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 Blood, 15 March 2006, Vol. 107, No. 6, pp. 2544-2547.
Prepublished online as a Blood First Edition Paper on November 22, 2005; DOI 10.1182/blood-2005-06-2601.

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NEOPLASIA
Brief report

c-FLIP confers resistance to FAS-mediated apoptosis in anaplastic large-cell lymphoma

Mauricio P. Oyarzo, L. Jeffrey Medeiros, Coralyn Atwell, Marianna Feretzaki, Vasiliki Leventaki, Elias Drakos, Hesham M. Amin, and George Z. Rassidakis

From the Department of Hematopathology, The University of Texas M. D. Anderson Cancer Center, Houston, TX.

We hypothesized that inhibition of the FAS-mediated apoptosis pathway by FLICE-like inhibitory protein (c-FLIP) may contribute to oncogenesis in ALK+ anaplastic large-cell lymphoma (ALCL). Treatment with increasing concentrations of CH-11 (CD95/FAS agonistic antibody) had no effect on cell viability of 2 ALK+ ALCL cell lines, Karpas 299 and SU-DHL1, each expressing high levels of c-FLIP. However, inhibition of endogenous c-FLIP expression by specific c-FLIP siRNA in Karpas 299 and SU-DHL1 cells treated with CH-11 resulted in FAS-mediated cell death associated with increased annexin V binding, apoptotic morphology, and cleavage of caspase-8. In 26 ALK+ ALCL tumors, assessed for expression of DISC-associated proteins, CD95/FAS and c-FLIP were commonly expressed, in 23 (92%) of 25 and 21 (91%) of 23 tumors, respectively. By contrast, CD95L/FASL was expressed in only 3 (12%) of 26 ALCL tumors, although it was strongly expressed by surrounding small reactive lymphocytes. Our findings suggest that overexpression of c-FLIP protects ALK+ ALCL cells from death-receptor-induced apoptosis and may contribute to ALCL pathogenesis. (Blood. 2006;107:2544-2547)


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