An improved understanding of the biology underlying leukemogenesis, including the determination of the cells of leukemia origin, is of great importance as it can have immediate implications on patient treatment and management. The article by Riemke et al (2016) provides further evidence that a subgroup of acute myeloid leukemia (AML), the most common acute leukemia in adults, might arise from T‐lymphoid progenitor cells. This study not only supports that the lymphoid fate of early T‐cell progenitors is not yet fully stabilized but also shows that under oncogenic conditions, this multilineage plasticity potential of T‐lymphoid progenitors can lead to transdifferentiation into myeloid leukemia. While gene expression profiles suggest that approximately 5% of all AML cases originate from T‐lymphoid progenitors, novel treatment strategies targeting JAK2/STAT3 signaling might open new avenues for this AML cohort.
See also: P Riemke et al (November 2016)
Based on the accumulation of genetic and epigenetic changes, acute myeloid leukemia (AML) arises from transformed immature hematopoietic cells, that is, hematopoietic stem cells (HSC) or committed progenitor cells (Pandolfi et al, 2013). First, this multistep process of transforming events gives rise to preleukemic stem cells (pre‐LSC), which precede leukemia stem cells (LSC; Fig 1). Unfortunately, the LSC compartment very often cannot be effectively eradicated despite the use of intensive chemotherapy and allogeneic stem cell transplantation. Thus, for the development of novel treatment …
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