arsenic trioxide induce apoptosis independent of tnfr-i and cd30 pathways in acute promyelocytic leukemia patient with t(15;17) translocation.

arsenic trioxide (ato) has been reported to induce apoptosis in leukemic cells of acute promyelo-cytic 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 postulated mechanisms.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 hr at clinically tolerable concentrations of ato (0.5-2.0 µmol/l) 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 combina tion with dual color immunofluorescence. our results suggest that the expression of tnfr-i and cd30 might not be related to  ato-induced apoptotic cell death.