Apoptosis and leukaemia

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Abstract
Defects in the intrinsic ability of haematopoietic progenitor cells to undergo apoptosis may allow the cell to acquire further mutations, survive inappropriately and eventually become malignant. Additionally, this defect could account for the resistance to cell death, observed in leukaemic cells, following treatment with chemotherapy. This review discusses some of the molecules known to influence apoptosis in leukaemic cells, particularly the novel fusion proteins produced as a result of leukaemia‐associated chromosomal translocations. The ultimate aim of understanding how apoptosis is altered in leukaemia cells is so that the process can be modulated to overcome resistance to chemotherapy and improve clinical outcomes. The relationship of leukaemia‐related fusion proteins such as PML‐RARα, BCR‐ABL, E2A‐HLF, AML1‐ETO and the various MLL fusions to the biochemical pathways involved in apoptosis are discussed as well as the consequences for therapeutic applications.