The face of remission induction

Abstract

Acute myeloid leukaemia (AML) is a heterogeneous disease in which prognosis is determined by cytogenetic and molecular aberrations as well as patient-related factors, including age, prior haematologic disorders, and comorbidities. Despite the diverse disease biology, the standard of care for remission induction therapy has changed very little since its inception in 1973. Next generation sequencing has helped to increase our knowledge of the disease pathogenesis, allowing us to develop targeted and possibly more effective treatment options. Seven new agents have been approved for the treatment of AML since 2017, all of which are directed toward a specific molecular subtype or patient population. With the advent of these therapies, a more optimal, patient-specific approach rather than the historical 'one-size fits all' model can be utilised. This review will discuss the role of these novel therapies in the remission induction setting.

SPOP accelerates acute myeloid leukemia initiation and development through miR-183-mediated METAP2 inhibition

“…Acute myeloid leukemia (AML) represents a malignant disorder originating in the bone marrow, which has been recognized to cause clonal spread as well as differentiation arrest of myeloid progenitor cells [1]. It is a heterogeneous disease accompanied by a warning mortality, where the prognosis status is dependent on cytogenetic and molecular changes as well as patient-related situations, such as age, and complications [2,3]. Furthermore, AML is a genetically heterogeneous malignant disorder of the hematopoietic system, which has been reportedly indicated to accompany with the increase of immature myeloid precursors with injured DNA [4,5].…”