Damon Runyon News

Dr. Yankielowicz-Keren studies cellular changes in breast cancer, the second leading cause of cancer death in women in the U.S. Recently, a new multiplexed ion beam imaging (MIBI) technology has been introduced, which enables simultaneous imaging of dozens of proteins at a single cell level within a tissue section with high sensitivity. She is applying MIBI to study expression patterns of human breast cancer samples in the spatial context of the microenvironment and the interactions with the immune system.

Dr. Flynn aims to understand the interplay between cancer metabolism and RNA biology at the level of protein modifications, such as glycosylation. The use of metabolites to fuel cellular processes including cell division and protein synthesis are critical in both healthy tissue and cancer growth. This work will define glycosylation events that respond to and regulate the cancer state within RNA-based networks, thereby establishing new layers of regulation for future therapeutic targeting.

Dr. Dong studies how injury and pathogen invasion trigger a chain of inflammatory and repair responses that restore the damaged tissue. Defects in wound repair result in painful, non-healing ulcers that frequently affect aged individuals and diabetes patients. Malignant tumors are particularly severe complications, which often occur at sites of repetitive irritation and chronic wounds.

Dr. Chung is focusing on the biology of fat storage organelles called lipid droplets (LDs). Many cancer cells are characterized by an increased number of LDs, and this accumulation has been proposed to be pathogenic. Key questions of LD biology remain unanswered, limiting the potential for therapeutic intervention. She will combine various imaging technologies and biochemical approaches to elucidate the molecular architecture of initial LD formation and its regulation.

Dr. Belyy studies how cancerous cells bypass normal signaling pathways and continue to grow uncontrollably, instead of either repairing themselves or dying in response to “unfolded protein stress.” Under these conditions, normal cells have evolved to sense this type of stress and either fix the problem or, if the fix fails, die in a controlled manner to protect the rest of the organism.

Dr. Burton studies how chemical modification of histone proteins leads to changes in the structure of chromatin, the physiologically relevant form of DNA, and how misregulation of this higher-order assembly can lead to aberrant gene transcription patterns and cancer. He will use chemical biology tools to carry out precise chemistry in live cells, and determine direct causality in the downstream effects on DNA accessibility and transcription.

Dr. Blair aims to address a key bottleneck in drug discovery by developing a generalizable strategy for synthesis of complex natural products to be used as therapeutics. Small molecules created by nature (natural products) often possess extraordinary functional potential and have led to many transformative human medicines. Unfortunately, despite important progress in the field of natural product synthesis, the methods available for synthesizing such complex natural products are typically too slow for practical drug discovery and development.

Dr. Baker seeks to understand the molecular mechanism of how large protein assemblies actively rearrange local areas of chromatin, acting as keystone regulators of gene expression. He focuses on the SWI/SNF family of proteins. Recent genomic studies have shown that nearly 20% of all tumors contain a mutation in SWI/SNF genes. Notably, these mutations frequently result in with aberrant or uncontrolled SWI/SNF activity, suggesting that they could be viable drug targets.

Many cancers result from an alteration in a cell's genetic material or DNA -- the basic instruction manual for life. Even a subtle change in DNA sequence can cause dramatic effects and reprogram normal cells, leading to cancer. While many cancers have genetic components, a more recent paradigm in cancer biology has been the study of cellular reprogramming founded in epigenetic or epitranscriptomic changes, which occur without alteration of the underlying DNA sequence. Dr.

Dr. Watson is taking advantage of high-throughput genetic screens to map gene networks involved in the response to metabolic stress. Cancer cells tap into growth-promoting metabolic programs, enabling them to robustly proliferate using limited resources from the tissue microenvironment and bloodstream. The metabolic plasticity observed in cancer cells can be at least partly attributed to metabolic stress response pathways that enable the cancer to mobilize resources for growth.