In this study we analyzed the expression of mRNA for PDGF-B and PDGF B-type receptor (PDGFrecB) in 42 biopsy specimens from human astrocytic gliomas and other brain tumors. All gliomas expressed PDGF-B mRNA at higher levels than found in peritumoral and normal nervous tissues. Levels of PDGF-B transcripts correlated strongly with those of mRNA for glial fibrillary acidic protein. Thus, the production of PDGF-B mRNA may be attributed mainly to tumoral glial cells. PDGFrecB transcripts were found in 24 out of 29 gliomas, in agreement with the hypothesis of an autocrine growth stimulation in these tumors. Moreover, mean levels of PDGFrecB expression were higher in glioblastomas than in astrocytomas and over 30-fold higher in meningiomas than in gliomas. This suggests that in gliomas PDGFrecB can be expressed also by vascular elements, in agreement with the hypothesized existence of a paracrine mechanism that may be responsible for the endothelial hyperplasias.

Coexpression of platelet-derived growth factor (PDGF) B chain and PDGF B-type receptor in human gliomas.

MAURO, Alessandro;TURCO, Emilia;
1991

Abstract

In this study we analyzed the expression of mRNA for PDGF-B and PDGF B-type receptor (PDGFrecB) in 42 biopsy specimens from human astrocytic gliomas and other brain tumors. All gliomas expressed PDGF-B mRNA at higher levels than found in peritumoral and normal nervous tissues. Levels of PDGF-B transcripts correlated strongly with those of mRNA for glial fibrillary acidic protein. Thus, the production of PDGF-B mRNA may be attributed mainly to tumoral glial cells. PDGFrecB transcripts were found in 24 out of 29 gliomas, in agreement with the hypothesis of an autocrine growth stimulation in these tumors. Moreover, mean levels of PDGFrecB expression were higher in glioblastomas than in astrocytomas and over 30-fold higher in meningiomas than in gliomas. This suggests that in gliomas PDGFrecB can be expressed also by vascular elements, in agreement with the hypothesized existence of a paracrine mechanism that may be responsible for the endothelial hyperplasias.
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432
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MAURO A; BULFONE A; TURCO E; SCHIFFER D
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2318/35604
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