Abstract
Glioblastoma Multiforme (GBM) tumors are the most common type of brain tumors. These tumors are in general very malignant and can be characterized as rapidly progressive astrocytomas. The pathological characteristics of these tumors are exemplified by an active invasiveness, necrosis and a specialized form of angiogenesis, known as microvascular hyperplasia. These pathological features are thought to be due to tissue hypoxia. Cells that are under hypoxic stress can either develop an adaptive response that includes increasing the rate of glycolysis and angiogenesis or undergo cell death by promoting apoptosis and/or necrosis. The ability of tumor cells to maintain a balance between an adaptation to hypoxia and cell death is regulated by a family of transcription factors called hypoxia-inducing factors (HIF), which are essential for the regulation of the expression of a large number of hypoxia-responsive genes. The hypothesis that tumor hypoxia would facilitate the likelihood of metastases, tumor recurrence, resistance to chemotherapy and radiotherapy and the invasive potential; all of which culminate in a decrease in patient survival. In this review we will summarize the role of hypoxia in GBM with regard to drug therapy and toxicity and attempt to describe the possible interactions between hypoxia and apoptosis.
Current Molecular Pharmacology
Title: Hypoxia and the Malignant Glioma Microenvironment: Regulation and Implications for Therapy
Volume: 2
Author(s): L. Oliver, C. Olivier, F. B. Marhuenda, M. Campone and F. M. Vallette
Affiliation:
Keywords: Apoptosis, hypoxia, glioma
Abstract: Glioblastoma Multiforme (GBM) tumors are the most common type of brain tumors. These tumors are in general very malignant and can be characterized as rapidly progressive astrocytomas. The pathological characteristics of these tumors are exemplified by an active invasiveness, necrosis and a specialized form of angiogenesis, known as microvascular hyperplasia. These pathological features are thought to be due to tissue hypoxia. Cells that are under hypoxic stress can either develop an adaptive response that includes increasing the rate of glycolysis and angiogenesis or undergo cell death by promoting apoptosis and/or necrosis. The ability of tumor cells to maintain a balance between an adaptation to hypoxia and cell death is regulated by a family of transcription factors called hypoxia-inducing factors (HIF), which are essential for the regulation of the expression of a large number of hypoxia-responsive genes. The hypothesis that tumor hypoxia would facilitate the likelihood of metastases, tumor recurrence, resistance to chemotherapy and radiotherapy and the invasive potential; all of which culminate in a decrease in patient survival. In this review we will summarize the role of hypoxia in GBM with regard to drug therapy and toxicity and attempt to describe the possible interactions between hypoxia and apoptosis.
Export Options
About this article
Cite this article as:
Oliver L., Olivier C., Marhuenda B. F., Campone M. and Vallette M. F., Hypoxia and the Malignant Glioma Microenvironment: Regulation and Implications for Therapy, Current Molecular Pharmacology 2009; 2 (3) . https://dx.doi.org/10.2174/1874467210902030263
DOI https://dx.doi.org/10.2174/1874467210902030263 |
Print ISSN 1874-4672 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-4702 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Recent Advances in Luminescent Carbon Dots
Current Analytical Chemistry Divergent Synthesis of Novel Dienylbenzothiazoles and Arylidenedibenzoxazepines and Evaluation of Their Antiproliferative and Cytotoxic Properties
Letters in Organic Chemistry Mechanisms of Action and Chemical-Biological Interactions Between Ozone and Body Compartments: A Critical Appraisal of the Different Administration Routes
Current Drug Therapy Prolyl-Specific Peptidases and Their Inhibitors in Biological Processes
Current Chemical Biology Himalayan Plants as a Source of Anti-Cancer Agents: A Review
The Natural Products Journal Gliomas: Current Issues in Diagnosis and Treatment
Current Medical Imaging Modulation of Nitric Oxide Pathway by Multiligands/RAGE Axis: A Crossing Point on the Road to Microvascular Complication in Diabetes
Current Enzyme Inhibition MicroRNAs as Regulators in Normal Hematopoietic and Leukemia Stem Cells: Current Concepts and Clinical Implications
Current Molecular Medicine Combined Treatment with JFKD and Gefitinib Overcomes Drug Resistance in Non-Small Cell Lung Cancer
Current Pharmaceutical Biotechnology Immune Checkpoint Inhibitors: Basics and Challenges
Current Medicinal Chemistry Multidisciplinary Cancer Therapy with Telomerase-Specific Oncolytic Adenovirus
Current Cancer Therapy Reviews Protein-Modified Magnetic Nanoparticles for Biomedical Applications
Current Organic Chemistry Therapeutic Application of Natural Medicine Monomers in Cancer Treatment
Current Medicinal Chemistry The Coordinated Role of CYP450 Enzymes and P-gp in Determining Cancer Resistance to Chemotherapy
Current Drug Metabolism Meet Our Editorial Board Member
Letters in Drug Design & Discovery Targeting the Tumor Proteasome as a Mechanism to Control the Synthesis and Bioactivity of Matrix Macromolecules
Current Molecular Medicine Cellular Immunotherapy for Neuroblastoma: A Review of Current Vaccine and Adoptive T Cell Therapeutics
Current Pharmaceutical Design Indoleamine 2,3-dioxygenase (IDO): Biology and Target in Cancer Immunotherapies
Current Cancer Drug Targets Improvement of Nonviral Gene Therapy by Epstein-Barr Virus (EBV)-based Plasmid Vectors
Current Gene Therapy Restoring TRAIL Induced Apoptosis Using Naturopathy. Hercules Joins Hand with Nature to Triumph Over Lernaean Hydra
Current Genomics