Leukaemia: Holding back

摘要

The AML1 (also known as RUNX1)-ETO (also known as RUNX1T1) fusion protein that can be present in acute myeloid leukaemia (AML) is not leukaemogenic on its own, as it suppresses proliferation and reduces cell survival. Hence, AML1-ETO requires additional cooperating mutations to induce AML. A recent paper published in Blood indicates that the interaction between AML1-ETO and the transcriptional co-repressor NCOR1 is partly responsible for limiting the leukaemogenic capacity of this fusion protein.