Abstract

Glioblastoma Multiforme (GBM) is the most lethal subtype of glioma (brain tumor), with a 5-year survival rate of merely 5.6% post diagnosis1. The traditional study of glioblastoma has investigated the role of multiple genes in advancing its progression, including the upregulation of Epidermal Growth Factor Receptor (EGFR). However, there is at yet little research into the epigenetic factors that control EGFR, both in the precursor astrocytes and in glioblastomas themselves2. EGFR and its regulation may play a significant role in the progression and development of GBM from astrocytes. Through modification of genomic pathways as observed in GBM, our lab generated an in vitro glioblastoma model that is representative of the pathways modulated in glioblastoma. The purpose of this study was to investigate the modulation of epigenetic factors that occurs upon conversion from astrocyte to glioblastoma-like cells using epigenetic and expression analysis methods, in hopes of revealing potential therapeutic venues for future study. The study revealed that activating marks present in astrocytes were in fact downregulated in the glioblastoma cells leading to decreased expression of wild-type EGFR mRNA. Further exploration may provide more clues as to why this modulation occurs.

Thesis Completion

2020

Semester

Spring

Thesis Chair/Advisor

Kim, Yoon-Seong

Degree

Bachelor of Science (B.S.)

College

College of Medicine

Department

Burnett School of Biomedical Sciences

Degree Program

Biomedical Sciences

Language

English

Access Status

Open Access

Release Date

5-1-2020

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