Genetics, Biology, and Treatment of Acute Myeloid Leukemia 2.0

Dear Colleagues,

Acute myeloid leukemia (AML) is a highly heterogeneous disease both in terms of its genetic etiology and outcome. In the 1960s, cytogenetic analyses yielded the first insights into the genetic alterations driving its emergence and evolution, and a panel of recurrent chromosome aberrations discovered decades ago still represents one of the main pillars of prognostication. The advent of molecular biology facilitated the discovery and characterization of the fusion genes formed as a consequence of these chromosome rearrangements. In recent years, next-generation sequencing has allowed the establishment of the full inventory of somatically acquired mutations in individuals with AML, as well as the investigation of the evolution of mutational patterns during the course of disease, including treatment, remission, and relapse. In addition to genetic alterations, epigenetic changes and changes in gene expression are of pivotal importance to AML pathogenesis. Together, these studies have identified molecular and genetic alterations that support the diagnosis of AML and facilitate prognostication and disease monitoring. In select cases, they also form the basis for targeted therapies. Indeed, the AML subtype acute promyelocytic leukemia was one of the earliest examples of targeted cancer therapy; all-trans retinoic acid, introduced into the treatment regimen over three decades ago, has impressively improved patient outcome. In the past two years, inhibitors of mutated IDH and FLT3 were approved for use in AML treatment, and several other targeted therapies are under development and hoped to ameliorate the outcome of this aggressive disease in the future.

Another important line of research concerns the role of stem cells in AML. Understanding their roles in disease formation, therapy resistance, and relapse and their interactions with the specific microenvironment of their niche in bone marrow is expected to lead to discoveries that can be exploited therapeutically.

In a recent IJMS Special Issue dedicated to the genetics, biology, and treatment of AML, colleagues contributed valuable articles discussing the genetic hierarchy of AML, the role of measurable residual disease monitoring, relapse of AML after stem cell transplantation, clonal evolution in myelodysplastic syndromes, mouse models of AML, the role of the epigenome in AML with RUNX1-ETO fusions, and therapeutic vulnerabilities in FLT3-mutant AML.

We now welcome additional articles concerning the topics outlined above and/or related to the key words listed below.

Prof. Rotraud Wieser
Guest Editor

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