Natasha Pinto Medici, PhD

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.