Document Detail


Tumor angiogenesis and anti-angiogenic therapy in malignant gliomas revisited.
MedLine Citation:
PMID:  23143192     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The cellular and molecular mechanisms of tumor angiogenesis and its prospects for anti-angiogenic cancer therapy are major issues in almost all current concepts of both cancer biology and targeted cancer therapy. Currently, (1) sprouting angiogenesis, (2) vascular co-option, (3) vascular intussusception, (4) vasculogenic mimicry, (5) bone marrow-derived vasculogenesis, (6) cancer stem-like cell-derived vasculogenesis and (7) myeloid cell-driven angiogenesis are all considered to contribute to tumor angiogenesis. Many of these processes have been described in developmental angiogenesis; however, the relative contribution and relevance of these in human brain cancer remain unclear. Preclinical tumor models support a role for sprouting angiogenesis, vascular co-option and myeloid cell-derived angiogenesis in glioma vascularization, whereas a role for the other four mechanisms remains controversial and rather enigmatic. The anti-angiogenesis drug Avastin (Bevacizumab), which targets VEGF, has become one of the most popular cancer drugs in the world. Anti-angiogenic therapy may lead to vascular normalization and as such facilitate conventional cytotoxic chemotherapy. However, preclinical and clinical studies suggest that anti-VEGF therapy using bevacizumab may also lead to a pro-migratory phenotype in therapy resistant glioblastomas and thus actively promote tumor invasion and recurrent tumor growth. This review focusses on (1) mechanisms of tumor angiogenesis in human malignant glioma that are of particular relevance for targeted therapy and (2) controversial issues in tumor angiogenesis such as cancer stem-like cell-derived vasculogenesis and bone-marrow-derived vasculogenesis.
Authors:
Karl H Plate; Alexander Scholz; Daniel J Dumont
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2012-11-11
Journal Detail:
Title:  Acta neuropathologica     Volume:  124     ISSN:  1432-0533     ISO Abbreviation:  Acta Neuropathol.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-28     Completed Date:  2013-06-10     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  0412041     Medline TA:  Acta Neuropathol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  763-75     Citation Subset:  IM    
Affiliation:
Institute of Neurology (Edinger Institute), Frankfurt University Medical School, Frankfurt, Germany. karl-heinz.plate@kgu.de
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MeSH Terms
Descriptor/Qualifier:
Angiogenesis Inhibitors / therapeutic use*
Brain Neoplasms / blood supply,  drug therapy*,  pathology
Glioma / blood supply,  drug therapy*,  pathology
Humans
Neovascularization, Pathologic / drug therapy*
Signal Transduction / physiology
Chemical
Reg. No./Substance:
0/Angiogenesis Inhibitors
Comments/Corrections

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