Journal
NEUROSURGERY CLINICS OF NORTH AMERICA
Volume 18, Issue 1, Pages 39-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.nec.2006.10.006
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Funding
- NATIONAL CANCER INSTITUTE [R01CA100688, R01CA099489] Funding Source: NIH RePORTER
- NCI NIH HHS [U01 CA894314-1, R01 CA100688, R01 CA099489] Funding Source: Medline
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Platelet-derived growth factor (PDGF) is a growth factor family of ligands and receptors known to activate phosphatidylinositol 3-kinase, mitogen-activated protein kinase, Jak family kinase, Src family kinase, and phospholipase C gamma signal transduction pathways, some of which have been causally linked to glioma formation. Extensive involvement of PDGF in development and its implication in a variety of pathologic conditions, including gliomagenesis, are mediated not only by autocrine effects but by paracrine effects. Many researchers view brain tumors as clonal entities derived from the cancer stem cell; however, recent documentation of the importance of the tumor microenvironment for glioma initiation and progression as well as the ability of neural stem or progenitor cells to migrate toward the sites of injury or tumor formation reveals additional complexities in brain tumorigenesis. Paracrine effects of PDGF in animal models of gliomagenesis, continued adult neurogenesis capable of increasing in response to brain injury, and the growth factor-rich environment of brain tumors suggest that recruitment may play a role in gliomagenesis. In this view, glioma formation involves recruitment of cells from the adjacent brain and possibly other sites.
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