Expression of BECN1 gene in Acute Myeloid Leukemia: Association with Hematological and Clinical Parameters

Abstract

Acute myeloid leukemia (AML) is characterized by the accumulation of immature blast cells in the bone marrow, resulting in a disruption of normal hematopoiesis. The growth advantage of leukemic cells over the normal hematopoietic stem and progenitor cells (HPSC) is linked to a perturbation in differentiation, metabolic and cell survival programming, as a result of a number of genetic and epigenetic defects. Autophagy, a catabolic cellular process conserved in all eukaryotes, plays an important role in cell proliferation, differentiation, survival and homeostasis. In cellular stress conditions such as nutrient deprivation, hypoxia, accumulation of protein aggregates and infection, double-layered membrane vesicles called auto-phagosomes engulf long-lived proteins, damaged organelles and pathogens. The auto-phagosomes fuse with lysosomes to degrade and recycle the enclosed contents. Aberrant autophagy is implicated in numerous diseases, including acute myeloid leukemia. In AML, loss in the autophagic genes as BECN1was recognized. BECN1 gene is essential for autophagy. As a critical mediator, BECN1gene influences the onset and advance of autophagy.