Abstract:
Translocation (8;21), AML1/ETO (A/E), is one the most common chromosomal translocations in AML patients, with an incidence of 10-15% – up to 40% in FAB-M2 subtype of AML – and it is associated with core-binding factor leukaemias. It has been implicated that A/E is insufficient to trigger leukaemia in a murine model, unless it cooperates with other somatic mutations. AML1/ETO9a (A/E9a) is an alternatively spliced isoform of A/E and it is sufficient to develop leukaemia in a murine model on its own. Therefore, A/E9a is a potentially suitable fusion protein to study the function of A/E in a retroviral transduction murine bone marrow transplantation leukaemia model (MBMTLM) to characterise leukaemia induced in this model.
