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International Journal of Cancer Research
  Year: 2006 | Volume: 2 | Issue: 2 | Page No.: 124-130
DOI: 10.3923/ijcr.2006.124.130
Evaluation of Apoptosis Induced by Arsenic Trioxide Through TNFR-I and CD30 Pathways in Acute Promyelocytic Leukemia Patient with t (15;17) Translocation
A.R. Ardjmand, K. Alimoghadam , S. Kaviani , A. Ghavamzadeh , M. Djahani and L. Moezzi

Abstract:
Arsenic trioxide (ATO) has been reported to induce apoptosis in Leukemic cells of Acute Promyelocytic Leukemia (APL) patients through different pathways. However, the exact mechanism of ATO-induced apoptosis is not yet clear. Co stimulation of death receptors CD30 and tumor necrosis factor receptor type one (TNFR-I) is one of the postulate mechanisms which in the present study we aimed to evaluate their involvement in fresh Promyelocytic cells separated from bone marrow of APL patients. Immunomagnetic separated cells were treated up to 48 h at clinically tolerable concentration of ATO (0.5-2.0 μmol L-1) and expression of TNFR-I and CD30 were evaluated within the apoptotic and live populations using a sensitive triple color flow cytometric method for measuring apoptosis in combination with dual color immunofluorescence. Present results suggest that the expression of TNFR-I and CD30 might not be related to ATO-induced apoptotic cell death.
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How to cite this article:

A.R. Ardjmand, K. Alimoghadam , S. Kaviani , A. Ghavamzadeh , M. Djahani and L. Moezzi , 2006. Evaluation of Apoptosis Induced by Arsenic Trioxide Through TNFR-I and CD30 Pathways in Acute Promyelocytic Leukemia Patient with t (15;17) Translocation. International Journal of Cancer Research, 2: 124-130.

DOI: 10.3923/ijcr.2006.124.130

URL: https://scialert.net/abstract/?doi=ijcr.2006.124.130

 
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