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Leukaemogenesis is a stepwise process of a delimited number of genetic aberrations, which lead to maturation impairment and promote proliferation and/or survival of the neoplastic clone.1 In acute myeloid leukaemia (AML) with t(8;21)(q22;q22)/RUNX1-RUNX1T1, genetic aberrations additional to the core-binding factor rearrangement are well known.2 Presumably further aberrations are also involved in leukaemogenesis of such AML, but are yet to be discovered.
Decrease/loss of function of the transcription factor GATA1 plays a central role in transient myeloproliferative disorders (TMDs) of newborns with trisomy 21.3–6 The presence of a short protein isoform, generated by a mutation, is complementary to trisomy 21 to initiate TMD.6 7 Since the potent oncogene RUNX1 is located …
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