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image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
Neuropathology
Article . 2007 . Peer-reviewed
License: Wiley Online Library User Agreement
Data sources: Crossref
Neuropathology
Article . 2008
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Immunohistochemical evaluation of the microvascular density through the expression of TGF‐β (CD 105/endoglin) and CD 34 receptors and expression of the vascular endothelial growth factor (VEGF) in oligodendrogliomas

Authors: Gabriel Corteze, Netto; Cristina Birlem, Bleil; Arlete, Hilbig; Lígia Maria Barbosa, Coutinho;

Immunohistochemical evaluation of the microvascular density through the expression of TGF‐β (CD 105/endoglin) and CD 34 receptors and expression of the vascular endothelial growth factor (VEGF) in oligodendrogliomas

Abstract

Angiogenesis has been proposed as essential for the growth of solid tumors. The determinants of this process, the growth factors and the vascular endothelial receptors have brought a potential in the tumor prognostic determination as well as perspectives of “targets” for antiangiogenic therapy. In oligodendrogliomas (OL), angiogenesis is little known and/or has generated conflicting results. In order to clarify angiogenesis in OL, we have evaluated the immunohistochemical expression of vascular endothelial growth factor (VEGF) and the microvascular density (MVD) through the expression of TGF‐β (CD105/endoglin) (MVD‐CD105) and CD34 (MVD‐CD34) receptors using the Chalkley point method in 30 OL. No significant immune reaction was found for the VEGF. There was expression in <10% of tumor cells and/or staining of weak intensity in 15 (50.0%), >10% of cells and moderate intensity staining in 1 (3.33%), and negative expression in 14 (46.67%). If present, the expression was restricted to tumor and endothelial cells. Our findings suggest that VEGF has little influence on OL angiogenesis. All specimens showed CD105 and CD34 expression in the intratumor vascular endothelium, suggesting involvement of CD105 in OL angiogenesis. The mean ± SD MVD‐CD105 and MVD‐CD34 were 10.83 ± 2.24 and 11.00 ± 2.76 in OL (P = 0.086; r = 0.319); 10.00 ± 2.00 and 10.40 ± 3.02 in OL grade II (n = 15) (P = 0.547; r = 0.105), and 11.67 ± 2.22 and 11.53 ± 2.45 in OL grade III (n = 15) (P = 0.817; r = 0.551), respectively. The absence of correlation between DMV‐CD105, DMV‐CD34 and tumor grades suggests that anti‐CD105 and anti‐CD34 antibodies have different vascular specificities. MVD‐CD105 was greater in OL grade III than in OL grade II (P = 0.0032), indicating an increase in the vascular neoformation, something which must be evaluated as a possible prognostic factor in OL. Both TGF‐β and CD105 bring perspectives as “targets” for antiangiogenic treatments in OL.

Keywords

Adult, Male, Vascular Endothelial Growth Factor A, Adolescent, Neovascularization, Pathologic, Brain Neoplasms, Oligodendroglioma, Endoglin, Antigens, CD34, Receptors, Cell Surface, Middle Aged, Immunohistochemistry, Antigens, CD, Humans, Female, Endothelium, Vascular, Child, Aged

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
32
Top 10%
Top 10%
Top 10%
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