Abstract Details Title Implications of TIGAR Within Glioblastoma Multiforme Drug Resistance Topic Neuro-oncology Presentation(s) Neuro-oncology Posters (7:00 AM-5:00 PM) Poster/Presentation Number 002 Objective To establish TIGAR's role in developing drug resistance within glioblastoma multiforme. To offer insights on TIGAR as a possible therapeutic target in the treatment for glioblastoma multiforme. To identify if TIGAR is dependent on p53 expression and whether p53 expression protects against TIGAR overexpression. Background The incidence of glioblastoma multiforme (GBM) has been rising throughout the last decade, yet interventional medical advances have not been able to keep up. With current literature focusing on hypoxia-inducible factor 1 and angiogenic properties of GBM, our study focuses on Tp53 glycolysis and apoptosis regulator (TIGAR) enzyme to supplement the limited amount of published literature. Recent literature implicates Tp53 glycolysis and apoptosis regulator (TIGAR) in tumor survival based on its function to shunt glycolytic intermediates to generate NADPH. We plan to fill in the gaps and determine if TIGAR protects GBM from therapeutic intervention. In hope to implicate TIGAR as a therapeutic target in the treatment of GBM. Design/Methods Both p53 and TIGAR protein expression were confirmed using western blot throughout the GBM subtypes. An MTT assay determined the minimal concentration of pifithrin-? required to inhibit p53 expression within live cultures of GBM. RT-PCR followed to monitor TIGAR expression after nullification of p53. Cells with nullified p53 were exposed to oxidative stress to establish a survival curve. A known p53 null line, SAOS-2, was used to monitor TIGAR expression using rt-PCR to determine p53 expression dependence. Results Throughout the cell cultures, p53 is absent in the proneuronal subtype of GBM. Western blot confirmed the absence of p53 and the presence of TIGAR in this cell line. GBM cells with increased TIGAR expression were more resistant to oxidative stress. Lastly p53 has minimal influence on the transcription of TIGAR. Conclusions We hypothesize that targeting TIGAR may make GBM more susceptible to modern treatment and decrease likelihood of recurrence. Authors/Disclosures Joseph Sahagun PRESENTER Mr. Sahagun has nothing to disclose.