Survivin, caspase-3 and MIB-1 expression in astrocytic tumors of various grades

Gliomas are the most common primary brain tumors. The etiology is still unclear and the progression from low to high-grade gliomas is frequent. The molecular mechanisms are quite established, however the heterogeneity of glioblastomas force the scientist to look for the new therapeutic targets. The aim of the study was to evaluate the caspase-3 and survivin expression in correlation with MIB-1 expression in gliomas of various grade to assess the apoptosis in gliomas and to determinate new possible targets for the future therapy.

We identified 131 patients with a histopathological diagnosis of astrocytic tumors (diffuse astrocytoma, anaplastic astrocytoma and glioblastoma). The evaluation of caspase-3, survivin and MIB-1 expression was done using immunohistochemical methods.

Caspase-3 and survivin expression was observed both in low- and high-grade astrocytomas. The differences in expression were the most evident in glioblastoma group. All primary glioblastomas (31 cases) expressed caspase-3. In secondary glioblastoma group only 17 out of 30 specimens were positive for caspase-3. Survivin expression was observed in 80.6% primary glioblastomas and in all examined secondary glioblastomas and the staining was strong and diffuse in all cases. MIB-1 expression was low in diffuse astrocytomas (DA) and ranged between 1 and 5%. In anaplastic astrocytoma group it was ranged between 5 and 10% and the highest percentage of the positive cells was observed in glioblastoma cases and ranged from 10% even to 30%. The most evident MIB-1 expression was observed in the cells surrounding the pathological blood vessels and necrosis.

The high incidence of survivin and caspase-3 expression in diffuse and anaplastic astrocytoma cases may suggest, that the regulation between pro- and antiapoptotic proteins may play an important role in tumor growth and progression. The overexpression of survivin and MIB-1 expression in glioblastoma cases also may confirm the theory about the important role of anti-apoptotic and proliferation processes in glioblastoma progression and as such may be potential therapeutic targets.