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ORIGINAL ARTICLE
Year : 2015  |  Volume : 11  |  Issue : 4  |  Page : 823-829

Doxorubicin enhances 131 I-rituximab induced cell death in Raji cells


1 Isotope Applications and Radiopharmaceuticals Division, Bhabha Atomic Research Centre, Mumbai, Maharashtra, India
2 Radiation Biology and Health Sciences Division, Bhabha Atomic Research Centre, Mumbai, Maharashtra, India
3 Department of Nuclear Sciences and Nuclear Applications, IAEA, Vienna, Austria

Correspondence Address:
G Samuel
Isotope Applications and Radiopharmaceuticals Division, Bhabha Atomic Research Centre, Mumbai - 400 085, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.140844

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Aim: There are various therapeutic modalities of treatment for non-Hodgkin's lymphoma, but with certain limitations, hence, investigating the scope of combined therapeutic approach. Materials and Methods: In this article, cellular toxicity, apoptosis and expression of mitogen-activated protein kinase signaling pathway proteins were investigated in Raji cells preincubated with doxorubicin followed by 131 I-rituximab (rituximab radiolabeled with Iodine-131) treatment. Results: It was found that the 131 I-rituximab in combination with doxorubicin showed a higher amount of cell toxicity and apoptosis compared to respective controls. Expression of anti-apoptotic protein (B-cell lymphoma-extra-large) was downregulated and cleavage of poly (ADP-ribose) polymerase, a marker of apoptosis was higher in cells treated with doxorubicin (2 μg/mL) and 131 I-rituximab (P ≤ 0.05). Moreover, in these cells the basal level of expression of p42/44 and p38 were increased while its phosphorylation was decreased. Conclusion: These results suggest that doxorubicin has the potential to sensitize 131 I-rituximab induced cell death in Raji cells.


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