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Mechanisms of neovascularization and resistance to anti-angiogenic therapies in glioblastoma multiforme.

Al's Comment:

 This is the type of thinking I love to see.  I have always thought that the cure is going to be in a well thought out cocktail of drugs - such as an anti-angiogenesis drug which does work pretty well for a while, as well as targetted therapies that shut down all of the possible resistance pathways. Perhaps throw in other treatments such as vaccines and tumor treating fields and we may hit a home run someday soon.


Posted on: 03/24/2013

J Mol Med (Berl). 2013 Mar 20. [Epub ahead of print]
Mechanisms of neovascularization and resistance to anti-angiogenic therapies in glioblastoma multiforme.
Soda Y, Myskiw C, Rommel A, Verma IM.
Laboratory of Genetics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA, 92037, USA.
 
Abstract
Glioblastoma multiforme (GBM) is the most malignant brain tumor and highly resistant to intensive combination therapies. GBM is one of the most vascularized tumors and vascular endothelial growth factor (VEGF) produced by tumor cells is a major factor regulating angiogenesis. Successful results of preclinical studies of anti-angiogenic therapies using xenograft mouse models of human GBM cell lines encouraged clinical studies of anti-angiogenic drugs, such as bevacizumab (Avastin), an anti-VEGF antibody. However, these clinical studies have shown that most patients become resistant to anti-VEGF therapy after an initial response. Recent studies have revealed some resistance mechanisms against anti-VEGF therapies involved in several types of cancer. In this review, we address mechanisms of angiogenesis, including unique features in GBMs, and resistance to anti-VEGF therapies frequently observed in GBM. Enhanced invasiveness is one such resistance mechanism and recent works report the contribution of activated MET signaling induced by inhibition of VEGF signaling. On the other hand, tumor cell-originated neovascularization including tumor-derived endothelial cell-induced angiogenesis and vasculogenic mimicry has been suggested to be involved in the resistance to anti-VEGF therapy. Therefore, these mechanisms should be targeted in addition to anti-angiogenic therapies to achieve better results for patients with GBM.
 
 PMID: 23512266 [PubMed - as supplied by publisher] 
 

 


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