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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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NEOPLASIA

Brief Report

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

Christofer Diakos1, Gerd Krapf1, Christopher Gerner2, Andrea Inthal1, Christof Lemberger1, Jozef Ban1, Alexander M. Dohnal1, and E. Renate Panzer-Gruemayer1,3

1 Children's Cancer Research Institute (CCRI), Vienna, Austria; 2 Institute of Cancer Research, Medical University of Vienna, Vienna, Austria; 3 St Anna Kinderspital, Vienna, Austria

The TEL/AML1 fusion gene results from the most frequent t(12;21)(p13;q22) translocation in childhood acute lymphoblastic leukemia (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 not only contributes to leukemogenesis by affecting an antiapoptotic 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 2 proteins.


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