Macrophage mediated chemoresistance in AML: from macrophage subset characterisation to the potential for therapeutic targeting.

Despite decades of research, we know very little of how cancer drug resistance can arise in acute myeloid leukaemia (AML), and approaches to overcome chemoresistance are important for curative therapies. Each year in the UK there are over 2,600 AML patient deaths. AML is currently incurable and for the majority of AML patient’s (≥65 years of age) 5-year survival is <20%, with little improvement in these figures observed in the last two decades. Chemoresistance is a major contributing factor towards treatment failure, disease relapse and death in AML patients (Burnett et al., 2012). The involvement of the bone marrow microenvironment (BMME) in the development of chemoresistance is well documented in AML, with mounting evidence suggesting that AML-macrophage (Mφ cross-talk influences the Mφ phenotype, which in turn blunts the response of AML blasts towards chemotherapeutics.