Antiangiogenesis -- therapeutic strategies and clinical implications for brain tumors.
The poor prognosis of patients with malignant brain tumors in spite of aggressive multimodality therapy has led to the search for novel therapeutic strategies. Among the targets for such treatment approaches, tumor angiogenesis has captured the attention of not only the medical field but also of the lay public because of its conceptual departure from traditional methods of cancer therapy. Angiogenesis and vascular proliferation are particularly important in the growth and progression of malignant gliomas and are used as indicators of the degree of malignancy. Recent studies have helped us gain a better understanding of the molecular mediators of this process. It is now evident that after the initial formation of malignancy the continued growth of a glioma is critically dependent on its angiogenic potential. Hence, several approaches to control angiogenesis are being developed and tested. In the present review, we examine some of these approaches from a therapeutic perspective and summarize the findings from early human trials of such agents.
Department of Neuro-Oncology, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA. vpuduval@mdanderson.org
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D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D043168:Angiostatins; D001932:Brain Neoplasms / Q000098:blood supply / Q000188:drug therapy*; D015687:Cell Hypoxia; D002465:Cell Movement / Q000187:drug effects; D002986:Clinical Trials as Topic; D003094:Collagen / Q000627:therapeutic use; D003510:Cyclohexanes; D043169:Endostatins; D016228:Endothelial Growth Factors / Q000037:antagonists & inhibitors; D004730:Endothelium, Vascular / Q000187:drug effects; D015316:Genetic Therapy; D005910:Glioma / Q000098:blood supply / Q000188:drug therapy*; D006801:Humans; D016023:Integrins / Q000037:antagonists & inhibitors; D007372:Interferons / Q000627:therapeutic use; D008222:Lymphokines / Q000037:antagonists & inhibitors; D061965:Matrix Metalloproteinase Inhibitors; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors; D009389:Neovascularization, Pathologic / Q000188:drug therapy*; D000077609:O-(Chloroacetylcarbamoyl)fumagillol; D010446:Peptide Fragments / Q000627:therapeutic use; D010958:Plasminogen / Q000627:therapeutic use; D011379:Prognosis; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D042787:Receptor, TIE-2; D012176:Retinoids / Q000627:therapeutic use; D012717:Sesquiterpenes / Q000627:therapeutic use; D013267:Stilbenes / Q000627:therapeutic use; D013792:Thalidomide / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000627:therapeutic use; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D020533:Angiogenesis Inhibitors; D003510:Cyclohexanes; D043169:Endostatins; D016228:Endothelial Growth Factors; D016023:Integrins; D008222:Lymphokines; D061965:Matrix Metalloproteinase Inhibitors; D009363:Neoplasm Proteins; D010446:Peptide Fragments; D012176:Retinoids; D012717:Sesquiterpenes; D013267:Stilbenes; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D013792:Thalidomide; D043168:Angiostatins; D010958:Plasminogen; D003094:Collagen; D007372:Interferons; D020794:Receptor Protein-Tyrosine Kinases; D042787:Receptor, TIE-2; C058728:fosbretabulin; D000077609:O-(Chloroacetylcarbamoyl)fumagillol