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The stroma of astrocytic tumours has been investigated in the past years by various authors. Among the proteins of the extracellular matrix tenascin is considered a very important molecule because of presumed links with the malignancy of the tumours and with the angiogenesis1 2 and also a possible target for therapy. To verify these opinions we have performed an immunohistochemical analysis of 10 astrocytic tumours of the cerebral hemispheres. The series of patients comprised six men and four women, ranging in age from 43 to 72 years; seven underwent gross total resection and three subtotal resection. The study focused on the following molecules of the extracellular matrix: tenascin, laminin, fibronectin, and type IV collagen. The results were evaluated in relation to the following indices: grading according to the St Anne/Mayo System,3proliferating cell nuclear antigen labelling index,4dimensions of the tumour evaluated radiologically (CT and MRI) and expressed according to the criteria of the manual for staging of cancer by means of the parameter “T”.5
Primary monoclonal antibodies were purchased from Dako and staining was performed by the labelled streptavidin biotin staining method on 10% formalin fixed and paraffin embedded tissue.
The tumours were grade II in two cases (one gemistocytic), grade III in three cases, and grade IV in five cases. Tenascin was present in the extracellular matrix in all grade IV astrocytomas and in the gemistocytic astrocytoma. In two grade III astrocytomas and in all grade IV astrocytomas the basement membranes of the vessels with or without endothelial proliferation showed a positive immunohistochemical staining for tenascin (figure).Tenascin and fibronectin were detected in some neoplastic cells of grade IV tumours and also in the gemistocytes. Laminin, fibronectin, and collagen type IV were found around the vessels of tumours of all grades.The PCNA labelling index was <1% in tumours of grade II and grade III. In grade IV tumours the areas of highest PCNA staining did not correspond to the greater expression of tenascin on serial sections. In some areas with strong staining for tenascin the PCNA labelling index was <5%, whereas the total percentage in grade IV tumours ranged from 5% to 18%.
Evaluation of the parameter “T” failed to provide a correlation between the size of the tumour and the presence of the molecules of the extracellular matrix. For instance, a grade IV tumour evaluated as T1 expressed the tenascin as well as a grade IV tumour evaluated as T4.
In conclusion, we have shown that tenascin does not correlate with the indices of malignancy we have studied—namely, grading, PCNA labelling index, and size of the tumour. The presence of tenascin in the extracellular matrix could only be a signal of progression of astrocytic tumours. This could explain its presence in the gemistocytic astrocytoma, which is well known as a tumour with a high probability of progression.
Furthermore, it is well known in oncology that the size of the tumour must correlate with neoangiogenesis.6 Our hypothesis is that if the expression of tenascin does not correlate with the dimension of the tumour it cannot really correlate with the angiogenesis.
This work was supported by the contribution of the Department of experimental and clinical medicine of the University of Reggio Calabria.
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