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The p53 Pathway in Glioblastoma

Department of Microbiology, Immunology & Cancer Biology, University of Virginia, Charlottesville, VA 22908, USA
Department of Neurology, University of Virginia, Charlottesville, VA 22908, USA
The Cancer Center, University of Virginia, Charlottesville, VA 22908, USA
Author to whom correspondence should be addressed.
These authors contributed equally to the manuscript.
Cancers 2018, 10(9), 297;
Received: 29 June 2018 / Revised: 17 August 2018 / Accepted: 28 August 2018 / Published: 1 September 2018
(This article belongs to the Special Issue p53 Signaling in Cancers)
The tumor suppressor and transcription factor p53 plays critical roles in tumor prevention by orchestrating a wide variety of cellular responses, including damaged cell apoptosis, maintenance of genomic stability, inhibition of angiogenesis, and regulation of cell metabolism and tumor microenvironment. TP53 is one of the most commonly deregulated genes in cancer. The p53-ARF-MDM2 pathway is deregulated in 84% of glioblastoma (GBM) patients and 94% of GBM cell lines. Deregulated p53 pathway components have been implicated in GBM cell invasion, migration, proliferation, evasion of apoptosis, and cancer cell stemness. These pathway components are also regulated by various microRNAs and long non-coding RNAs. TP53 mutations in GBM are mostly point mutations that lead to a high expression of a gain of function (GOF) oncogenic variants of the p53 protein. These relatively understudied GOF p53 mutants promote GBM malignancy, possibly by acting as transcription factors on a set of genes other than those regulated by wild type p53. Their expression correlates with worse prognosis, highlighting their potential importance as markers and targets for GBM therapy. Understanding mutant p53 functions led to the development of novel approaches to restore p53 activity or promote mutant p53 degradation for future GBM therapies. View Full-Text
Keywords: glioblastoma; wild type p53; mutant p53; gain-of-function glioblastoma; wild type p53; mutant p53; gain-of-function
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Zhang, Y.; Dube, C.; Gibert, M., Jr.; Cruickshanks, N.; Wang, B.; Coughlan, M.; Yang, Y.; Setiady, I.; Deveau, C.; Saoud, K.; Grello, C.; Oxford, M.; Yuan, F.; Abounader, R. The p53 Pathway in Glioblastoma. Cancers 2018, 10, 297.

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