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Rituximab-Dependent Cytotoxicity by Natural Killer Cells

Data up to Jan 2025

Published2004
Citations413
References51

Total Citations Per Year

Abstract

References (51)

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Complement Activation Determines the Therapeutic Activity of Rituximab In Vivo

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Rituximab (anti-CD20 monoclonal antibody) as single first-line therapy for patients with follicular lymphoma with a low tumor burden: clinical and molecular evaluation

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Association of serum Rituximab (IDEC–C2B8) concentration and anti-tumor response in the treatment of recurrent low-grade or follicular non-Hodgkin’s lymphoma

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Rituximab as First-Line and Maintenance Therapy for Patients With Indolent Non-Hodgkin’s Lymphoma

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CD20 levels determine the in vitro susceptibility to rituximab and complement of B-cell chronic lymphocytic leukemia: further regulation by CD55 and CD59

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The relationship of FcγRIIIa genotype to degree of B cell depletion by rituximab in the treatment of systemic lupus erythematosus

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Mapping of the C1q Binding Site on Rituxan, a Chimeric Antibody with a Human IgG1 Fc

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Polymorphisms in FcγRIIIA (CD16) Receptor Expression Are Associated With Clinical Response to Rituximab in Waldenström’s Macroglobulinemia

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Rituximab (Anti‐CD20) Therapy of B‐Cell Lymphomas: Direct Complement Killing is Superior to Cellular Effector Mechanisms

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Expression of complement inhibitors CD46, CD55, and CD59 on tumor cells does not predict clinical outcome after rituximab treatment in follicular non-Hodgkin lymphoma

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Binding to CD20 by Anti-B1 Antibody or F(ab') 2 is sufficient for induction of apoptosis in B-cell lines

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Feasibility and pharmacokinetic study of a chimeric anti-CD20 monoclonal antibody (IDEC-C2B8, rituximab) in relapsed B-cell lymphoma

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Rituximab-Dependent Cytotoxicity by Natural Killer Cells (2004) – Cancer Research | Metascience Observatory Explorer