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Acute Myeloid Leukemia (AML) has been reported to arise from Pre-Leukemic Stem Cells (pre-LSCs), which are derived from Hematopoietic Stem and Progenitor Cells (HSPCs). Pre-LSCs can survive chemotherapy thus indicating that they play a role in disease recurrence in AML patients. In AML, somatic mutations of TP53 occurs in approximately 20% of patients and are associated with poor survival rates and increased resistance to intensive therapy. More recently, it has been suggested that TP53 mutations may play a role in the early events of AML, hence the rationale of this study.
In a Letter to the Editor of Blood on 3rd March 2017, Ridhimal Lal from the Medical University of Graz, Graz, Austria, and colleagues discussed their study which investigated the effect of somatic TP53 mutations on early events of AML development.
In summation, somatically acquired TP53 mutations characterize pre-LSCs, initiate genetic events and are mediators of resistant disease in AML.
The authors concluded by highlighting that their study adds further evidence to “recent claims of TP53 mutated AML as a distinct disease entity”. They further suggested that their study would have implications for the development of targeted treatment approaches for TP53 mutated AML.
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