Postdoctoral Associate
I am a microbiologist/immunologist with background in host-pathogen interactions and in molecular immunology that spans over 10 years of training. My doctoral work led to the discovery of how virulence factors activate inflammation responses in macrophages, and these findings impact our understanding of how we can develop therapeutics suitable for auto-immune diseases. With my thorough understanding that the immune system is a principal site that determines disease prognosis, I became motivated to pursue the study of its molecular regulation in pancreatic cancer, based on its high resistant to the best standard-of-care therapeutics we have and very short survival. In addition, while immunotherapy has shown promise in many cancers, pancreatic cancer is refractory to the current best immunotherapies available, suggesting that additional work is required to understand what makes the immune system in pancreatic cancer different and whether these differences can reveal therapeutic opportunities.
My goal as a scientist is to understand essential mechanisms that can serve as targets for the development of new and more effective therapies to fight acute and chronic diseases. As a James Hudson Brown - Alexander Brown Coxe postdoctoral fellow in the lab of Dr. Luisa Escobar-Hoyos, and based on my lab’s prior work that uncovered the importance of altered RNA splicing in pancreatic cancer biology and that this aberrant process leads to a diversified proteome in PDAC cells, my ongoing studies seek to determine how mutations in critical proteins that control splicing, such as the splicing factor SF3B1, can drive tumorigenesis and alter the expression of proteins that signal to the immune system. Through understanding these mechanisms, we hope to test novel anti-splicing therapies to disrupt tumor growth and sensitize pancreatic cells to be recognized and targeted by the immune system.
My laboratory discovered that pancreatic cancer cells with activating mutations in p53 change mRNA splicing to promote the expression of isoform proteins that license tumors to be more aggressive and less responsive to current standard-of-care treatment. We also found that targeting the spliceosome and the aberrant RNA splicing events are novel therapeutic approaches that prevent tumor growth and extend animal survival, suggesting novel therapeutic strategies for tumors with these alterations in PDAC patients.