Original Paper

Journal of Cancer Research and Clinical Oncology

, Volume 128, Issue 6, pp 302-306

First online:

Expression of survivin in primary glioblastomas

  • Asha DasAffiliated withDepartment of Neurology, National Neuroscience Institute, 11 Jalan Tan Tock Seng, Singapore 308443
  • , Wan-Loo TanAffiliated withDepartment of Neurology, National Neuroscience Institute, 11 Jalan Tan Tock Seng, Singapore 308443
  • , Jennifer TeoAffiliated withNeuropathology Laboratory, National Neuroscience Institute, Singapore
  • , Duncan R. SmithAffiliated withLaboratory of Molecular Pathology, Institute of Molecular Biology and Genetics, Mahidol University, Salaya Campus, 25/25 Phutamonton Sai 4, Nakorn Pathom, Thailand 73170

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Purpose. Studies in several tumour types have suggested that the inappropriate expression of the novel inhibitor of apoptosis protein survivin may play a key role in tumourigenesis. This study presents the first immunohistochemical examination of survivin expression in glioblastomas.

Method. The cohort consisted of 39 ethnic Chinese patients diagnosed with primary glioblastoma multiforme. Samples were archival paraffin-embedded blocks. Concomitant with examination for survivin expression, samples were also examined for over-expression of the p53 protein as well as for evidence of apoptotic cells via the terminal deoxynucleotide transferease (TdT) mediated nick end labelling (TUNEL) technique.

Results. Results showed that survivin was expressed in nearly 80% (31/39) of samples. Over-expression of moderate or high levels of survivin was correlated with the absence of apoptotic cells (P=0.03). Expression of survivin and p53 was found to be significantly related (P=0.037), and 70% (27/39) of tumours showed co-ordinate expression of p53 and survivin.

Conclusion. Given that p53 over-expression in primary glioblastomas is predominantly detected in the absence of mutations of the gene, and that both survivin and p53 are regulated at the level of the protein by the same ubiquitin-proteosome degradation pathway, these results suggest that primary glioblastomas may occur as a result of a failure of appropriate protein degradation regulation.

Survivin Apoptosis p53 Glioblastoma