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

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 (P<0.0001) correlation was demonstrated between A1 and Ki-67 labelling index (LI). Immunolabelling with the bcl-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.