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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Annals of oncology 8 (1997), S. 1023-1029 
    ISSN: 1569-8041
    Keywords: double-staining ; glioma ; growth factors ; immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Growth factors play a role in proliferation and motility of malignant glial cells, through autocrine and paracrine mechanisms. Also, proliferation of non-tumour cells, e.g., endothelial cells, is likely to be controlled by growth factors. Several growth factors with their appropriate receptors can be involved, but studies on tissue specimens evaluating this in glioma are rare. Materials and methods: We evaluated the potential role of Transforming growth factor-α (TGF-α) and Epidermal growth factor receptor (EGF-R), the Platelet-derived growth factor A- and B-chain (PDGF-A and PDGF-B) and its receptors (PDGFRα and PDGFRβ), and basic fibroblast growth factor (bFGF) in gliomas by analysing 86 of these tumours on the single cell level for the presence of immunoreactive growth factors and receptors. In a few cases double-staining experiments were done to directly visualize co-expression of factor and receptor. Results: Multiple growth factors and their receptors are present in astrocytic tumours; the higher the grade, the more growth factors and the more positive cells are found. Oligodendroglial tumours and pilocytic astrocytomas showed little expression. Autocrine and paracrine mechanisms were frequently possible in the astrocytic tumours, often more than one loop could be involved. Interestingly, it was also frequently possible that non-tumour cells produced a growth factor for which the tumour cells expressed the receptor. Conclusions: Multiple growth factors appear to be involved in astrocytic tumours, with frequent autocrine and paracrine loops. Expression of these molecules seems to increase with increasing grade. The results argue for a contribution of non-tumour cells to the growth of a tumour.
    Type of Medium: Electronic Resource
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