New York, NY (August 27, 2018) - The Damon Runyon Cancer Research Foundation, a non-profit organization focused on supporting innovative early career researchers, named 18 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 total) to work on innovative projects.
May 2018 Damon Runyon Fellows:
Matthew Bakalar, PhD, with his sponsor Nir Hacohen, PhD, at The Broad Institute, Cambridge, is developing new methods to discover the millions of interactions between T-cell receptors and foreign antigens that trigger an immune response. In many cancers, such as metastatic melanoma, immunotherapy depends on the ability of T cells to recognize and respond to tumor-specific neoantigens--new proteins found on cancer cells, which let the immune system know that these are not normal cells. Collecting the data on this relationship can help create computational models to predict the antigen-target of a patient's individual T cell receptor, which could then guide the design of patient-specific cancer vaccines and engineering of new, tumor-targeting T cells.
Robert S. Banh, PhD [Merck Fellow] with his sponsors Alec Kimmelman, MD, PhD, and Michael Pacold, MD, PhD, at New York University School of Medicine, New York City, is focusing on the role of sensory neurons in promoting pancreatic tumor growth. Interestingly, most pancreatic tumors display increased number of sensory nerves, which cause pain in patients. Dr. Banh hypothesizes that sensory neurons may metabolically support pancreatic tumor growth in nutrient poor environments by directly releasing nutrients or by changing the cancer's nutritional demands. Elucidating this crosstalk in regulation and function will help gain insight into the contributions of neurons on the development of pancreatic tumors, and potentially other cancers, with the ultimate goal of identifying novel treatment strategies.
Geoffrey P. Dann, PhD [Merck Fellow] with his sponsor Benjamin A. Garcia, PhD, at University of Pennsylvania, Philadelphia, is studying how the addition of the amino acid arginine to proteins regulates their biological activity. When this process malfunctions, cancerous genes are transcribed into proteins. Dr. Dann will use high-resolution mass spectrometry to identify arginine-modified proteins in cells, chemical biological tools to decipher the role of such modification in determining protein function, and functional genomics to understand how this process regulates the genome.
Allison Didychuk, PhD, with her sponsor Britt A. Glaunsinger, PhD, at University of California, Berkeley, is investigating the mechanism by which the Kaposi's sarcoma herpesvirus (KSHV) co-opts the cellular host machinery to produce its own gene products in a manner distinct from other viruses and host cells. This research should reveal insights into this unique mode of transcriptional control. KHSV is an oncogenic virus that causes various cancers including, Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease, in immunocompromised individuals.
Kelsie A. Eichel, PhD [Robert A. Swanson Family Fellow] with her sponsor Kang Shen, PhD, at Stanford University, Stanford, is studying how proteins travel across cellular membranes and are sorted to different areas of the cell. This highly regulated mechanism generates distinct membrane domains of the cell with unique protein compositions, which are essential for cellular functions. Dr. Eichel hopes to understand how membrane trafficking plays a role in cancer biology, including loss of cellular polarization, uncontrolled cell growth, invasion, and metastasis.
Eric E. Gardner, PhD [Kenneth G. and Elaine A. Langone Fellow] with his sponsor Harold E. Varmus, MD, at Weill Cornell Medicine, New York City, is studying acquired resistance to targeted therapies in lung cancer. Many targeted therapies used in cancer treatment are capable of controlling disease for a period of time, but in most cases, the disease finds a way to resist or adapt. For instance, some patients treated with epidermal growth factor receptor (EGFR) inhibitors for adenocarcinoma develop resistance to this class of drugs when their cancer transforms to small cell lung cancer (SCLC). Dr. Gardner is investigating this process using both human and mouse models of lung cancer to identify therapeutic approaches that may treat, prevent, or reverse this type of acquired resistance.
Stephanie Gates, PhD [HHMI Fellow] with her sponsor Andreas Martin, PhD, at University of California, Berkeley, is focusing on the 26S proteasome, part of the Ubiquitin Proteasome System (UPS), which is important for protein quality control and cellular regulation. The proteasome degrades aggregated and misfolded proteins, which are tagged with a ubiquitin molecule for disposal in normal cells. Proteasomes are also critical in helping cancer cells survive by disposing of malfunctioning proteins, so inhibiting the proteasomal degradation mechanism is an effective cancer drug target. Dr. Gates is investigating how the cell's disposal machinery recognizes ubiquitin, which may help in designing proteasome inhibitors for cancer treatment.
Marsha M. Hirschi, PhD [Dennis and Marsha Dammerman Fellow] with her sponsor Gabriel C. Lander, PhD, at The Scripps Research Institute, La Jolla, is creating a tool to investigate specific glutamate receptor subpopulations and elucidate their role in cancer mechanisms. Glutamate receptors on neurons are involved with learning and memory in a time- and tissue-specific manner and abnormal function can lead to cancer. Detailed understanding of how glutamate receptors work may provide insight into new therapies for cancers ranging from gliomas to peripheral malignancies, such as pancreatic cancer.
Whitney Johnson, PhD, with her sponsor David S. Pellman, MD, at Dana-Farber Cancer Institute, Boston, is studying how genome rearrangements occur in cancer, using artificial pancreatic cancer organoids--clusters of cells that act as a model system. Cancer cells have unstable genomes that mutate and rearrange at a high rate compared to normal cells. Ultimately, Dr. Johnson hopes to understand how genome instability may be exploited to improve cancer treatments, including immunotherapy.
Jamie Lahvic, PhD [The Mark Foundation for Cancer Research Fellow], with her sponsor Iswar K. Hariharan, PhD, at University of California, Berkeley, is investigating how neighboring normal cells will try to impede the growth of cancer cells, and how a tumor escapes these controls. Dr. Lahvic aims to understand the genetic predispositions to cancer and find clues to a new way of preventing and treating cancer: activation of normal cells to directly fight a nearby tumor. While this work could hold relevance for all carcinomas, she is focusing on Ras mutations, which are especially common in pancreatic and colon cancers.
Chuan Li, PhD [Connie and Bob Lurie Fellow], with her sponsor Dmitri Petrov, PhD, at Stanford University, Stanford, is focusing on quantifying how different tumor suppressor genes interact to determine the mechanisms underlying cancer growth. Using mouse lung adenocarcinoma as a model system, she is developing high-throughput experimental approaches to quantify the combinatorial effects of inactivating tumor suppressor pairs. This approach may enable an in-depth understanding of the pathways that underlie cancer progression and potentially hint at new therapeutic targets.
Daniel H. Lin, PhD [HHMI Fellow] with his sponsor David P. Bartel, PhD, at Whitehead Institute, Cambridge, is studying how the three-dimensional organization of messenger RNAs affects protein synthesis and how this mode of control is affected in cancer. Dr. Lin is developing high-throughput sequencing technologies to measure the three-dimensional organization and protein production of messenger RNAs to decipher the rules governing the relationship between these two properties and how they change in cancer.
Nagarajan (Sandy) Nandagopal, PhD [Philip O'B Montgomery, Jr., MD, Fellow] with his sponsors Galit Lahav, PhD, and Sean Megason, PhD, at Harvard Medical School, Cambridge, is focusing on genes in the bHLH family and their role in signal integration to help decide whether cells grow and divide, differentiate, migrate, or even die. bHLH genes are involved in fate choices in stem cells of the brain, intestines, skin, and other tissues. They are also commonly misregulated in cancers, such as neuroblastomas and glioblastomas. By comparing signal integration by bHLH circuits in normal and cancer cells, Dr. Nandagopal aims to discover how errors in fate decisions occur, and how they can be corrected.
Trang Nguyen, PhD, with her sponsor Arthur Weiss, MD, PhD, at University of California, San Francisco, is focusing on the key molecular pathways involved in T-cell unresponsive states, which prevents a full immune response against cancer. Within the suppressive cancer environment, T cells stop recognizing and fighting cancer cells. Dr. Nguyen is examining new genes and pathways that activate T cells and overcome the defects of unresponsive T cells. The insights gained from these studies may inspire new therapeutic strategies for cancer immunotherapy.
Christopher Wilson, PhD [Marion Abbe Fellow] with his sponsor David R. Liu, PhD, at Harvard College, Cambridge, is developing molecular tools to specifically modify RNA as a potential pathway to novel cancer therapeutics. RNA modification affects RNA fate and influences the way genes are expressed, including cell cycle control, cell differentiation, and transcript stability, which have been linked to a variety of diseases, including cancer. Dr. Wilson aims to use the CRISPR/Cas9 homologs to alter RNA translation, ultimately leading to an increased understanding of the role of the transcriptome-- all of the messenger RNA molecules expressed from the genes of an organism.
Dian Yang, PhD, with his sponsors Jonathan S. Weissman, PhD, and Trever G. Bivona, MD, PhD, at University of California, San Francisco, is examining tumor heterogeneity in search of new diagnostic markers and potential therapeutic targets. A tumor consists of not only cancer cells, but also immune cells, fibroblasts and other stromal components. The diverse cell types and cell states may promote disease progression and lead to therapeutic resistance, which is one of the greatest challenges in precision medicine. Dr. Yang aims to understand how heterogeneity is generated and regulated by using single cell functional genomic tools.
Xiaoyu Zhang, PhD, with his sponsor Benjamin F. Cravatt, PhD, at The Scripps Research Institute, La Jolla, is developing small molecules that promote targeted protein degradation in human cancers. Although targeted cancer therapies have been successful in recent years, many oncogenic proteins are still considered "undruggable" because the conventional drug design strategy often fails to interfere with these proteins. One potential way to address "undruggable" oncogenic proteins may be to create a new type of bifunctional small molecule that delivers these proteins to the cellular degradation system, therefore promoting their destruction.
Yuxiang Zhang, PhD [HHMI Fellow] with his sponsor Frederick W. Alt, PhD, at Boston Children's Hospital, Boston, is studying the mechanisms that promote recurrent DNA double strand break clusters (RDCs) in the brain and liver, and how these breaks in the DNA are repaired to maintain genomic stability and suppress tumors. Recently, RDCs were found in neural stem and progenitor cells. This work may reveal if DNA breaks in RDC genes predispose individuals to genomic variations that could contribute to cancers and other diseases.
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 nearly $355 million and funded nearly 3,700 young scientists. This year, it will commit approximately $18 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.
Yung S. Lie, PhD
Deputy Director and Chief Scientific Officer
Damon Runyon Cancer Research Foundation