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.

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.

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.