Rituximab causes a polarization of B cells that augments its therapeutic function in NK-cell-mediated antibody-dependent cellular cytotoxicity.
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Rituximab: how approval history is reflected by a corresponding patent filing strategyPrioritizing therapeutic targets using patient-derived xenograft modelsCellular immune dysfunction in immune thrombocytopenia (ITP).Pathogenesis and Therapeutic Mechanisms in Immune Thrombocytopenia (ITP)A phase I study of PRO131921, a novel anti-CD20 monoclonal antibody in patients with relapsed/refractory CD20+ indolent NHL: correlation between clinical responses and AUC pharmacokineticsNeonatal natural killer cell function: relevance to antiviral immune defenseRefractory myasthenia gravis - clinical profile, comorbidities and response to rituximab.Somatic alterations as the basis for resistance to targeted therapies.The central role of the cytoskeleton in mechanisms and functions of the NK cell immune synapse.Three major uncertainties in the antibody therapy of cancer.Natural killer (NK) cells and anti-tumor therapeutic mAb: unexplored interactions.Neurotrophins and B-cell malignancies.Emerging therapies in systemic lupus erythematous: from clinical trial to the real life.Macrophage-Mediated Trogocytosis Leads to Death of Antibody-Opsonized Tumor CellsFollicular lymphoma: in vitro effects of combining lymphokine-activated killer (LAK) cell-induced cytotoxicity and rituximab- and obinutuzumab-dependent cellular cytotoxicity (ADCC) activity.Entinostat, a novel histone deacetylase inhibitor is active in B-cell lymphoma and enhances the anti-tumour activity of rituximab and chemotherapy agents.Antitumor activity of an anti-CD98 antibody.c-Abl modulates tumor cell sensitivity to antibody-dependent cellular cytotoxicity.Acute myeloid leukemia impairs natural killer cells through the formation of a deficient cytotoxic immunological synapse.Rituximab induces phenotypical and functional changes of NK cells in a non-malignant experimental setting.SILAC-Based Quantitative Proteomic Analysis of Diffuse Large B-Cell Lymphoma Patients.Integrin receptors on tumor cells facilitate NK cell-mediated antibody-dependent cytotoxicity.RFX1 participates in doxorubicin-induced hepatitis B virus reactivation.
P2860
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P2860
Rituximab causes a polarization of B cells that augments its therapeutic function in NK-cell-mediated antibody-dependent cellular cytotoxicity.
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2013 nî lūn-bûn
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2013 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2013年の論文
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2013年論文
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2013年論文
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2013年論文
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2013年論文
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2013年論文
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2013年论文
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name
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@ast
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@en
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@nl
type
label
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@ast
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@en
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@nl
prefLabel
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@ast
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@en
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@nl
P2093
P1433
P1476
Rituximab causes a polarizatio ...... pendent cellular cytotoxicity.
@en
P2093
Anna Oszmiana
Darren J Schofield
David C Lowe
Dominika Rudnicka
Donna K Finch
Ian Strickland
Matthew A Sleeman
P304
P356
10.1182/BLOOD-2013-02-482570
P407
P577
2013-04-23T00:00:00Z