Hypoxia and the malignant glioma microenvironment : regulation and implications for therapy

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.

Medienart:

E-Artikel

Erscheinungsjahr:

2009

Erschienen:

2009

Enthalten in:

Zur Gesamtaufnahme - volume:2

Enthalten in:

Current molecular pharmacology - 2(2009), 3 vom: 15. Nov., Seite 263-84

Sprache:

Englisch

Beteiligte Personen:

Oliver, L [VerfasserIn]
Olivier, C [VerfasserIn]
Marhuenda, F B [VerfasserIn]
Campone, M [VerfasserIn]
Vallette, F M [VerfasserIn]

Themen:

Hypoxia-Inducible Factor 1
Journal Article
Research Support, Non-U.S. Gov't
Review

Anmerkungen:

Date Completed 02.08.2010

Date Revised 11.11.2019

published: Print

Citation Status MEDLINE

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM193859769