The Damon Runyon Cancer Research Foundation has selected 14 postdoctoral scientists as its May 2026 Fellows, awarding each researcher independent support to pursue high-risk, potentially transformative studies in cancer biology, immunology, metabolism, development, and infectious disease. The four-year fellowship provides $300,000, giving early-career scientists the freedom to investigate questions that may be difficult to fund through conventional grant programs. Working in laboratories led by prominent investigators across the United States, the new Fellows will examine how cancer cells reprogram genomes, evade immune attack, alter metabolism, and exploit mechanisms normally used by healthy tissues.
The fellowship arrives at a moment when cancer research is increasingly shaped by connections between disciplines once treated as separate. Cancer is not only a disease of uncontrolled cell division; it is also a disease of altered gene regulation, disrupted communication between organs, immune dysfunction, metabolic rewiring, and persistent interactions with infectious agents. The new projects reflect that broader view. Several researchers will study the regulatory architecture that determines which genes are active, while others will develop technologies for mapping cell surfaces, identify hidden immune targets, or investigate the molecular machinery that makes tumors vulnerable to treatment. Together, the projects illustrate how fundamental biology can generate new routes toward prevention, diagnosis, and therapy.
Nicholas Aboreden, PhD, a Robertson Foundation Fellow working with Kimberly Stegmaier, MD, at Dana-Farber Cancer Institute, will investigate the poorly understood regulatory elements known as silencers. Although only about 2 percent of the human genome encodes proteins, much of the remaining sequence controls when genes are activated or repressed. Cancer cells frequently exploit enhancers to increase the expression of growth-promoting genes, but the mechanisms by which they use silencers to maintain malignancy remain less clear. Aboreden will map the regulatory genome of an aggressive pediatric leukemia marked by widespread gene repression. By identifying silencer elements essential for the leukemia state, he hopes to uncover vulnerabilities that can be targeted without damaging normal cells. His work could also clarify how gene repression contributes to other tumor types.
At the California Institute of Technology, Timmerman Traverse Fellow Shihui Chen, PhD, will explore the relationship between embryonic development and cancer. During early embryogenesis, genetically identical cells acquire different identities through carefully coordinated changes in gene expression. Similar developmental programs can be reactivated in cancer, allowing malignant cells to adopt abnormal states and invade surrounding tissues. Working with Magdalena Zernicka-Goetz, PhD, Chen will use mouse embryos to study CARM1, a gene regulator frequently overexpressed in human tumors. She will determine how CARM1 influences early cell-fate decisions and how the same regulatory logic may be hijacked during cancer initiation. At The J. David Gladstone Institutes, Timmerman Traverse Fellow Stephanie A. Gaglione, PhD, will pursue another underexplored dimension of tumor biology: cryptic antigens. These immune targets arise from unusual or noncoding regions of viral and tumor genomes and may be shared among patients. With Alexander Marson, MD, PhD, Gaglione will profile the antigens displayed by virally driven cancers and identify those capable of stimulating tumor-specific T cells. The results could support engineered T-cell therapies and cancer vaccines directed at targets that conventional approaches overlook.
Several Fellows are developing tools to see cancer biology at unprecedented molecular resolution. Connie and Bob Lurie Fellow Yi Hua, PhD, working with Alice Y. Ting, PhD, at Stanford University School of Medicine, plans to create SortID, a labeling technology based on an engineered bacterial enzyme. The method is designed to rapidly label exposed protein residues on cell surfaces without requiring researchers to attach pre-existing molecular tags. Hua will use SortID to map the surface of SLAMF7, a protein already considered an important therapeutic target in multiple myeloma. A detailed map of the protein’s interactions could reveal how tumor cells communicate with immune cells and identify opportunities for more selective immunotherapies. At Stanford, Lurie Fellow Zhuoran Li, PhD, will examine a different communication system: peptide hormones produced by the brain. Computational analyses suggest that the brain generates many previously unrecognized peptides, but their biological functions remain unknown. Working with Katrin J. Svensson, PhD, Li will identify these signals and determine how they influence appetite and whole-body metabolism, potentially revealing brain–tumor connections relevant to the well-being of cancer patients.
Other projects focus on the molecular systems that determine whether cells survive stress or become malignant. Devon Jeltema, PhD, at the University of California, Berkeley, will study how PARP enzymes modify RNA. PARPs are best known for chemically modifying proteins involved in DNA repair and cellular stress responses, and several PARP inhibitors are already used in cancer treatment. Jeltema’s research will investigate whether RNA modification represents an additional layer of immune defense against viral infection and cancer. By combining biochemical experiments with sequencing technologies, she aims to map modified RNA molecules and determine how these chemical marks alter immune signaling. At The Rockefeller University, Hope Funds for Cancer Research Fellow Jaejin Kim, PhD, will investigate how tissues retain molecular memories of inflammation. Conditions such as eczema, psoriasis, and inflammatory bowel disease can recur in the same anatomical locations, suggesting that stem cells preserve information about previous injury. Kim, working with Elaine Fuchs, PhD, will identify the genes and mechanisms that encode these memories and distinguish beneficial regenerative responses from persistent programs that increase cancer risk.
Metabolism is another central theme among the new fellowships. At The J. David Gladstone Institutes, Connie and Bob Lurie Fellow Rachael A. McMinimy, PhD, will study the pyruvate dehydrogenase complex, an enzymatic switch that determines whether glucose-derived carbon enters mitochondrial respiration. Normal cells often use mitochondria to generate energy efficiently, while many cancer cells redirect glucose through alternative pathways that support rapid proliferation and the production of cellular building blocks. McMinimy is investigating a newly identified mechanism that regulates the pyruvate dehydrogenase complex through selective protein degradation. Manipulating this pathway could force tumor cells to rely more heavily on mitochondrial metabolism and reduce their ability to grow. At Stanford, Robertson Foundation Fellow Gayathri Muthukumar, PhD, will examine post-translational modifications on cell-surface and intracellular membrane proteins. Tumor cells often carry unusually dense coatings of sugar molecules, known as glycans, which may alter signaling and help cancers avoid immune attack. Muthukumar will combine molecular mapping with precision genetic screens to determine which modifications promote oncogenesis. The findings could yield new therapeutic targets and diagnostic markers.
At the Massachusetts Institute of Technology, Timmerman Traverse Fellow Angelos Pistofidis, PhD, will investigate transcription termination factor 2, or TTF2, a protein involved in the mechanics of cell division. During mitosis, duplicated chromosomes must be compacted and accurately separated so that each daughter cell receives a complete genome. Alterations in TTF2 have been linked to defective chromosome segregation, DNA damage, and cell death, and many cancers appear to depend on the protein for survival. Pistofidis will use structural biology, biochemistry, and single-molecule biophysics to determine how TTF2 functions at the molecular level and identify weaknesses that could be exploited by future drugs. At Columbia University, National Mah Jongg League Fellow Christina A. Stephens, PhD, will study adhesion G protein-coupled receptors, or aGPCRs, a class of surface proteins increasingly associated with cancer. These receptors can influence cell growth and communication, but their activation mechanisms remain obscure. Using single-molecule microscopy and molecular dynamics simulations, Stephens will define how aGPCRs switch between inactive and active states and use that information to optimize therapeutic strategies against tumors carrying these receptors.
Two Fellows will investigate problems at the intersection of cancer and infectious disease. At The Rockefeller University, Timmerman Traverse Fellow Bailey Schultz, PhD, will study the growth and division of Mycobacterium tuberculosis, the bacterium responsible for tuberculosis. Approximately one-quarter of the global population is estimated to have been infected with M. tuberculosis, and the disease kills more people than any other pathogen. Tuberculosis and cancer intensify one another: previous infection is associated with increased risk of some cancers, while tumors and chemotherapy can weaken immunity and make infection more dangerous. Some cancer immunotherapies may also reactivate dormant tuberculosis. Schultz will use genome-wide CRISPR-based approaches to identify bacterial genes that control cell growth and division, pointing to potential drug targets while anticipating genetic routes to antibiotic resistance. At Weill Medical College of Cornell University, Robertson Foundation Fellow Yang Su, PhD, will focus on c-MYC, a master regulator of cancer growth that has long been considered difficult to drug directly. Su will investigate a newly described form of chemical modification in c-MYC messenger RNA involving the addition of two methyl groups. Determining which enzyme installs the modification and how it changes c-MYC stability or activity could expose a new strategy for suppressing tumors driven by this oncogene.
The final project addresses the evolution of cancer within individual tumors. At Dana-Farber Cancer Institute, Robertson Foundation Fellow Shuya Wang, PhD, will work with David S. Pellman, MD, to understand how genome instability creates epigenetic diversity. Cancer cells in the same tumor can activate different genes, enabling some subpopulations to survive treatment, adapt to changing conditions, or become more aggressive. Wang will identify the genes and pathways that connect genomic instability with changes in the epigenome, the regulatory layer that controls gene activity without altering the underlying DNA sequence. Understanding how this heterogeneity arises could reveal ways to slow tumor evolution and treatment resistance. “There’s so much talent and excitement and passion and energy at this stage of a scientist’s career,” said current Damon Runyon-Timmerman Traverse Fellow Antonio J. LaPorte, PhD, emphasizing the importance of independent support for young investigators. Yung S. Lie, PhD, President and CEO of Damon Runyon, said the Foundation remains committed to backing researchers whose discoveries in prevention, diagnostics, and therapeutics might otherwise go unfunded. Since its founding in 1946, Damon Runyon says it has invested more than $491 million in nearly 4,100 scientists, including 13 researchers who later received Nobel Prizes.
Web References: http://damonrunyon.org/
Keywords: Damon Runyon Cancer Research Foundation, cancer research, postdoctoral fellows, cancer biology, cancer immunotherapy, gene regulation, epigenetics, cancer metabolism, tuberculosis, molecular therapeutics, CARM1, c-MYC, TTF2, cryptic antigens, RNA modification
Tags: cancer biology and immunologycancer cell reprogrammingcancer metabolism and gene regulationcancer research fellowshipscancer research fundingearly-career cancer scientistsImmune Evasion Mechanismsinfectious disease and cancerinnovative cancer research projectsmultidisciplinary cancer studiestransformative cancer research studiestumor vulnerability and treatment
