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 Blood, 15 March 2007, Vol. 109, No. 6, pp. 2607-2610.
Prepublished online as a Blood First Edition Paper on November 9, 2006; DOI 10.1182/blood-2006-04-019612.

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Submitted April 27, 2006
Accepted November 2, 2006

RNAi-mediated silencing of TEL/AML1 reveals a heat shock protein and survivin dependent mechanism for survival

Christofer Diakos, Gerd Krapf, Christopher Gerner, Andrea Inthal, Christof Lemberger, Jozef Ban, Alexander M Dohnal, and E. Renate Panzer-Grumayer*

Children's Cancer Research Institute, Austria
Medical University of Vienna, Austria
St. Anna Kinderspital, Austria

* Corresponding author; email: renate.panzer{at}ccri.at.

The TEL/AML1 fusion gene results from the most frequent t(12;21)(p13;q22) translocation in childhood ALL. Its contribution to transformation is largely unknown, in particular with respect to survival and apoptosis. We therefore silenced TEL/AML1 expression in leukemic REH cells by RNA inhibition, which eventually led to programmed cell death. Microarray and 2D-gel electrophoresis data demonstrated a differential regulation of heat-shock proteins (HSPs), among them HSP90, as well as of its client, survivin. Consistent with these findings, ectopic expression of TEL/AML1 in Ba/F3 cells increased protein levels of HSP90 and survivin and conferred resistance to apoptotic stimuli. Our data suggest that TEL/AML1 does not only contribute to leukemogenesis by affecting an anti-apoptotic network but also seems to be indispensable for maintaining the malignant phenotype. The functional relationship between TEL/AML1, HSP90 and survivin provides the rational for targeted therapy, be it the fusion gene or the latter two proteins.


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