadelphia, Philadelphia

Dr. Waanders is committed to developing more effective treatments for the many children diagnosed with brain tumors each year. Mutations in BRAF, an oncogene that can drive cancer growth, are prevalent in pediatric astrocytomas. Her research has shown that different BRAF mutations identified in these tumors respond differently to targeted BRAF treatments and suggests that combination therapies may be highly effective. Her continued studies will be the basis for moving novel, targeted treatment strategies into the clinic to treat the children afflicted by this devastating cancer.

Arun P. Wiita, MD, PhD (Damon Runyon Fellow '12-'14)
University of California, San Francisco

Dr. Wiita is using emerging technologies to study response to chemotherapy in multiple myeloma. He aims to characterize the genetic changes that underlie development and progression of the disease, and determine how these changes may predict sensitivity to chemotherapy. His goal is to use this information to enable more effective individualized chemotherapeutic regimens for cancer patients.

November 2014 Damon Runyon Fellows:

Anupam K. Chakravarty, PhD [HHMI Fellow] with his sponsor Daniel F. Jarosz, PhD, at Stanford University School of Medicine, Stanford, is investigating heritable physical structures, called higher order assemblies, formed upon overexpression of RNA binding proteins. These proteins are consistently overexpressed in multiple cancers. His research will illuminate the mechanism of assembly formation and its role in altering gene regulation, thereby suggesting novel avenues to potential therapeutic intervention.

Matthew R. Clay, PhD [HHMI Fellow] with his sponsor David R. Sherwood, PhD, at Duke University, Durham, is studying how cells in their natural environment move across basement membranes-the extracellular matrix of proteins that surrounds tissues. Basement membrane "breaching" is the first step of cell invasion, which underlies cancer metastasis. These studies will uncover fundamental mechanisms that govern cell invasion and drive the deadly progression of cancers.

Ronald J. Hause, PhD, with his sponsor Jay A. Shendure, MD, PhD, at the University of Washington, Seattle, is developing new experimental and analytical methods to better understand, interpret and predict how genetic mutations affect individuals' risks for cancers and responses to chemotherapy. He will use a combination of genomic, biochemical, and machine learning approaches to investigate and model the effects of all possible mutations of a gene involved in chemotherapeutic drug response and relate these results to patient outcome.

Kai Mao, PhD, with his sponsor Gary Ruvkun, PhD, at Massachusetts General Hospital, Boston, is studying the cell's cytoskeleton, which provides the physical structure and shape of a cell. The cytoskeleton is an attractive target for cancer chemotherapy because of its central function in mitosis or cell division, but these chemotherapeutic agents have very high toxicity. He hypothesizes that the next generation of chemotherapy will benefit from the inhibition of these toxin response pathways.

Rand M. Miller, PhD, with his sponsor Tarun M. Kapoor, PhD, at The Rockefeller University, New York, is interested in understanding the mechanisms by which cancers become resistant to chemotherapeutic agents. Many cancers acquire resistance to drugs by overproducing molecular "pumps" called multidrug resistance proteins, which actively export the toxic drug molecules out of cells. Using a variety of chemical techniques, he will investigate how these pumps mediate drug resistance in cancers, as well as their roles in the maintenance of healthy cellular function.

Sigrid Nachtergaele, PhD, with her sponsor Chuan He, PhD, at The University of Chicago, Chicago, is investigating the roles of a chemical modification of mRNA called methylation. Many enzymes that add and remove RNA modifications impact developmental processes and cancer proliferation, but how they are regulated remains a mystery. She aims to identify the mechanisms by which mRNA methylation alters gene expression and eventually results in altered cell signaling and growth.

Thomas Norman, PhD, with his sponsor Jonathan Weissman, PhD, at the University of California, San Francisco, is investigating the role that "epigenetic" differences play in cancer cells' ability to develop drug resistance. These epigenetic changes result in altered gene expression. He will use a new technique called CRISPRi to systematically tune the expression of different parts of the genome and measure their effects on drug resistance. He hopes that these studies will identify new avenues for reducing resistance and expand our knowledge of the role epigenetic factors play in leukemia and other cancers.

Magdalena E. Potok, PhD [HHMI Fellow] with her sponsor Steven E. Jacobsen, PhD, at University of California, Los Angeles, is investigating how gene expression is controlled by heterochromatin (the physically compacted form of DNA) and genomic instability. In certain plants, reduction in a chemical mark on the chromatin, called H3K27me1, results in heterochromatin decompaction, abnormal gene expression and the production of extra DNA from certain regions. Extra copies of DNA are a sign of genomic instability often observed in cancers.

William Razzell, PhD [HHMI Fellow] with his sponsor Jennifer A. Zallen, PhD, at Memorial Sloan Kettering Cancer Center, New York, is using cell biological, molecular genetic, and biophysical approaches to understand how cell-derived mechanical forces contribute to tumorigenesis through the modulation of cellular signaling pathways. He will focus on one pathway that is responsive to mechanical forces, the Hippo pathway, which prevents excessive tissue growth during development.

David W. Taylor, PhD, with his sponsor Eva Nogales, PhD, at the University of California, Berkeley, is studying the structural biology of bacterial CRISPR-Cas surveillance complexes, which have been adopted as versatile genome engineering tools. He aims to decipher the principles by which these complexes function and to apply them for cancer research and therapeutics.

Albert Tsai, PhD, with his sponsor Robert H. Singer, PhD, at HHMI Janelia Farm Research Campus, Ashburn, is studying a process called translation, by which messenger RNAs (mRNAs) are decoded into proteins. A hallmark of cancer cells is distorted patterns of protein production, leading to uncontrolled growth and invasive behavior. He is using novel microscope technology to image live cells in real-time and developing techniques to image individual protein molecules during their synthesis, thereby linking the time, location and amount of protein production to individual mRNAs.

Jeanine L. Van Nostrand, PhD, with her sponsor Reuben J. Shaw, PhD, at the Salk Institute, La Jolla, aims to understand how signaling pathways involved in the energetic and metabolic stress responses prevent cancer. She will generate models harboring specific mutations that prevent the stress response, and evaluate the effects of these mutations on lung cancer development.

Aaron D. Viny, MD, with his sponsor Ross L. Levine, MD, at Memorial Sloan Kettering Cancer Center, New York, is studying the oncogenic role of abnormalities in the cohesin complex--a group of proteins that function to align and stabilize sister chromatids (copies of the chromosomes) during cell division. Mutations within several proteins in this complex have been identified in solid tumors and hematologic malignancies, particularly acute myeloid leukemia, the most common adult leukemia.

Jonathan R. Whicher, PhD, with his sponsor Roderick MacKinnon, MD, at The Rockefeller University, New York, focuses on a cellular structure called the voltage-gated potassium channel Eag1, which can promote tumor growth and is aberrantly expressed in many types of cancer including breast, colon, prostate, lung, and liver. He is determining the structure and mechanism of Eag1 in order to elucidate how Eag1 promotes cancer growth, with the eventual goal of developing Eag1 modulators as potential anti-cancer therapies.

Andrew L. Wolfe, PhD, with his sponsor Ramon Parsons, MD, PhD, at the Icahn School of Medicine at Mount Sinai, New York, studies PTEN, an anti-cancer protein that opposes cell growth and can induce cancer cells to die. Loss of PTEN protein has been detected in nearly every form of cancer and is associated with drug resistance and poor clinical outcome. A new, longer form of PTEN, called PTEN-L, was recently discovered. He aims to answer fundamental questions about the mechanism and function of PTEN-L, which will characterize the expression and regulation of this important anti-cancer protein for the first time.

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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, the Foundation has invested over $287 million and funded more than 3,460 young scientists. This year it will commit over $15 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

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