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Pronier, Elodie; Bowman, Robert L.; Ahn, Jihae; Glass, Jacob; Kandoth, Cyriac; Merlinsky, Tiffany R.; Whitfield, Justin T.; Durham, Benjamin H.; Gruet, Antoine; Hanasoge Somasundara, Amritha Varshini; Rampal, Raajit; Melnick, Ari; Koche, Richard P.; Taylor, Barry S.; Levine, Ross L.
Blood, 09/2018, Letnik: 132, Številka: 12Journal Article
Genetic studies have identified recurrent somatic mutations in acute myeloid leukemia (AML) patients, including in the Wilms' tumor 1 (WT1) gene. The molecular mechanisms by which WT1 mutations contribute to leukemogenesis have not yet been fully elucidated. We investigated the role of Wt1 gene dosage in steady-state and pathologic hematopoiesis. Wt1 heterozygous loss enhanced stem cell self-renewal in an age-dependent manner, which increased stem cell function over time and resulted in age-dependent leukemic transformation. Wt1-haploinsufficient leukemias were characterized by progressive genetic and epigenetic alterations, including those in known leukemia-associated alleles, demonstrating a requirement for additional events to promote hematopoietic transformation. Consistent with this observation, we found that Wt1 depletion cooperates with Flt3-ITD mutation to induce fully penetrant AML. Our studies provide insight into mechanisms of Wt1-loss leukemogenesis and into the evolutionary events required to induce transformation of Wt1-haploinsufficient stem/progenitor cells. •Wt1 heterozygous loss enhanced stem cell self-renewal in an age-dependent manner.•Wt1-haploinsufficient leukemias require additional events to promote hematopoietic transformation. Display omitted
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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