1. ¹State Key Laboratory of Oncology in Southern China, Cancer Center, Sun Yat-Sen University, Guangzhou, China
2. ²Department of Neurosurgery, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
3. ³Department of Pathology, Zhong Shan Medical College, Sun Yat-Sen University, Guangzhou, China
4. ⁴Department of Clinical Oncology, University of Hong Kong, Hong Kong, China

Correspondence: Dr D Xie or Dr XY Guan, State Key Laboratory of Oncology in Southern China, Cancer Center, Sun Yat-Sen University, 651 Dongfeng Road East, Guangzhou, china. E-mail: danxie@graduate.hku.hk or Department of Clinical Oncology, University of Hong Kong, Room 109, School of Chinese Medicine Building, 10 Sassoon Road, Hong Kong, China. E-mail: xyguan@hkucc.hku.hk

Received 10 June 2005; Revised 27 October 2005; Accepted 15 November 2005; Published online 13 December 2005.

Abstract

Clinically, human glioblastoma (GBM) may develop de novo or from a low-grade glioma (secondary GBM), and molecular alterations in the two pathways may differ. This study examined the status of Survivin expression and apoptosis in 30 primary and 26 secondary GBMs. Our results show that cytoplasmic Survivin positivity was significantly (P<0.001) more frequent in primary GBMs (83%) than that in secondary GBMs (46%). In addition, an inverse correlation of cytoplasmc Survivin positivity with GBM apoptotic index, and a positive association between cytoplasmic Survivin and size of the tumours were observed. These results suggest that cytoplasmic Survivin, via its antiapoptotic function, may be involved in the tumorigenesis of many primary GBMs, but only in a small fraction of secondary GBMs. Furthermore, the overall progression times from low-grade precursor lesions to secondary GBMs were significantly shorter (P<0.05) in cytoplasmic Survivin-positive cases (mean, 15.6 months) than those in Survivin-negative cases (mean, 23.8 moths), and the positive expression level of Survivin in cytoplasm was upregulated in most secondary GBMs when compared to matched pre-existing low-graded lesions. These results suggest that the increased accumulation of Survivin in the cytoplasm of more malignant glioma cells may prove to be a selective advantage, thus accelerating progression to a more aggressive phenotype.