Kayla Hernandez-Zirofsky

Glioblastoma is a lethal form of cancer that grows in the brain. Despite radiation therapy, glioblastoma cells continue to survive. Researchers predicted this is due to a mechanism of resistance being exhibited by the tumor cells. The Vanpouille-Box lab’s previous study suggests that a major mechanism of resistance is lipid accumulation and fatty acid pooling. There are two main pathways of this lipid pooling: de novo synthesis mediated by FASN or lipid uptake mediated by CD36. This paper seeks to determine which pathway is responsible for lipid accumulation in irradiated cells to identify a resistance mechanism, which could improve outcomes of radiation treatment for glioblastoma. Mouse cell lines of glioblastoma were used for flow cytometry experiments to determine (1) apoptosis to assess the percent of the inhibition induced in the cells; (2) the accumulation of lipids in the presence of genetic and pharmacological inhibitors of FASN and/or CD36 by BODIPY/lipid intensity; (3) the expression of CD36. The results of this study indicate that FASN inhibition, using the drug Boehringer Ingelheim, is an effective method for increasing cancer cell death and lowering lipid accumulation. Additionally, inhibiting CD36 did not impact cell death or lipid accumulation in this study. In fact, some results suggest that inhibiting CD36 may cause an increase in lipid accumulation. Alongside this research, in vivo studies suggest that treatments with CD36 inhibitors may yield positive survival outcomes. This prompts the investigation of the effect CD36 inhibition has on other aspects of the tumor microenvironment of glioblastomas.

2024 Terra NYC STEM Fair Finalist

2024 JSHS Regional Semi-Finalist

2022 Independent Science Research Award

Research Paper