Close
Help





JOURNAL

Clinical Medicine Insights: Oncology

Inhibitors of Glioma Growth that Reveal the Tumour to the Immune System

Submit a Paper


Clinical Medicine Insights: Oncology 2011:5 265-314

Review

Published on 21 Sep 2011

DOI: 10.4137/CMO.S7685


Further metadata provided in PDF



Sign up for Email Alerts and keep in touch with Clinical Medicine Insights: Oncology journal news, updates, events and articles

The Editor-in-Chief has endorsed this article

Gliomas is one of the most devastating diseases as they are difficult to treat and with high mortality. The authors conducted a comprehensive review on gliomas with a focus on cellular pathways that mediate tumor proliferation and invasion as well as current therapies on gliomas.

About this endorsement

Abstract

Treated glioblastoma patients survive from 6 to 14 months. In the first part of this review, we describe glioma origins, cancer stem cells and the genomic alterations that generate dysregulated cell division, with enhanced proliferation and diverse response to radiation and chemotherapy. We review the pathways that mediate tumour cell proliferation, neo-angiogenesis, tumor cell invasion, as well as necrotic and apoptotic cell death. Then, we examine the ability of gliomas to evade and suppress the host immune system, exhibited at the levels of antigen recognition and immune activation, limiting the effective signaling between glioma and host immune cells.

The second part of the review presents current therapies and their drawbacks. This is followed by a summary of the work of our laboratory during the past 20 years, on oligosaccharide and glycosphingolipid inhibitors of astroblast and astrocytoma division. Neurostatins, the O-acetylated forms of gangliosides GD1b and GT1b naturally present in mammalian brain, are cytostatic for normal astroblasts, but cytotoxic for rat C6 glioma cells and human astrocytoma grades III and IV, with ID50 values ranging from 200 to 450 nM. The inhibitors do not affect neurons or fibroblasts up to concentrations of 4 µM or higher.

At least four different neurostatin-activated, cell-mediated antitumoral processes, lead to tumor destruction: (i) inhibition of tumor neovascularization; (ii) activation of microglia; (iii) activation of natural killer (NK) cells; (iv) activation of cytotoxic lymphocytes (CTL). The enhanced antigenicity of neurostatin-treated glioma cells, could be related to their increased expression of connexin 43. Because neurostatins and their analogues show specific activity and no toxicity for normal cells, a clinical trial would be the logical next step.



Downloads

PDF  (9.62 MB PDF FORMAT)

RIS citation   (ENDNOTE, REFERENCE MANAGER, PROCITE, REFWORKS)

BibTex citation   (BIBDESK, LATEX)

XML




What Your Colleagues Say About Clinical Medicine Insights: Oncology
It is an honor that my manuscript was accepted by the Clinical Medicine Insights: Oncology.  The comments from reviewers were professional, the emails from the editor were friendly, and the procedure was very quick.  I will submit further manuscripts to Clinical Medicine Insights: Oncology in the near future.
Dr Cheng Tan (Hamamatsu University School of Medicine, Shizuoka, Japan)
More Testimonials

Quick Links


New article and journal news notification services