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. 2013 Oct 17;369(16):1561-3.
doi: 10.1056/NEJMcibr1309402.

Angiogenesis in glioblastoma

Sunit Das, Philip A Marsden

Angiogenesis in glioblastoma

Sunit Das et al. N Engl J Med. .
No abstract available

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Figures

Figure 1
Figure 1. Angiogenesis in Glioblastoma Multiforme
A variety of pathways have been described for the formation of new blood vessels in glioblastoma multiforme. Hypoxic tumor cells, especially those surrounding the necrotic core, release vascular growth factors, such as vascular endothelial growth factor (VEGF), that stimulate the formation of new blood vessels from preexisting normal endothelial cells (Panel A). This process involves both endothelial-cell proliferation and enhanced vascular permeability. New blood-vessel formation also occurs through the recruitment of bone marrow-derived endothelial progenitor cells or through mesenchymal or hematopoietic stem cells (Panel B). These cells migrate from the systemic circulation into the tumors. Recent work shows that glioma stem cells contribute to the formation of tumor blood vessels by differentiating into endothelial cells or pericytes, contractile cells that wrap around the endothelial cells of small blood vessels (Panel C). In the normal brain, the neurovascular unit is composed of neurons, astrocytes, endothelial cells, and pericytes. Pericytes play a critical role in the regulation of blood-vessel function: they control local blood flow and the permeability of the blood–brain barrier, and they communicate directly with endothelial cells through gap junctions and soluble paracrine signals.
See this image and copyright information in PMC

References

    1. Chen J, Li Y, Yu TS, et al. A restricted cell population propagates glioblastoma growth after chemotherapy. Nature. 2012;488:522–6. - PMC - PubMed
    1. Wang R, Chadalavada K, Wilshire J, et al. Glioblastoma stem-like cells give rise to tumour endothelium. Nature. 2010;468:829–33. - PubMed

    1. Ricci-Vitiani L, Pallini R, Biffoni M, et al. Tumour vascularization via endothelial differentiation of glioblastoma stem-like cells. Nature. 2010;468:824–8. [Errata, Nature 2011;469:432, 477:238.]

    1. Soda Y, Marumoto T, Friedmann-Morvinski D, et al. Trans-differentiation of glioblastoma cells into vascular endothelial cells. Proc Natl Acad Sci U S A. 2011;108:4274–80. - PMC - PubMed
    1. Cheng L, Huang Z, Zhou W, et al. Glioblastoma stem cells generate vascular pericytes to support vessel function and tumor growth. Cell. 2013;153:139–52. - PMC - PubMed

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