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Date of Award


Document Type

Restricted Thesis: Campus only access

Degree Name

Bachelor of Science



First Advisor

Valerie Kish


Glial cells are brain cells that provide nutritional, metabolic, and mechanical support to neural tissue. Glial cells can multiply abnormally to create tumors of which the most aggressive is glioblastoma multiforme (GBM). After diagnosis with GBM, patients usually die within two years. P53 is a tumor suppressor protein involved in protecting against the proliferation of potentially tumorigenic cells. It acts primarily as a transcription factor capable of the upregulation of other proteins that are involved in cell cycle control and apoptosis. Loss of function of the P53 protein has been correlated to GBM tumor progression. P53 activity is lost either through mutation of its gene (TP53) or functional inactivation by other cellular factors. An attractive model for treatment of glioblastomas would be to restore the p53 wild-type phenotype to the cells through transfection with exogenous p53. The addition of ionizing radiation following p53 transduction could enhance the effect of the transduced p53 by activating it. This study was aimed at the development of an assay to examine p53 function in the T98G and GEPE glioblastoma cell lines in order to predict the effects of p53 transduction. Toward this end, the p53 gene was cloned from these cell lines and analyzed by sequencing for mutations. T98G-derived p53 contained the characteristic mutation at codon 237 that causes an amino acid substitution from methionine to isoleucine. The gene also contained base substitutions in codons 118 and 119 that cause a silent mutation and an amino acid change from threonine to alanine respectively. GEPE-derived p53 contained a common polymorphism at codon 72 along with 4 other probable mutations, which included a silent mutation at codon 78, an amino acid substitution from threonine to alanine at codon 79 and single base deletions at codons 129 and 141 which result in frameshifts.