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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. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-06-2601v1 107/6/2544    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Oyarzo, M. P. Articles by Rassidakis, G. Z. Search for Related Content PubMed PubMed Citation Articles by Oyarzo, M. P. Articles by Rassidakis, G. Z. Related Collections Apoptosis Brief Reports Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  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) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: X. Wang, W. Chen, W. Zeng, L. Bai, Y. Tesfaigzi, S. A. Belinsky, and Y. Lin Akt-mediated eminent expression of c-FLIP and Mcl-1 confers acquired resistance to TRAIL-induced cytotoxicity to lung cancer cells Mol. Cancer Ther., May 1, 2008; 7(5): 1156 - 1163. [Abstract] [Full Text] [PDF] L. E. Perez, N. Parquet, K. Shain, R. Nimmanapalli, M. Alsina, C. Anasetti, and W. Dalton Bone Marrow Stroma Confers Resistance to Apo2 Ligand/TRAIL in Multiple Myeloma in Part by Regulating c-FLIP J. Immunol., February 1, 2008; 180(3): 1545 - 1555. [Abstract] [Full Text] [PDF] J. Yang, P. K. Epling-Burnette, J. S. Painter, J. Zou, F. Bai, S. Wei, and T. P. Loughran Jr Antigen activation and impaired Fas-induced death-inducing signaling complex formation in T-large-granular lymphocyte leukemia Blood, February 1, 2008; 111(3): 1610 - 1616. [Abstract] [Full Text] [PDF]

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