The Damon Runyon Cancer Research Foundation has named 13 new Damon Runyon Fellows, exceptional postdoctoral scientists conducting basic and translational cancer research in the laboratories of leading senior investigators. This prestigious Fellowship encourages the nation's most promising young scientists to pursue careers in cancer research by providing them with independent funding to investigate cancer causes, mechanisms, therapies, and prevention. In July 2023, the Board of Directors announced at 15% increase in the Fellowship stipend, bringing the total to $300,000 over the award's four-year term.

“Over the past three decades, the rate of cancer mortality in the U.S. has dropped by a third, saving an estimated 3.8 million lives. This is because of earlier diagnoses, a better fundamental understanding of the genetic changes that take place in a cancer cell, and personalized treatment options like targeted therapy and immunotherapy. Damon Runyon scientists have been a part of each and every one of these advances,” said Yung S. Lie, PhD, President and CEO of Damon Runyon. “We fund the best young talent—risk takers and innovators. I am confident that because of the research being done by our scientists, this trend will continue, such that ultimately cancer will be a fully treatable disease. My optimism is shared by the cancer research community.”

May 2023 Damon Runyon Fellows

Gabriel Cavin-Meza, PhD [Merck Fellow], with his sponsor Rebecca W. Heald, PhD, at the University of California, Berkeley

Proper cell division, including equal partitioning of DNA into two “daughter” cells, is critical for cell viability. However, many cancers continue to divide despite having atypical numbers of chromosomes and can even contain additional copies of the entire genome (polyploidy). Understanding how large increases in chromosome number affect cell division machinery has been limited by the methods used to generate polyploid cells. Serendipitously, stable polyploidy has arisen in multiple organisms, such as plants, fish, and amphibians. By utilizing the natural polyploidy found in Xenopus clawed frogs (ranging from two copies to twelve copies of the genome), Dr. Cavin-Meza will explore the mechanisms that lead to increased but stable genome size. He will also analyze the proteome across Xenopus species to reveal how proteins have adapted to promote stable polyploidy over time, giving valuable insight into how stable polyploidy could arise in cancers. Dr. Cavin-Meza received his PhD from Northwestern University, Evanston and received his BS from the University of California, San Diego.

Alon Chappleboim, PhD, with his sponsor Sharad Ramanathan, PhD, at Harvard University, Cambridge

Dr. Chappleboim studies how cells communicate during a developmental process called somitogenesis, which drives the formation of repeated structures such as the spinal vertebrae. The signals that guide cell communication during this process can get misinterpreted by cancer cells, resulting in uncontrolled growth. These pathways are implicated in numerous cancer types but are notably associated with colorectal, ovarian, and breast cancer. Using cutting-edge techniques in human stem cells and 3D-models called organoids, along with the tools of computational biology, Dr. Chappleboim aims to deliberately perturb and examine these signaling pathways to gain a comprehensive understanding of how they function. Dr. Chappleboim received his PhD, MS, and BS from Hebrew University of Jerusalem, Jerusalem.

Wei (Will) Chen, PhD, with his sponsor David Baker, PhD, at University of Washington, Seattle

For gene activation, transcription factors (TFs) must bind to enhancers, often with multiple TFs binding at the same site, and recruit other proteins known as cofactors and polymerases. The interactions between TFs and cofactors are usually nonspecific, meaning the cofactors are interchangeable, which limits our understanding of precise gene activation. Dr. Chen will design new proteins that bind the cofactors with high specificity to clarify the contribution of each cofactor. This research will not only provide new insights into the mechanism of gene regulation but also provide new platforms to modulate gene expression with high precision. Dr. Chen received his PhD from the University of Washington, Seattle, his MS from Cornell University, Ithaca and his BS from Shandong University, Jinan.

Anders B. Dohlman, PhD, with his sponsor Matthew L. Meyerson, MD, PhD, at Dana-Farber Cancer Institute, Boston

In many cancer types, microbiota have emerged as an influential component of the tumor environment. Dr. Dohlman studies Fusobacterium nucleatum, a bacterial species that colonizes around half of colorectal tumors. The reasons for F. nucleatum’s preferential colonization of these tissues are poorly understood, and investigating this phenomenon could lead to improvements in cancer diagnosis and treatment. To this end, Dr. Dohlman is using computational methods to study strains of cancer-associated F. nucleatum, searching for genomic features that promote colonization of colorectal cancers. In parallel, he is analyzing the genomes of colorectal tumors to identify genetic changes that in turn promote F. nucleatum colonization. Dr. Dohlman received his PhD from Duke University, Durham and his BA from Wesleyan University, Middletown.

Isabella Fraschilla, PhD [Merck Fellow], with her sponsor Tyler E. Jacks, PhD, at Massachusetts Institute of Technology – MIT, Cambridge

Pancreatic cancer remains unresponsive to current chemotherapy and immunotherapy treatments. However, with the recent development of mRNA vaccines and drugs that target cancer cell mutations, there is hope for a new generation of immune-based therapies. The ability of adaptive immune cells, called cytotoxic T cells, to kill cancer cells is central to anti-tumor immunity. Using mouse models of human pancreatic cancer, Dr. Fraschilla plans to identify the flags presented by cancer cells that enable T cells to recognize them as foreign and kill them. One category of flags that label cancer cells as foreign may be proteins from bacteria that prefer to replicate within the tumor environment. This investigation of cancer cell targets will inform the development of future vaccines to treat cancer and prevent tumor regrowth or metastases. Dr. Fraschilla received her PhD from Harvard University, Cambridge and her BS from Emory University, Atlanta.

Nicole Marie Hoitsma, PhD [HHMI Fellow], with her sponsor Karolin Luger, PhD, at University of Colorado, Boulder

Human cells have complex mechanisms to repair DNA damage, such as that caused by exposure to sunlight or chemical substances. If DNA is not properly repaired, however, it can lead to cancer. In fact, faulty DNA repair has been associated with the initiation and progression of all types of cancer and is often targeted in cancer treatment to stop uncontrolled cell growth. A better understanding of how cells naturally defend against DNA damage will allow for the development of better drugs to treat cancer. Dr. Hoitsma aims to investigate specialized proteins, known as chromatin remodelers, that make damaged DNA accessible for repair. This research will provide insight for the development of novel therapeutic strategies to target these critical pathways. Dr. Hoitsma received her PhD from University of Kansas Medical Center, Kansas City and her BS from South Dakota State University, Brookings.

Lucia Ichino, PhD [HHMI Fellow], with her sponsor Joanna K. Wysocka, PhD, at Stanford University School of Medicine, Stanford

Epithelial to Mesenchymal Transition (EMT) is a crucial biological process that occurs during early development. It allows epithelial cells, which line the inner and outer surfaces of the body, to undergo a profound transformation in cellular identity and migrate and populate the embryo. Unfortunately, numerous cancer types exploit this mechanism, allowing cancer cells to detach from the tissue of origin and disseminate throughout the body, significantly worsening patients’ prognoses. Dr. Ichino is studying the process of developmental EMT with the goal of discovering novel ways to interfere with it in the context of cancer progression. Dr. Ichino’s research takes advantage of a lab-grown system that mimics the EMT and migration of neural cells. Using this system, she plans to study how EMT-promoting transcription factors orchestrate this global change in cellular identity, and how genetic variations can influence this process. Dr. Ichino received her PhD from University of California, Los Angeles and her MS and BS from San Raffaele University, Milan.

Grant Austin King, PhD [HHMI Fellow], with his sponsor Harmit S. Malik, PhD, at Fred Hutchinson Cancer Center, Seattle

Like changes in key genes that control the cell cycle, changes to chromosomes can result in abnormal cell operation and sometimes even cancer. Recently, a new type of genetic change has been linked to diverse cancers: the formation of circular DNA molecules from chromosomes. These molecules, known as extrachromosomal DNA or ecDNA, are dangerous because they do not follow the same rules of inheritance as normal chromosomes. Understanding the behavior of ecDNA within cells may uncover strategies to eliminate ecDNA and restore cellular health. Using a model ecDNA in budding yeast, Dr. King will identify and characterize pathways that either limit or enhance ecDNA propagation. He will then determine whether these pathways play a consistent role in human cancer cells, with the goal of identifying novel therapeutic vulnerabilities in treatment-resistant ecDNA-driven cancers. Dr. King received his PhD from the University of California, Berkeley and his BA from Columbia University, New York.

Fanglue Peng, PhD [Connie and Bob Lurie Fellow], with his sponsor Jason G. Cyster, PhD, at the University of California, San Francisco

Accumulating evidence shows that specialized structures of white blood cells (lymphocytes), named tertiary lymphoid organs (TLOs), can form inside tumors and play a crucial role in fighting cancer progression. Unlocking the formation and functions of TLOs holds great promise for advancing cancer immunotherapy, but studying TLOs remains challenging due to the substantial disparities between humans and animal models. To address this, Dr. Peng will leverage single-cell sequencing data and high-throughput screening methods to investigate a key initiator of TLO formation in human tumors. He further plans to develop innovative genetic models that enable the study of TLOs in a human-specific context within living organisms. By unraveling the intricacies of TLO biology, Dr. Peng aims to uncover novel therapies that can augment cancer immunotherapy and enhance treatment outcomes across various cancer types. Dr. Peng received his PhD from Baylor College of Medicine, Houston and his BS from Zhejiang University, Hangzhou, Zhejiang.

Wendy Xueyi Wang, PhD, with her sponsors Xiao Wang, PhD (Broad Institute), and Jia Liu, PhD (Harvard University), at the Broad Institute, Cambridge

Dr. Wang is investigating how brain cell activity (e.g., neurons “firing”) and the intracellular signaling pathways triggered by this activity influence glioma and pediatric brain cancer development. Using high-throughput approaches to map neuronal activity, gene expression, and cell structure at the single-cell level, Dr. Wang aims to understand the normal progression of these activity-dependent signaling pathways in the healthy brain, and how these mechanisms are hijacked during cancer progression. This work may reveal new molecular and cellular targets and lead to the development of novel therapeutic strategies. Dr. Wang received her PhD and MS from the University of Toronto, Toronto and her BS from the University of Western Ontario, London, Ontario.

Juner Zhang, PhD, with his sponsor Tom W. Muir, PhD, at Princeton University, Princeton

In cells, DNA wraps around a protein complex consisting of proteins called histones. Chemical modifications to histones can affect gene expression, which is key to activating or suppressing cancer progression. Histone monoaminylation, in which an amine (e.g., serotonin, dopamine, or histamine) attaches itself to a histone, is a newfound type of epigenetic modification whose role remains elusive in these processes. Dr. Zhang is using chemical biology tools to study the functions of these modifications as well as their effects on other adjacent, pre-existing cancer-associated modifications. This research may establish a foundation for how this epigenetic modification regulates gene expression and offer insight into the role of amines in the progression of cancer and human neurodegenerative disorders. Dr. Zhang received his PhD from the California Institute of Technology, Pasadena and his BS from Tsinghua University, Beijing.

Pu Zheng, PhD [Fayez Sarofim Fellow], with his sponsor Jonathan S. Weissman, PhD, at the Whitehead Institute for Biomedical Research, Cambridge

Dr. Zheng is dedicated to the development of technologies for studying tumor evolution within their native contexts. Understanding the complex processes of cancer growth and progression requires a deep exploration of the dynamic interactions between tumor cells and the tumor microenvironment. “Spatial-omics” technologies are powerful tools that offer direct visualization of cells and their interactions in natural contexts, enabling systematic investigation of these intricate processes. Dr. Zheng aims to develop novel spatial-omics technologies that combine imaging and gene sequencing approaches to uncover the mechanisms underlying the spatially distinguished features of tumor evolution. Dr. Zheng received his PhD from Harvard University, Cambridge and his BS from Peking University, Beijing.

Ronghui Zhu, PhD [Connie and Bob Lurie Fellow], with his sponsors Alexander Marson, MD, PhD (The J. David Gladstone Institutes), and Jonathan K. Pritchard, PhD (Stanford University School of Medicine), at Gladstone Institutes, San Francisco

Our immune system can help us prevent or slow cancer development. Human CD4+ T cells play critical roles in regulating our immune responses to fight cancer. Upon encountering a pathogen, naïve CD4+ T cells differentiate into different T helper (Th) cells to perform diverse immune-modulatory functions. Variability in this differentiation process is associated with variable responses to cancer immunotherapy. While several genes necessary for differentiation have been identified, researchers lack a comprehensive map and a predictive model of the larger gene regulatory network (GRN) controlling this process. Dr. Zhu plans to combine functional genomics with mathematical modeling to systematically map and model the human CD4+ T cell differentiation GRN and use the GRN model to predict and control the differentiation process. His work promises to provide a quantitative understanding of the CD4+ T cell differentiation process and open up new strategies for safer and more effective cell-based cancer therapy. Dr. Zhu received his PhD from the California Institute of Technology, Pasadena and his BS from Hong Kong University of Science and Technology, Hong Kong.