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Blood, 15 August 2004, Vol. 104, No. 4, pp. 1166-1173.
Prepublished online as a Blood First Edition Paper on May 11, 2004; DOI 10.1182/blood-2004-01-0277.
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NEOPLASIA
Rituximab antiproliferative effect in B-lymphoma cells is associated with acid-sphingomyelinase activation in raft microdomains
Christine Bezombes,
Solène Grazide,
Céline Garret,
Claire Fabre,
Anne Quillet-Mary,
Sabina Müller,
Jean-Pierre Jaffrézou, and
Guy Laurent
From the Institut National de la Santé et de la Recherche Médicale U563-CPTP, Centre Hospitalier et Universitaire Purpan Pavillon Lefebvre, Toulouse, France; and the Service d'Hématologie, Centre Hospitalier Universitaire Purpan, Toulouse, France.
Rituximab is a chimeric human immunoglobulin G1 (IgG1) anti-CD20 monoclonal antibody with significant activity against CD20+ malignant B cells. Rituximab is currently used with success in the treatment of B-cell-derived lymphoid neoplasias either alone or in combination with chemotherapy. However, the predominant mechanism by which rituximab exerts its antitumor properties in vivo remains unknown. In the present study, we demonstrate that in Daudi and RL B-lymphoma cells, rituximab (without cross-linking) used at the saturating dose of 10 µg/mL induced moderate accumulation in G1 phase, growth inhibition, and significant loss in clonogenic potential. However, in these cells, rituximab induced no apoptosis. Furthermore, we observed that treatment with rituximab resulted in a rapid and transient increase in acid-sphingomyelinase (A-SMase) activity and concomitant cellular ceramide (CER) generation in raft microdomains. We also observed that rituximab-treated cells externalized both A-SMase and CER that colocalized with the CD20 receptor. Finally, we present evidence that rituximab-induced growth inhibition may be mediated through a CER-triggered signaling pathway, leading to the induction of cell cycle-dependent kinase inhibitors such as p27(Kip1) through a mitogen-activated protein kinase (MAPK)-dependent mechanism. (Blood. 2004;104: 1166-1173)
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