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Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives
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| Zeitschriftentitel: | Molecular Cancer Research |
|---|---|
| Personen und Körperschaften: | , , |
| In: | Molecular Cancer Research, 9, 2011, 11, S. 1435-1442 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Association for Cancer Research (AACR)
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| Schlagwörter: |
| author_facet |
Bezombes, Christine Fournié, Jean-Jacques Laurent, Guy Bezombes, Christine Fournié, Jean-Jacques Laurent, Guy |
|---|---|
| author |
Bezombes, Christine Fournié, Jean-Jacques Laurent, Guy |
| spellingShingle |
Bezombes, Christine Fournié, Jean-Jacques Laurent, Guy Molecular Cancer Research Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives Cancer Research Oncology Molecular Biology |
| author_sort |
bezombes, christine |
| spelling |
Bezombes, Christine Fournié, Jean-Jacques Laurent, Guy 1541-7786 1557-3125 American Association for Cancer Research (AACR) Cancer Research Oncology Molecular Biology http://dx.doi.org/10.1158/1541-7786.mcr-11-0154 <jats:title>Abstract</jats:title> <jats:p>The anti-CD20 monoclonal antibody rituximab is the backbone of treatment for the B-cell malignancies non-Hodgkin lymphoma and chronic lymphocytic leukemia. However, there is a wide variability in response to rituximab treatment, and some patients are refractory to current standard therapies. Rituximab kills B cells by multiple mechanisms of action, including complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, which are immune-mediated mechanisms, as well as by direct effects on cell signaling pathways and cell membranes following CD20 binding. A large number of events that are affected by rituximab binding have been identified, including lipid raft modifications, kinase and caspase activation, and effects on transcription factors and apoptotic/antiapoptotic molecules. Studies on cell lines and isolated tumor cells have shown that by targeting these pathways, it may be possible to increase or decrease susceptibility to rituximab cell killing. An increased understanding of the direct effects of rituximab may therefore aid in the design of new, rational combinations to improve the outcome of CD20-based therapy for patients who currently have suboptimal outcome following standard treatments. Mol Cancer Res; 9(11); 1435–42. ©2011 AACR.</jats:p> Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives Molecular Cancer Research |
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1541-7786 1557-3125 |
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| title |
Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_unstemmed |
Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_full |
Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_fullStr |
Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_full_unstemmed |
Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_short |
Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_sort |
direct effect of rituximab in b-cell–derived lymphoid neoplasias: mechanism, regulation, and perspectives |
| topic |
Cancer Research Oncology Molecular Biology |
| url |
http://dx.doi.org/10.1158/1541-7786.mcr-11-0154 |
| publishDate |
2011 |
| physical |
1435-1442 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>The anti-CD20 monoclonal antibody rituximab is the backbone of treatment for the B-cell malignancies non-Hodgkin lymphoma and chronic lymphocytic leukemia. However, there is a wide variability in response to rituximab treatment, and some patients are refractory to current standard therapies. Rituximab kills B cells by multiple mechanisms of action, including complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, which are immune-mediated mechanisms, as well as by direct effects on cell signaling pathways and cell membranes following CD20 binding. A large number of events that are affected by rituximab binding have been identified, including lipid raft modifications, kinase and caspase activation, and effects on transcription factors and apoptotic/antiapoptotic molecules. Studies on cell lines and isolated tumor cells have shown that by targeting these pathways, it may be possible to increase or decrease susceptibility to rituximab cell killing. An increased understanding of the direct effects of rituximab may therefore aid in the design of new, rational combinations to improve the outcome of CD20-based therapy for patients who currently have suboptimal outcome following standard treatments. Mol Cancer Res; 9(11); 1435–42. ©2011 AACR.</jats:p> |
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| author | Bezombes, Christine, Fournié, Jean-Jacques, Laurent, Guy |
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| description | <jats:title>Abstract</jats:title> <jats:p>The anti-CD20 monoclonal antibody rituximab is the backbone of treatment for the B-cell malignancies non-Hodgkin lymphoma and chronic lymphocytic leukemia. However, there is a wide variability in response to rituximab treatment, and some patients are refractory to current standard therapies. Rituximab kills B cells by multiple mechanisms of action, including complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, which are immune-mediated mechanisms, as well as by direct effects on cell signaling pathways and cell membranes following CD20 binding. A large number of events that are affected by rituximab binding have been identified, including lipid raft modifications, kinase and caspase activation, and effects on transcription factors and apoptotic/antiapoptotic molecules. Studies on cell lines and isolated tumor cells have shown that by targeting these pathways, it may be possible to increase or decrease susceptibility to rituximab cell killing. An increased understanding of the direct effects of rituximab may therefore aid in the design of new, rational combinations to improve the outcome of CD20-based therapy for patients who currently have suboptimal outcome following standard treatments. Mol Cancer Res; 9(11); 1435–42. ©2011 AACR.</jats:p> |
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| imprint_str_mv | American Association for Cancer Research (AACR), 2011 |
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| spelling | Bezombes, Christine Fournié, Jean-Jacques Laurent, Guy 1541-7786 1557-3125 American Association for Cancer Research (AACR) Cancer Research Oncology Molecular Biology http://dx.doi.org/10.1158/1541-7786.mcr-11-0154 <jats:title>Abstract</jats:title> <jats:p>The anti-CD20 monoclonal antibody rituximab is the backbone of treatment for the B-cell malignancies non-Hodgkin lymphoma and chronic lymphocytic leukemia. However, there is a wide variability in response to rituximab treatment, and some patients are refractory to current standard therapies. Rituximab kills B cells by multiple mechanisms of action, including complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, which are immune-mediated mechanisms, as well as by direct effects on cell signaling pathways and cell membranes following CD20 binding. A large number of events that are affected by rituximab binding have been identified, including lipid raft modifications, kinase and caspase activation, and effects on transcription factors and apoptotic/antiapoptotic molecules. Studies on cell lines and isolated tumor cells have shown that by targeting these pathways, it may be possible to increase or decrease susceptibility to rituximab cell killing. An increased understanding of the direct effects of rituximab may therefore aid in the design of new, rational combinations to improve the outcome of CD20-based therapy for patients who currently have suboptimal outcome following standard treatments. Mol Cancer Res; 9(11); 1435–42. ©2011 AACR.</jats:p> Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives Molecular Cancer Research |
| spellingShingle | Bezombes, Christine, Fournié, Jean-Jacques, Laurent, Guy, Molecular Cancer Research, Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives, Cancer Research, Oncology, Molecular Biology |
| title | Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_full | Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_fullStr | Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_full_unstemmed | Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_short | Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| title_sort | direct effect of rituximab in b-cell–derived lymphoid neoplasias: mechanism, regulation, and perspectives |
| title_unstemmed | Direct Effect of Rituximab in B-Cell–Derived Lymphoid Neoplasias: Mechanism, Regulation, and Perspectives |
| topic | Cancer Research, Oncology, Molecular Biology |
| url | http://dx.doi.org/10.1158/1541-7786.mcr-11-0154 |