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High expression of the transcriptional regulator EVI1 encoded at the MECOM locus at 3q26 is one of the most aggressive oncogenic drivers in acute myeloid leukaemia (AML) and carries a… Click to show full abstract
High expression of the transcriptional regulator EVI1 encoded at the MECOM locus at 3q26 is one of the most aggressive oncogenic drivers in acute myeloid leukaemia (AML) and carries a very poor prognosis. How EVI1 confers leukaemic transformation and chemotherapy resistance in AML is subject to important ongoing clinical and experimental studies. Recent discoveries have revealed critical details about genetic mechanisms of the activation of EVI1 overexpression and downstream events of aberrantly high EVI1 expression. Here we review and discuss aspects concerning the protein interactions of EVI1 and the related proteins MDS-EVI1 and ΔEVI1 from the perspective of their potential for therapeutic intervention.
Journal Title: Experimental hematology
Year Published: 2021
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