Although most patients with acute myeloid leukaemia (AML) initially respond to anti-leukaemic chemotherapy, the majority of patients subsequently relapses and dies of relapsed or refractory disease. Recent studies have suggested that therapeutic relapse is the result of persistent, chemo-resistant AML cells that survive initial therapy, who serve as a reservoir for genetic/epigenetic evolution and subsequent clinical relapse. Although many AML patients have evidence of residual leukemia at clinical remission, the mechanisms leading to chemo-resistance and to the survival of AML cells in response to chemotherapy have not been delineated. During EHA 2015, a study was presented showing that mutant DNMT3A promotes chemoresistance in AML, suggesting the possibility of unique vulnerabilities in DNMT3A-mutant cells that can be exploited therapeutically. In a second presentation, tyrosine kinase inhibition was for the first time identified as a therapeutic option in this leukaemia subtype.

(BELG J HEMATOL 2015;6(3):99–100)