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British Journal of Cancer logoLink to British Journal of Cancer
. 2001 Nov;85(10):1557–1563. doi: 10.1054/bjoc.2001.2146

The prognostic significance of apoptosis-associated proteins BCL-2, BAX and BCL-X in clinical nephroblastoma

M A Ghanem 1, T H Van der Kwast 2, J C Den Hollander 2, M K Sudaryo 3, M M Van den Heuvel 4, M A Noordzij 1, R J M Nijman 1, E H Soliman 5, G J van Steenbrugge 1
PMCID: PMC2363928  PMID: 11720445

Abstract

Apoptotic cell death represents an important mechanism for the precise regulation of cell numbers in normal tissues. Various apoptosis-associated regulatory proteins, such as Bcl-2, Bax and Bcl-X, may contribute to the rate of apoptosis in neoplasia. The present study was performed to evaluate the prognostic value of these molecules in a group of 61 Wilms' tumours of chemotherapeutically pre-treated patients using an immunohistochemical approach. Generally, Bcl-2, Bax and for Bcl-X S/L were expressed in the blastemal and epithelial components of Wilms' tumour. Immunoreactive blastema cells were found in 53%, 41% and 38% of tumours for Bcl-2, Bax and for Bcl-X S/L, respectively. An increased expression of Bcl-2 was observed in the blastemal component of increasing pathological stages. In contrast, a gradual decline of Bax expression was observed in the blastemal component of tumours with increasing pathological stages. Also blastemal Bcl-X S/L expression decreased with stage. Univariate analysis showed that blastemal Bcl-2 expression and the Bcl-2/Bax ratio were indicative for clinical progression, whereas epithelial staining was of no prognostic value. Multivariate analysis showed that blastemal Bcl-2 expression is an independent prognostic marker for clinical progression besides stage. These findings demonstrate that alterations of the Bcl-2/Bax balance may influence the clinical outcome of Wilms' tumour patients by deregulation of programmed cell death.   http://www.bjcancer.com © 2001 Cancer Research Campaign

Keywords: Wilms’, tumour, Bcl-2, Bax, Bcl-X, prognosis

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Selected References

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