Tet2-mutated myeloid progenitors possess aberrant in vitro self-renewal capacity

摘要

Ten-Eleven-Translocation 2 (TET2) is one of the most frequently mutated genes in various hematologic malignancies. Li et al have previously reported that the deletion of Tet2 in mice led to dysregulated hematopoietic stem cells (HSCs) and subsequent development of myeloid malignancies. We and others have also reported similar findings using different strains of Tet2-mutant mice.These observations led us to speculate that enhanced HSC function of Tet2-mutant mice sets a critical background for malignant transformation, and such dysregulated HSCs are the cell of origin for myeloid malignancies.