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Correlation between TSP-1, TGF-β and PPAR-γ expression levels and glioma microvascular density
Gliomas are the most common type of primary tumor in the central nervous system and are characterized by abundant capillary angiogenesis. It is important to study the underlying molecular mechanisms of angiogenesis in order to aid the identification of potential therapeutic targets. The aim of the c...
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Published in: | Oncology letters 2014-01, Vol.7 (1), p.95-100 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Gliomas are the most common type of primary tumor in the central nervous system and are characterized by abundant capillary angiogenesis. It is important to study the underlying molecular mechanisms of angiogenesis in order to aid the identification of potential therapeutic targets. The aim of the current study was to investigate the expression levels of thrombospondin-1 (TSP-1), transforming growth factor-β (TGF-β) and peroxisome proliferator-activated receptor-γ (PPAR-γ) in gliomas, and determine their relationships with angiogenesis. Immunohistochemical methods were used to detect TSP-1, TGF-β and PPAR-γ expression levels and to assess microvascular density (MVD) in 99 glioma tissue samples of various grades. The total positive expression rates of TSP-1 and PPAR-γ were 78.4 and 94.1% in low-grade gliomas and 45.8 and 39.6% in high-grade gliomas. These values suggest that their expression negatively correlated with tumor grade. However, TGF-β expression positively correlated with tumor grade; the total positive expression rate of TGF-β in high-grade gliomas (93.8%) was significantly increased compared with that in low-grade gliomas (43.1%). The MVD in the low-grade group was 28±7.2 vessels/field, which was significantly lower than in the high-grade group (45±6.2 vessels/field). TSP-1 and PPAR-γ expression levels were negatively correlated with MVD (P |
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ISSN: | 1792-1074 1792-1082 |
DOI: | 10.3892/ol.2013.1650 |