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August 1, 2016

Grants totaling nearly $3.95M give early career investigators independence to pursue novel ideas

New York, NY (August 1, 2016) – The Damon Runyon Cancer Research Foundation, a non-profit organization focused on supporting innovative early career researchers, named 17 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 ($231,000 for basic scientists; $248,000 for physician-scientists) to work on innovative projects that have the potential to impact cancer prevention, diagnosis, and treatment.

May 2016 Damon Runyon Fellows:

Sudeep Banjade, PhD [HHMI Fellow], with his sponsor Scott Emr, PhD, at Cornell University, Ithaca, studies how cellular membranes are remodeled. The ESCRT family of proteins (endosomal sorting complexes required for transport) regulate this remodeling process; misregulation has been found to be involved in many cancers. He aims to understand the specific roles of the ESCRT-III proteins for polymer remodeling and membrane deformation, using biochemical, biophysical and genetic approaches.

Kyle G. Daniels, PhD, with his sponsor Wendell Lim, PhD, at the University of California, San Francisco, aims to improve the ability of engineered T cells to kill cancer. Specifically, his goal is to understand how signaling events during T cell activation determine the therapeutic properties of activated T cells. He uses synthetic immunology techniques and computational methods to search for synthetic receptors that confer desired functions upon T cells. Ultimately, he hopes to design and create receptors that improve the ability of T cells to proliferate, persist, recruit other immune cells, and kill cancer cells.

Ivana Gasic, Dr.Sc. [Merck Fellow], with her sponsor Timothy Mitchison, PhD, at Harvard Medical School, Boston, aims to elucidate the “microtubule integrity response,” mechanisms that monitor the health of microtubules in cell division under normal physiological conditions and in cancer. Microtubules are frequent chemotherapy targets in treatment of various cancers, such as leukemia, lymphomas, melanoma, lung, ovarian, and breast cancer. Microtubule-targeting chemotherapeutics are believed to kill cancer cells through mitotic arrest. There is, however, growing evidence that they impact non-dividing “interphase” cells as well; this mechanism remains largely unexplored. She seeks to explore the microtubule integrity response, which may reveal how microtubule poisons kill non-dividing cancer cells, and help design better anti-cancer therapies.

Daniel H. Goldman, PhD [Merck Fellow], with his sponsor Rachel Green, PhD, at Johns Hopkins School of Medicine, Baltimore, studies the process of protein synthesis, which is often misregulated in cancer, causing uncontrolled cell growth and proliferation. The balance of protein production in healthy cells is maintained in part by RNA-binding proteins, which modulate the efficiency of mRNA translation by the ribosome. However, the mechanisms underlying such regulation are not well understood. He is combining high-throughput sequencing technologies with single-molecule imaging in living cells to elucidate the mechanisms by which RNA-binding proteins regulate protein synthesis.

Jeffrey A. Hussmann, PhD [Rebecca Ridley Kry Fellow], with his sponsor Carol Gross, PhD, at the University of California, San Francisco, is studying how translation is regulated in healthy cells and how this regulation goes awry in disease. Cells control protein abundance by modulating how frequently messenger RNAs are translated by ribosomes, but the mechanisms that determine how densely ribosomes are packed onto each individual transcript are poorly understood. He is developing experimental approaches to produce transcriptome‐wide single‐molecule measurements of ribosome density in order to advance this understanding. These approaches will provide insights into the the key role that this process plays in the development and progression of many cancers.

Megan Insco, MD, PhD, with her sponsor Len Zon, MD, at Boston Children's Hospital, Boston, studies advanced melanoma. Melanoma initiation and drug resistance rely heavily on factors that control gene expression. Proteins called Cyclin Dependent Kinases (CDKs) show promise as drug targets in multiple difficult-to-treat cancers and are enabling a method to “drug” the previously “undruggable” process of gene expression. She aims to determine whether any of the transcriptional CDKs could be an effective drug target in advanced melanoma. 

Alexander Jaeger, PhD [HHMI Fellow], with his sponsor Susan Lindquist, PhD, at the Whitehead Institute, Cambridge, is investigating how a protein called the Heat Shock Transcription Factor 1 (HSF1), a potent pro-survival transcription factor, orchestrates changes in the three-dimensional architecture of chromosomes to activate tumor supportive gene expression programs in diverse cancer types. Increasing evidence suggests that the three dimensional architecture of chromosomes can influence the unique gene expression programs that support tumor growth. He aims to determine how gene expression is significantly altered in cancer cells when compared to normal cells.

Elise C. Jeffery, PhD, with her sponsor Sean Morrison, PhD, at the University of Texas Southwestern Medical Center, Dallas, studies “stromal cells” that support the function of blood stem cells in the bone marrow. Cancer treatments such as irradiation and chemotherapy damage the bone marrow, and the repair of this tissue is crucial for the recovery of the blood system. She is characterizing the role of a newly identified factor produced by stromal cells in this rebuilding process. These studies have the potential to enhance our understanding of bone marrow repair, and to identify new methods for improving the recovery of the blood system in cancer patients following irradiation or chemotherapy.

Brian J. Laidlaw, PhD, with his sponsor Jason Cyster, PhD, at the University of California, San Francisco, is investigating the mechanisms underlying immune cell positioning following viral infection and tumor challenge. Localization of immune cells to particular sites within the tissue is critical for their maintenance and protective capacity upon reencountering an antigen. How immune cell migration within the tissue is regulated remains poorly understood. His studies should significantly enhance our understanding of immune cell trafficking and inform the development of new immunotherapies against cancer that modulate these pathways to promote tumor regression.

Natasha M. O'Brown, PhD, with her sponsor Chenghua Gu, PhD, at Harvard Medical School, Boston, is investigating the molecular mechanisms that govern the blood-brain barrier (BBB), which acts as the gatekeeper for the brain. While the BBB protects the brain from pathogens and provides the necessary environment for normal brain function, the BBB also acts as an obstacle to drug delivery for the treatment of neurological diseases, including brain tumors. A key regulator of BBB integrity, Mfsd2a, limits transcellular movement across the barrier and therefore prevents leakage into the brain. Using a combination of zebrafish genetics, small molecule screens, and live imaging, she aims to understand how this protein regulates these BBB processes. By investigating the cellular signals that induce or remove barrier properties, she hopes to identify ways by which she can selectively manipulate the barrier to allow for drug delivery to the brain.

Jose M. Ordovas-Montanes, PhD [HHMI Fellow], with his sponsor Alex Shalek, PhD, at the Massachusetts Institute of Technology, Cambridge, studies how inflammation in the gut influences individual epithelial and immune cells. Inflammation is one of the largest risk factors for developing colon cancer. A better understanding of the cellular factors involved in precipitating malignancy may lead to novel approaches for blocking the initiation of cancer and restoring the gut to a healthy balanced state.

Ying Qi Shirleen Soh, PhD, with her sponsor Jesse Bloom, PhD, at the Fred Hutchinson Cancer Research Center, Seattle, focuses on how viruses such as influenza evolve to infect diverse host species. Zoonotic transmissions of influenza from avian and swine hosts to humans have the potential to result in pandemics with severe public health consequences. Cancer patients, in particular, are disproportionately susceptible to complications arising from infection. Dissecting the pathways and mechanisms by which influenza can adapt to the human host will aid in the ability to predict and prevent pandemics resulting from zoonotic infection.

Sarah Z. Tasker, PhD [HHMI Fellow], with her sponsor Paul Hergenrother, PhD, at the University of Illinois, Urbana-Champaign, is synthesizing a new set of small molecules based on natural products, designed to have structural features to allow them to cross the blood-brain barrier. The blood-brain barrier protects the brain, but it also prevents most chemotherapeutic agents from reaching tumor cells in brain cancers, meaning prognoses for cancers such as glioblastoma multiforme and brain metastases are often poor. She will test these new compounds for anticancer activity, and will study whether active compounds cross the blood-brain barrier.  The goal of these studies is to discover new anticancer small molecules and to better understand how these molecules penetrate the blood-brain barrier.  

Iva Tchasovnikarova, PhD, with her sponsor Robert Kingston, PhD, at Massachusetts General Hospital, Boston, is investigating the role of chromatin remodeling in epigenetic gene silencing by the recently discovered HUSH complex. Her research aims to delineate how heterochromatin formation is achieved through the concerted action of heterochromatin-associated proteins, heterochromatic histone modifications, and ATP-driven chromatin remodeling. As heterochromatin formation has been shown to be associated with oncogenic events, her future work will define general principles that could be exploited to design cancer therapies aimed at heterochromatin dysregulation.

Eric Wang, PhD, with his sponsor Nathanael Gray, PhD, at the Dana-Farber Cancer Institute, Boston, is applying a chemical biology approach to identify kinases and small molecule inhibitors that enhance the immune system’s tumor surveillance capabilities. Therapies that enhance the anti-tumor activity of the immune system have shown tremendous promise in patients; however, only a subset of patients and tumors respond well to such treatments, so identifying complementary strategies to increase the effectiveness of existing immunotherapies is increasingly important. His goal is to obtain mechanistic insight into the anti-tumor immune response and to identify small molecule drugs that may improve the efficacy of immunotherapies in patients.

Emma Watson, PhD [Suzanne and Bob Wright Fellow], with her sponsor Stephen Elledge, PhD, at Brigham and Women's Hospital, Boston, is taking advantage of high-throughput genetic screens to map gene networks involved in the response to metabolic stress. Cancer cells tap into growth-promoting metabolic programs, enabling them to robustly proliferate using limited resources from the tissue microenvironment and bloodstream. The metabolic plasticity observed in cancer cells can be at least partly attributed to metabolic stress response pathways that enable the cancer to mobilize resources for growth. Identifying the genes involved in sensing and enacting responses to metabolic stress will provide potentially novel therapeutic targets in the treatment of cancer.

Linghe Xi, PhD [Dale F. and Betty Ann Frey Fellow], with her sponsor Elaine Fuchs, PhD, at The Rockefeller University, New York, is studying signaling events that drive squamous cell carcinomas (SCCs), a common form of skin cancer. She focuses on WNT signaling, which is an important player in cell fate determination. It appears that WNT signaling is essential for SCC tumor formation, but exactly where and how it is required remains unknown. She is dissecting the activity of WNT signaling during the progression from normal epithelial cells to benign papillomas, and then to malignant SCC tumors. She is also investigating the critical downstream effectors of WNT signaling in this process, in order to identify improved targets for cancer therapeutics.


About the 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 $300 million and funded over 3,500 young scientists. This year it will commit over $17 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. 


Yung S. Lie, PhD

Deputy Director and Chief Scientific Officer

Damon Runyon Cancer Research Foundation