Jacksonville State University
We are a group of cancer biologists who study the behavior of oncogenes and seek therapeutic targets.
We use cell and molecular biology techniques in combination with bioinformatic analysis to explore cancer’s Achilles heel, such as gene mutations and deregulated signaling pathways. The ultimate goal is to find new biomarkers and drug targets that can be used to battle cancer better.
Our work focuses on sarcomas, a class of life-threatening musculoskeletal tumors in children and young adults, and major research topics are related to:
a) gene fusions and their oncogenic functions
b) regulation of cancer gene expression by histone modifications
c) synergistic drug interactions in cancer treatment
Fusion proteins, often resulting from chromosomal translocations, are hallmark drivers of many sarcomas. We are interested in understanding how fusion proteins deliver signals that transform normal cells into cancer. A major component of our efforts is the application of functional proteomics to map protein interaction networks perturbed by disease-specific fusion events.
Chromatin occurs in two structural states, "closed" and "open", which represent repressive and active gene expression, respectively. While histone deacetylase (HDAC) fosters chromatin condensation, histone acetyltransferase (HAT) acts to relax chromatin structure. We study the relation of HDAC and HAT to the oncogenic activity of fusion proteins in sarcoma cells.
Fusion proteins are appealing targets for sarcoma treatment due to their unique appearance and driver function. However, it is very difficult to disrupt fusion proteins directly. Through genetic and pharmacologic screens, the objective of our study is to find drugs that work coordinately to block the key molecules/pathways dictated by sarcoma cell dependency on fusion proteins.