Jacobs Journal of Cancer Science and Research

Mechanisms of Resistance to Rituximab in B-cell Lymphoma

Published on: 2015-03-14


Rituximab or Anti-CD20, is a chimeric monoclonal antibody (MoAb)that has become a ubiquitous component for improved therapeutic options for patients with B-cell non-Hodgkin lymphoma (B-NHL)and other known hematological malignancies. The MoAbs has the direct antiproliferative effect on the B cells in vitro. This review article focuses on the mechanism of resistance to the Rituximab(anti CD-20)mediated cytotoxicity.Understanding of the complexity of mechanism facilitates the progressof pharmacological strategies to reduce resistance.Unluckily, the common responses to single-agent Rituximab are inadequate, It has multiple mechanisms which commonly includes antibody-dependent cell- mediated cytotoxicity and complement- dependent cytotoxicity. Tumor/host -associated factors contribute to the Rituximab resistance. There are many approaches to overcome rituximab resistance such as engineered antibodies, radio-immunoconjugates and rational biologic combination immunotherapy, which provide a comprehensive understanding of interactions between its multiple mechanisms of action.Furthermore, few discussed studies in this review show that treatment with rituximab can be modified and may have a significant role in newer therapeutical strategies.


B-cell non-Hodgkin Lymphoma (B-NHL); Antibody Dependent Cell Mediated Cytotoxicity (ADCC); Complement Dependent Cytotoxicity (CDC); Anti-CD20, Monoclonal-Antibody; B-cell depletion