A family of enzymes called PARPs help cells defend against viruses and other stressors by chemically modifying other molecules. While research on PARPs has historically focused on their modification of proteins, Dr. Jeltema’s research explores the modification of RNA by PARPs. Her project aims to investigate how RNA modification affects immune responses to threats like viral infection and cancer. Using biochemical and sequencing tools to map which RNA molecules are modified, Dr. Jeltema hopes to identify a new facet of immune defense that can be harnessed to treat cancer. Dr. Jeltema received her PhD from the University of Texas Southwestern Medical Center, Dallas, and her BS from Wheaton College, Norton.

The oncogene c-MYC is a “master regulator” that drives aggressive cancer growth but is widely considered “undruggable” due to its lack of an accessible drug-binding pocket. Inside a cell, the levels of c-MYC protein are tightly controlled at both the RNA and protein levels by various chemical modifications. For example, c-MYC messenger RNA (mRNA) is frequently modified with the addition of a methyl group, which typically triggers rapid mRNA decay. Dr. Su and his colleagues recently discovered that c-MYC mRNA can also be decorated with two methyl groups, a completely new class of modification. Crucial questions remain unanswered: What is the biological impact of this modification on c-MYC? Which enzyme installs it? How does it alter c-MYC function? Dr. Su will address these questions using multidisciplinary approaches, revealing a fundamentally new mechanism of c-MYC regulation and paving the way for novel therapeutics designed to interfere with c-MYC modifications in cancer cells. Dr. Su received his PhD from the University of Georgia, Athens, and his BS from Zhejiang University, Hangzhou.

Estimates suggest that a quarter of the world’s population has been infected with Mycobacterium tuberculosis, which causes tuberculosis (TB) and kills more people than any other pathogen. The relationship between TB and cancer is bidirectional: a history of TB is associated with a higher risk of developing cancer (especially respiratory cancers), while many cancers and chemotherapies increase the risk of contracting TB by weakening the immune system, and some immunotherapies can even reactivate dormant TB infections. Better anti-TB drugs are urgently needed, but drug development efforts have been hampered by an incomplete molecular-level understanding of how M. tuberculosis grows and divides. Dr. Schultz is using genome-wide CRISPR-based approaches to identify and study genes that regulate mycobacterial cell growth and division. His work will point to new drug targets and help anticipate possible routes of antibiotic resistance, hopefully leading to new treatments for TB that will ease its burden on cancer patients. Dr. Schultz received his PhD from Harvard University, Cambridge, and his BS from Stanford University, Stanford. 

Normal cells convert glucose into energy via cellular respiration in the mitochondria, but cancer cells often rely on alternative metabolic pathways that support rapid growth. Central to this strategy is the pyruvate dehydrogenase complex, an enzymatic switch that controls how cells use glucose. Dr. McMinimy studies a newly discovered pathway that regulates this switch through selective protein degradation. By understanding and manipulating this pathway, she hopes to redirect cancer cell metabolism back toward the mitochondria, potentially slowing tumor growth. Dr. McMinimy received her PhD from the University of California, Berkeley, and her BA from Oberlin College, Oberlin.

Only two percent of the human genome contains instructions for making proteins. Much of the remaining 98 percent, once referred to as “genomic dark matter,” consists of regulatory elements that act as molecular switches to turn genes on or off. These molecular switches are broadly categorized into two groups: enhancers (on-switches) and silencers (off-switches). While it is well-known that cancers exploit enhancer elements to amplify the expression of growth-promoting genes, silencers remain poorly understood. Dr. Aboreden’s research focuses on the repressive mechanisms that cancer cells use to sustain uncontrolled growth. He is mapping the regulatory genome of an aggressive type of pediatric leukemia characterized by widespread gene repression. By identifying silencer elements that these cancer cells use to maintain a malignant state, his work aims to identify new therapeutic vulnerabilities to selectively target cancer. The insights gleaned from this work will have broad relevance across diverse tumor types. Dr. Aboreden received his PhD from the University of Pennsylvania, Philadelphia, his MS from Johns Hopkins University, Baltimore, and his BS from Liberty University, Lynchburg.

Even within the same tumor, cancer cells can differ in which genes they turn on or off, allowing some cells to adapt, survive treatment, or become more aggressive. These differences are often driven by changes in the epigenome, a layer of regulation that controls gene activity. Dr. Wang’s project explores the origin of epigenetic heterogeneity in cancer, focusing on the role of genome instability in driving epigenetic changes. By identifying the genes and pathways that connect these processes, she aims to better understand how cancer cells generate and maintain epigenetic heterogeneity, revealing new ways to limit tumor evolution, adaptation, and treatment resistance across all cancer types. Dr. Wang received her PhD from the University of California, Los Angeles, and her BS from Emory University, Decatur.

During the first days of embryogenesis, genetically identical cells begin the process of differentiation, switching genes “on” or “off” to establish distinct cell lineages that will ultimately form the embryo and supporting tissues. Aberrant reactivation of these embryonic gene regulatory programs later in life is a hallmark of many cancers. Dr. Chen’s research investigates how genetically identical cells acquire distinct fates during early mammalian development and explores the shared gene regulatory mechanisms that govern both development and cancer. Using mouse embryos as a model system, she will determine how CARM1, a regulator that is frequently overexpressed in human cancers, controls gene expression programs that drive early cell fate decisions. This work will reveal fundamental mechanisms that establish and maintain cellular identity and provide insight into how developmental pathways are hijacked during cancer initiation and progression. Dr. Chen received her PhD from the University of Southern California, Los Angeles, and her BS from Huazhong University of Science and Technology, Wuhan.

Changes in appetite and metabolism can affect how tumors develop, how they progress, and overall patient prognosis. Peptide hormones are small signaling molecules that help organs communicate and coordinate whole-body metabolism. Recent computational studies suggest that the brain may produce many more peptides than previously recognized—yet for most of these, we still do not know what they do, where they act, or how they work together. Dr. Li aims to identify new peptide signals produced by the brain and determine how they affect appetite and regulate metabolism. This work may reveal new brain-body signaling pathways that could ultimately help support cancer treatment and improve patient well-being. Dr. Li received her PhD from Stanford University, Stanford, and her BS from Peking University, Beijing.  

More than half of all FDA-approved biotherapeutics target proteins on the cell surface involved in intercellular communication. The vast majority of these proteins are decorated with post-translational modifications (PTMs), such as the addition of a sugar molecule, but our understanding of how individual PTMs affect communication in a disease context is poor. As aggressive tumors often have surface proteins thickly coated in sugar molecules, they are suspected to play a role in in driving oncogenic growth and tumor immune evasion. Dr. Muthukumar will map cell surface and intracellular membrane PTMs in cancer cells, and then interrogate the role each of these PTMs play in oncogenesis with precise mutational genomic screens. This will highlight the PTMs that drive tumor pathology, allowing for the development of new precision therapeutics and cancer diagnostic markers. Dr. Muthukumar received her PhD from the Massachusetts Institute of Technology, Cambridge, and her BA from Columbia University, New York.

During mitosis, two copies of the genome condense and segregate, a process catalyzed by a protein known as transcription termination factor 2 (TTF2). Mutations in TTF2 have been associated with incomplete genome segregation, DNA damage, and cell death. Research has shown that TTF2 is necessary for many cancers, making it a prime target for future cancer therapeutics. Dr. Pistofidis aims to use a combination of structural biology, biochemistry, and single-molecule biophysics to outline the molecular mechanism of TTF2. Ultimately, this work will reveal vulnerabilities in the mechanism of TTF2 that can be exploited for the development of cancer therapeutics. Dr. Pistofidis received his PhD from McGill University, Montréal, and his MSc from the University College London, London.