摘要: One event that accompanies glioma progression is the upregulation of angiogenesis. Low-grade gliomas are moderately vascularized tumors whereas high-grade show prominent microvascular proliferations and areas high vascular density. To analyze molecular mechanisms underlying angiogenesis, we studied expression endothelial growth factor (VEGF) its tyrosine kinase receptors VEGFR-1 VEGFR-2 during normal brain development glioma-induced Our results suggest a paracrine control angiogenesis cell proliferation tightly regulated transient in embryonic brain, switched off adult turned on tumor cells host vasculature (VEGFR-1 -2) progression. It unknown how VEGF upregulated but there recent evidence as well endogenous inhibitors could be under suppressor genes p53 VHL.
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