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‘Ayn al ‘Arab, Syria

Abulayha A.,Cell Biology Research Group | Bredan A.,Inflammation Research Center | Bredan A.,Ghent University | El Enshasy H.,University of Technology Malaysia | Daniels I.,University of Nottingham
Future Oncology | Year: 2014

Less than two decades ago, immunotherapy joined chemotherapy and radiotherapy as an effective approach for the treatment of cancer. The anti-CD20 monoclonal antibody, rituximab, is now used to treat almost all types of non-Hodgkin's B-cell lymphomas, and it could be useful in the treatment of other diseases with B-cell involvement. Upon binding, rituximab induces death of the target cells. It seems to act not only by activating immune system defense mechanisms such as complement-dependent and antibody-dependent cellular cytotoxicity, but also by inducing direct cell death. In this paper, we review current knowledge on rituximab mechanisms of action, with particular attention to its direct effects, and also highlight potential future avenues of research. © 2014 Future Medicine Ltd.

Abulayha A.M.,Cell Biology Research Group | Tabal S.A.,Cell Biology Research Group | Shawesh E.I.,Academy of Graduate Studies | Elbasir M.A.,Cell Biology Research Group | And 4 more authors.
Leukemia Research | Year: 2010

The monoclonal antibody Rituximab is useful for treatment of patients with B-cell non-Hodgkin's lymphoma. We phenotypically analyzed reconstitution of peripheral B cells in a male patient with follicular lymphoma following their depletion with Rituximab. CD19+ and CD20+ B cell counts in peripheral blood decreased rapidly following Rituximab treatment. Six months after the end of treatment, a few CD19+ B cells were detected in peripheral blood. These cells had a naive B cell phenotype (IgD+, CD27-) and they expressed high levels of CD38 and CD24, which show that the B cell pool was repopulated mainly with immature, naive B cells. © 2009 Elsevier Ltd.

Deyab M.,Cell Biology Research Group | Elbanani A.,Cell Biology Research Group | Tabal S.,Cell Biology Research Group | Geriani H.,Cell Biology Research Group | And 4 more authors.
Cancer Biotherapy and Radiopharmaceuticals | Year: 2014

Rituximab is an effective immunotherapy for CD20-positive B-cell non-Hodgkin's lymphoma. However, some patients show resistance, particularly those suffering from more aggressive lymphoma types, such as Burkitt's lymphoma. Hence, Rituximab is commonly combined with several chemotherapeutic drugs. With a view to reduce the number of such drugs, we examined the effect of combining Rituximab individually with hydroxyurea, vincristine, or etoposide on the killing of Ramos Burkitt lymphoma cell line type I. Cell death was examined by using Annexin-V/propidium iodide staining. Combining Rituximab with hydroxyurea or vincristine resulted in a synergistic effect, whereas combining it with etoposide resulted in a subadditive effect. In single treatments, the percentage of cell death ranged from 23% (Rituximab) to 36% (hydroxyurea). Combining Rituximab with hydroxyurea or vincristine resulted in a synergistic effect (83% and 74% killing, respectively). In contrast, only a subadditive effect was noticed with etoposide (36%). We conclude that the synergistic effect of Rituximab with hydroxyurea or vincristine is worthy of further study, and that further in vitro screening of chemotherapeutics might identify chemo-immunotherapeutic combinations that are effective in vivo but less toxic than currently used regimens. © Mary Ann Liebert, Inc.

Tabal S.,Cell Biology Research Group | Elbanani A.,Cell Biology Research Group | Deyab M.,Cell Biology Research Group | Abulayha A.,Cell Biology Research Group
Cancer Biotherapy and Radiopharmaceuticals | Year: 2015

In the treatment of B cell non-Hodgkin's lymphoma, rituximab is used in combination with different chemotherapeutics to improve its efficacy, but the mechanisms involved are not fully understood. The authors examined the mechanism by which rituximab combined with hydroxyurea or vincristine induces cell death in the human Burkitt's lymphoma Ramos cell line. Cell death was analyzed by phosphatidylserine exposure, caspase activation, and mitochondrial membrane changes. Their results indicate that the cell death initiated by the combination of rituximab and hydroxyurea is caspase-independent. In contrast, preincubation of the cells with the same concentrations of caspase inhibitors used with hydroxyurea eliminated the synergistic effect of the rituximab and vincristine combination. This was confirmed by the presence of the active fragment of caspase-3 in vincristine-treated cells. These preliminary results demonstrate that rituximab can activate different downstream signals to induce direct cell effects. Furthermore, the findings support the important role of mitochondria in the regulation of both pathways. © 2015, Mary Ann Liebert, Inc.

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