Elijah Uribe
Pronouns: hehim
Research Mentor(s): Maria Castro
Research Mentor School/College/Department: Neurosurgery / Medicine
Program: UROPF
Session: Session 4 (1:40pm – 2:30pm)
Authors: Elijah Uribe
Abstract
mIDH1 gliomas start like normal brain tumors, but grow more aggressively due to gain of function mutations. These mutations (TP53 & ATRX) cause an increase in autophagy related genes (Atgs) allowing the tumor to use autophagy to recycle dead cell parts and incorporate them into its mass. Tumor-causing plasmids were transposed into infant mice to grow mIDH1 glioma models. Through analysis of these mIDH1 tumors, it was seen that the gliomas cells were sensitive to autophagy inhibition. In-vivo autophagy blocking via synthetic protein nanoparticles (SPNPs) targeting Atgs proved to increase radiation sensitivity within the glioma cells. These findings suggest that autophagy is a vital part of mIDH1 glioma growth and that by inhibiting it, radiation therapy is more effective resulting in tumor regression, increased survival rate, and a more optimistic prognosis.
