Document Detail


Activation of alternative pathways of angiogenesis and involvement of stem cells following anti-angiogenesis treatment in glioma.
MedLine Citation:
PMID:  22419019     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Malignant gliomas are hypervascular tumors that are highly resistant to all the currently available multimodal treatments. Therefore, anti-angiogenic therapies targeting VEGF or VEGF receptors (VEGFRs) were designed and thought to be an effective tool for controlling the growth of malignant gliomas. However, recent results of early clinical trials using humanized monoclonal antibodies against VEGF (Bevacizumab), as well as small-molecule tyrosine kinase inhibitors that target different VEGF receptors (VEGFRs) (Vatalanib, Vandetanib, Sunitinib, Sorafenib, etc) alone or in combination with other therapeutic agents demonstrated differing outcomes, with the majority of reports indicating that glioma developed resistance to the employed anti-angiogenic treatments. It has been noted that continued anti-angiogenic therapy targeting only the VEGF-VEGFR system might affect pro-angiogenic factors other than VEGF, such as basic fibroblast growth factor (bFGF), stromal derived factor 1 (SDF-1) and Tie-2. These factors may in turn stimulate angiogenesis by mobilizing bone marrow derived precursor cells, such as endothelial progenitor cells (EPCs), which are known to promote angiogenesis and vasculogenesis. In this short review, the current antiangiogenic treatments, possible mechanisms of activation of alternative pathways of angiogenesis, and possible involvement of bone marrow derived progenitor cells in the failure of anti-angiogenic treatments are discussed.
Authors:
Ali S Arbab
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Histology and histopathology     Volume:  27     ISSN:  1699-5848     ISO Abbreviation:  Histol. Histopathol.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-03-15     Completed Date:  2012-07-16     Revised Date:  2014-09-12    
Medline Journal Info:
Nlm Unique ID:  8609357     Medline TA:  Histol Histopathol     Country:  Spain    
Other Details:
Languages:  eng     Pagination:  549-57     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Angiogenesis Inhibitors / therapeutic use*
Animals
Glioma / blood supply*,  drug therapy*,  pathology
Hematopoietic Stem Cells / drug effects*,  pathology
Humans
Neovascularization, Pathologic / drug therapy*,  etiology,  pathology
Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors
Vascular Endothelial Growth Factor A / antagonists & inhibitors
Grant Support
ID/Acronym/Agency:
R01 CA122031/CA/NCI NIH HHS; R01 CA122031-04/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Angiogenesis Inhibitors; 0/Vascular Endothelial Growth Factor A; EC 2.7.10.1/Receptors, Vascular Endothelial Growth Factor
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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