Publication: Expression of survivin in primary glioblastomas
Issued Date
2002-06-08
Resource Type
ISSN
01715216
Other identifier(s)
2-s2.0-0036261383
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Journal of Cancer Research and Clinical Oncology. Vol.128, No.6 (2002), 302-306
Suggested Citation
Asha Das, Wan Loo Tan, Jennifer Teo, Duncan R. Smith Expression of survivin in primary glioblastomas. Journal of Cancer Research and Clinical Oncology. Vol.128, No.6 (2002), 302-306. doi:10.1007/s00432-002-0343-4 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/20062
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Expression of survivin in primary glioblastomas
Author(s)
Other Contributor(s)
Abstract
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.