Abstract
Background & Objective: Gliomas constitute 81% of malignant brain tumors and exhibit a poor prognosis. Two main events involved in the progression of gliomas are the deregulation of genes via genetic events and the cellular damage resulting from the formation of reactive oxygen species (ROS). In gliomas, epigenetic abnormalities implicated in the deregulation of deoxyribonucleic acid (DNA) methylation, nucleosome rearrangement, and acetylation of histones, have been depicted. The overproduction of ROS has been implicated in the promotion of these modifications.
Conclusion: In this review, we discuss the epigenetic mechanisms and oxidative events that impact gene silencing and its association with the establishment and development of gliomas. Some of these epigenetic marks, or their related proteins, are under investigation for their potential use as biomarkers in clinical trials to propose personalized therapies for patients with glioblastoma.
Keywords: Brain tumors, clinical trials, epigenetics, glioma, malignant, oxidative stress.
Graphical Abstract
CNS & Neurological Disorders - Drug Targets
Title:Role of Epigenetics and Oxidative Stress in Gliomagenesis
Volume: 16 Issue: 10
Author(s): Yesennia Sanchez-Perez, Ernesto Soto-Reyes, Claudia M. Garcia-Cuellar, Bernardo Cacho-Diaz, Abel Santamaria and Edgar Rangel-Lopez*
Affiliation:
- National Institute of Neurology and Neurosurgery, Laboratory of Excitatory Amino Acids. Av. Insurgentes Sur #3877 Col. La Fama. Delegacion Tlalpan, C.P. 14269 Mexico City,United States
Keywords: Brain tumors, clinical trials, epigenetics, glioma, malignant, oxidative stress.
Abstract: Background & Objective: Gliomas constitute 81% of malignant brain tumors and exhibit a poor prognosis. Two main events involved in the progression of gliomas are the deregulation of genes via genetic events and the cellular damage resulting from the formation of reactive oxygen species (ROS). In gliomas, epigenetic abnormalities implicated in the deregulation of deoxyribonucleic acid (DNA) methylation, nucleosome rearrangement, and acetylation of histones, have been depicted. The overproduction of ROS has been implicated in the promotion of these modifications.
Conclusion: In this review, we discuss the epigenetic mechanisms and oxidative events that impact gene silencing and its association with the establishment and development of gliomas. Some of these epigenetic marks, or their related proteins, are under investigation for their potential use as biomarkers in clinical trials to propose personalized therapies for patients with glioblastoma.
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Cite this article as:
Sanchez-Perez Yesennia, Soto-Reyes Ernesto , Garcia-Cuellar M. Claudia, Cacho-Diaz Bernardo , Santamaria Abel and Rangel-Lopez Edgar *, Role of Epigenetics and Oxidative Stress in Gliomagenesis, CNS & Neurological Disorders - Drug Targets 2017; 16 (10) . https://dx.doi.org/10.2174/1871527317666180110124645
DOI https://dx.doi.org/10.2174/1871527317666180110124645 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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