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Elevated expression of survivin-splice variants predicts a poor outcome for soft-tissue sarcomas patients

Abstract

The aim of this study was to investigate the level and the prognostic value of the expression of different survivin transcript variants – survivin, survivin-ΔEx3 and survivin-2B – in tumours of 76 soft tissue sarcoma (STS) patients. The expression of survivin transcript variants in STS tissue samples and in 12 nonmalignant control tissues was analysed by quantitative RT–PCRs. Expression levels of all survivin transcript variants were strongly elevated in STS compared to normal tissues. A positive correlation between expression of splice variants and tumour stage was found (P=0.02; χ2 test). The multivariate Cox's proportional hazards regression model revealed a 7.3-fold increased risk of tumour-related death for patients with survivin-ΔEx3 overexpressing tumours (P=0.007). The effect of surivivin (wildtype variant) and survivin-2B was less pronounced but still significant (2.2- and 1.9-fold, resp., P<0.05 each). Our results show for the first time that mRNA expression of survivin-variants is significantly correlated to a poor prognosis for STS patients, and we suggest expression of survivin splice variants together with tumour stage as independent predictor of survival.

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Abbreviations

STS:

soft-tissue sarcoma(s)

PBS:

phosphate-buffered saline

CI 95%:

confidence interval

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Acknowledgements

We appreciate the contributions of other members of our laboratory: Birgit Wypior, Ute Rolle and Kathrin Spröte. The work in the authors' laboratory is supported by the Land Sachsen-Anhalt (Grant Number 3347A/0021B) and the NBL-3/W. Roux-program (Grant Number FKZ: 4/18). FB was supported by a grant from the Deutsche Krebshilfe (Grant 10-2130-Ta2) and KB was supported by a grant from the Chiron Behring GmbH & Co. (Marburg, Germany).

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Correspondence to Helge Taubert.

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Taubert, H., Kappler, M., Bache, M. et al. Elevated expression of survivin-splice variants predicts a poor outcome for soft-tissue sarcomas patients. Oncogene 24, 5258–5261 (2005). https://doi.org/10.1038/sj.onc.1208702

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