Apoptosis in cerebral astrocytic tumours and its relationship to expression of the bcl‐2 and p53 proteins

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Abstract
Apoptosis is an important determinant of tumour growth which can be regulated by the bcl‐2 and p53 genes. This study examines the relationship between apoptosis, growth fraction (Ki‐67 immunolabelling index), and accumulation of the bcl‐2 and p53 proteins in a spectrum of cerebral astrocytic tumours (n=81). including fibrillary astrocytomas (n=16), anaplastic astrocytomas (n=19), and glioblastomas (n=46). Median apoptosis indices (AIs) increased across this spectrum of tumours, and a significant (Pbcl‐2 antibody was found in 44% of fibrillary astrocytomas, 42% of anaplastic astrocytomas, and 28% of glioblastomas. It was also found in the vascular endothelial proliferation typically seen in glioblastomas, and in the giant, multinucleated cells of some glioblastomas. No clear relationship between AI and bcl‐2 accumulation was evident. Immunolabelling with the p53 antibody was found in 56% of fibrillary astrocytomas, 79% of anaplastic astrocytomas, and 50% of glioblastomas. No clear relationship between AI and patterns of p53 immunolabelling was evident. Equal proportions of p53‐positive tumours were bcl‐2 positive and bcl‐2 negative, but a small proportion of p53‐negative tumours was bcl‐2 positive. The correlation between A1 and Ki‐67 LI is in line with findings in other malignant tumours. We suggest that the regulation of apoptosis in astrocytic tumours is too complex for a clear association between A1 and bcl‐2 and p53 protein expression to be demonstrated.