Apoptosis is a form of programmed cell death characterized by specific morphologic and biochemical properties. Tumorgenesis is the consequence not only of cell proliferation but also the loss of the ability to undergo apoptosis [2]. Bcl-2 is a protooncogene which has the ability to block apoptosis in many cell types. Astrocytic neoplasms are very aggressive tumors which many times fail to respond to surgery, radiation or chemotherapy. They frequently overexpress wild-type p53 which is associated with the expression of bcl-2, and thus they may have evolved a mechanism to subvert apoptosis and allow continued growth. We examined the apoptotic index in fifty-nine astrocytic tumors of various histological grades (Oncor ApopTag Plus In Situ Detection Kit) and compared this with the level of bcl-2 expression. Low grade astrocytomas (0.21 +/- 0.05; range 0.0-0.9) and anaplastic astrocytomas (0.27 +/- 0.13; range 0.0-2.6) had significantly less apoptosis than glioblastomas (0.70 +/- 0.13; range 0.0-2.1; Kruskal-Wallis test, P < or = 0.01). In contrast, bcl-2 expression was similar in all grades of astrocytic tumors and did not correlate with the apoptotic index. Cells of low grade and anaplastic astrocytomas are less likely to undergo apoptosis; however, this does not seem to be a direct consequence of the regulation of bcl-2 expression. The difference in growth potential despite differences in apoptotic index is likely to be attributed to differences in mitotic not apoptotic activity.