Damon Runyon News

Dr. Starr focuses on the process of how the immune system produces antibodies that specifically recognize and bind to antigens on pathogens and cancer cells. He is combining computational analyses of antibody sequences with experimental methods to test the effects of possible mutations on antibody function. This iterative process, similar to what the body does naturally, will help identify the most effective antibodies for an infection.

Dr. Reyes [HHMI Fellow] focuses on Complex-Karyotype Acute Myeloid Leukemia (CK-AML), an aggressive form of AML with poor prognosis and limited treatment options. Dr. Reyes is using mouse models and single-cell technologies to follow the parallel evolution of cancer cells from the time of disease onset until its terminal stage.

Dr. Reimer [Merck Fellow] investigates the cell cytoskeleton which is comprised of a network of microtubules that act as roadways for motor proteins to transport a multitude of different cargoes around the cell. She studies how the motor dynein walks along microtubules to transport cargo from the cell periphery to the interior of the cell. Dynein has essential roles in cell division and is regulated by the protein Lis1. Misregulation of dynein by Lis1 can lead to aberrant cell division and has been implicated in some cancers. Dr.

Dr. Orellana Vinueza is investigating whether changes that modify the shape, stability and function of transfer RNAs (tRNAs) play a role in the development of cancer. The tRNA molecules are involved in the process that translates messenger RNA into a protein. Dr. Orellana Vinueza focuses on a tRNA methyltransferase complex that malfunctions in glioblastoma and liposarcoma. He will assess how alterations in the activity of this enzyme affect global patterns of methylation in normal and human cancer cells.

Dr. Neggers is focusing on validating a new drug target for pancreatic cancer. Using large-scale genetic screening, Dr. Neggers discovered that a subset of cancers, including over 50% of pancreatic cancers, selectively require the VPS4A gene to proliferate and grow. When VPS4A is turned off, the cells stop dividing and die. He will study this vulnerability in clinically relevant patient-derived and mouse models of pancreatic cancer to understand how it functions.

Dr. LaBar [Candy and William Raveis Fellow] is using budding yeast and computational modeling to study the basic processes that determine how cancer cell populations evolve in response their environment. Dr. LaBar aims to understand how the number of cells in a tumor may drive the evolution of cancer cells based on their supply of new mutations.

Dr. Kenney [Merck Fellow] studies how microbes make natural products, a major source of new chemotherapy drug candidates. Dr. Kenney is identifying the chemical reactions used by microbes in nature to synthesize compounds that have the potential to act as chemotherapeutic drugs.

Dr. Hueschen studies the motility of Apicomplexan parasites, which cause malaria, foodborne illness (toxoplasmosis) and infections in immunocompromised cancer patients. These parasites move through the human body using a mechanism called "gliding" to migrate over host cells and through the surrounding extracellular matrix. Dr. Hueschen's goal is to understand how molecules inside the parasite are organized, coordinated and regulated to produce forces that direct movement.

Dr. Chung is developing a new engineering approach to create intelligent and tenacious T cells with durable anti-tumor activity. Her aim is to create enhanced T cells that will infiltrate tumors, kill cancer cells, and persist long-term to prevent recurrence. Dr. Chung will use cutting-edge, multi-disciplinary approaches, including bioinformatics, protein and genetic engineering, and tumor immunology, to design a synthetic T cell differentiation pathway.

Cancers originating from different tissue types harbor distinct genetic mutations. Using molecular and systematic approaches in genetics, Dr. Chiba will dissect the mechanisms of how distinct combinations of oncogenic mutations drive tumors from different tissue origins. Due to the differing genetic background of these tumors, the efficacy of therapies that target the same oncogenic mutations varies between tumor types. Thus, understanding multiple different mutations in a tissue-specific context is critical for effective precision therapies.