Epigenetics in Myeloproliferative Neoplasms and Acute Myeloid Leukemia

Dear Colleagues,

Research over the past years has revealed the increasingly intricate landscape of acute myeloid leukemia (AML) and myeloproliferative neoplasms (MPN). Today it is well-appreciated that the heterogeneity of malignant cells in both diseases is triggered by sets of cytogenetic abnormalities and somatic mutations. Besides this genetic complexity, diversification in the epigenome has also been identified as a key player in both tumors. The multidimensional epigenetic picture integrates several layers of (dys)regulated DNA methylation, histone modification, and microRNA modulation. Indeed, abnormal epigenetic signatures, some of which may be linked to specific somatic mutations, frequently present in AML and MPN can profoundly disrupt the phenotype of hematopoietic cells. Furthermore, epigenetic (dys)regulation has emerged as an intersection of several key hallmarks of cancer such as immunology and metabolism.

Thus, understanding the functional link between genetic and epigenetic heterogeneity in AML and MPN, and what they contribute to the disease is an important area of research that would aid clinical decision-making and enhance drug development.

In this Topical Collection, we will discuss the current trends in epigenetic dysregulation in AML and MPN, their interactions with other cancer mechanisms, the interrelation between epigenetics and genetics, and the research on the development of drugs targeting epigenetic regulators, such as IDH1/2 inhibitors and BET proteins, as monotherapies or combination therapies in AML and MPN.

Dr. Haifa Kathrin Al-Ali
Collection Editor

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