Acute myeloid leukemia (AML) is the most common neoplastic transformation of the myeloid lineage of blood cells. Unfortunately, despite numerous studies, the main treatment remains chemotherapy, and the 5-year survival rates vary from 12% to 70%, depending on the type of AML; these statistics highlight the need for new therapies. To make matters worse, the observation that these types of blood cancers are associated with few genomic mutations contributes to shifting research toward epigenetic therapies, which have been proving highly effective. Our research group is studying the effect of a possible combination of an enzyme, phospholipase C beta 1 (PLCβ1), and epigenetic factors in the treatment of AML. The enzyme PLCβ1 is involved in the regulation of phosphatidylinositols (PI), molecules that can localize to different parts of the cell, where they regulate various and numerous biological processes, such as growth, differentiation, or gene expression. The aim is to use PLCβ1 and PI to "reprogram" the function of epigenetic factors so that the neoplastic cell returns to expressing the correct genes, thus becoming a healthy cell, while also minimizing side effects on normal hematopoietic stem cells.
