Abstract
The cellular and molecular events that initiate and promote malignant glioma development are not completely understood. The treatment modalities designed to promote its demise are all ultimately ineffective, leading to disease progression. In this issue of the JCI, Kioi et al. demonstrate that vasculogenesis and angiogenesis potentially play distinct roles in the etiology of primary and recurrent malignant gliomas, suggesting that patient therapy should perhaps be tailored specifically against the predominant vasculature pathway at a given specific stage of gliomagenesis.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Comment
MeSH terms
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Animals
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Anti-HIV Agents
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Antibodies, Neutralizing
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Antineoplastic Agents / pharmacology*
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Antineoplastic Agents / therapeutic use
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Benzylamines
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Bone Marrow Cells / metabolism
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Bone Marrow Cells / pathology
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Brain Neoplasms / metabolism
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Brain Neoplasms / pathology
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Brain Neoplasms / therapy*
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CD11b Antigen / metabolism
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Cell Line, Tumor
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Cell Movement / drug effects
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Cell Movement / radiation effects
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Chemokine CXCL12 / antagonists & inhibitors
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Chemokine CXCL12 / metabolism
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Cyclams
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Glioblastoma / metabolism
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Glioblastoma / pathology
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Glioblastoma / therapy*
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Heterocyclic Compounds / pharmacology*
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Heterocyclic Compounds / therapeutic use
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Humans
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Hypoxia-Inducible Factor 1 / metabolism
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Mice
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Mice, Nude
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Monocytes / metabolism
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Monocytes / pathology
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Neoplasm Recurrence, Local / metabolism
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Neoplasm Recurrence, Local / pathology
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Neoplasm Recurrence, Local / therapy*
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Neoplasm Transplantation
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Neovascularization, Pathologic / metabolism
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Neovascularization, Pathologic / pathology
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Neovascularization, Pathologic / therapy*
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Receptors, CXCR4 / antagonists & inhibitors
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Receptors, CXCR4 / metabolism
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Transplantation, Heterologous
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Whole-Body Irradiation
Substances
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Anti-HIV Agents
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Antibodies, Neutralizing
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Antineoplastic Agents
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Benzylamines
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CD11b Antigen
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CXCR4 protein, human
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CXCR4 protein, mouse
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Chemokine CXCL12
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Cxcl12 protein, mouse
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Cyclams
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Heterocyclic Compounds
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Hypoxia-Inducible Factor 1
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ITGAM protein, human
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Receptors, CXCR4
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plerixafor