Abstract
TP-53 deficient cells of human leukaemia HL-60 die by massive apoptosis after treatment by high (50-100 nmol/l) doses of DNA damaging agent Idarubicin, regardless of the cell-cycle phase, in which they are affected. In contrary, after relatively low dose 10 nmol/l the cells die after cell-cycle arrest in G2 phase. The results show, that apoptosis induced by idarubicin could appear independently of the cell-cycle phase and that period in which apoptosis is observed is related to the dose of Idarubicin.
Highlights
Acute myeloid leukaemia (AML) accounts for over 80% of all adult acute leukaemias [7] and is a characterised by a clonal expansion of immature myeloid cells in all haematopoietic tissues
Many patients progress to AML from preleukaemic myelodysplastic syndrome (MDS) or from chronic myelogenous leukaemia (CML)
The result suggest that the total length of time available for DNA damage repair, prior to potential activation of apoptosis, is a critical determinant of radiosensitivity in human haematopoietic cell lines
Summary
Acute myeloid leukaemia (AML) accounts for over 80% of all adult acute leukaemias [7] and is a characterised by a clonal expansion of immature myeloid cells in all haematopoietic tissues. The first described and best characterized mechanism of resistance is mdr gene product, P-glycoprotein. This molecule spans the cell membrane and act as an efflux pump for toxins, including chemotherapy drugs such as anthracyclines, vinca alkaloids and topoisomerase II inhibitors. Aldrige and Radford [1] showed that differences between human haematopoietic cell lines, in the rate of induction of apoptosis after irradiation were generally related to the functioning of cell cycle checkpoints. The result suggest that the total length of time available for DNA damage repair (regard less of whether this time occures as arrest in G1, S or G2), prior to potential activation of apoptosis, is a critical determinant of radiosensitivity in human haematopoietic cell lines
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