ArticleBlood2012
Stress hematopoiesis reveals abnormal control of self-renewal, lineage bias, and myeloid differentiation in Mll partial tandem duplication (Mll-PTD) hematopoietic stem/progenitor cells.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Synergistic adverse prognosis ofFrontiers in cell and developmental biology · 2026Article
- 'Nomadic' Hematopoietic Stem Cells Navigate the Embryonic Landscape.Stem cell reviews and reports · 2025Review
- Hydrogels Containing Gradients in Vascular Density Reveal Dose-Dependent Role of Angiocrine Cues on Stem Cell Behavior.Advanced functional materials · 2021Article
- Review
- Connecting secretome to hematopoietic stem cell phenotype shifts in an engineered bone marrow niche.Integrative biology : quantitative biosciences from nano to macro · 2020Article
- Article
- DNMT3A mutants provide proliferating advantage with augmentation of self-renewal activity in the pathogenesis of AML in KMT2A-PTD-positive leukemic cells.Oncogenesis · 2020Article
- Clinical implications of recurrent gene mutations in acute myeloid leukemia.Experimental hematology & oncology · 2020Review
- SETD2 mutations confer chemoresistance in acute myeloid leukemia partly through altered cell cycle checkpoints.Leukemia · 2019Article
- Soluble Signals and Remodeling in a Synthetic Gelatin-Based Hematopoietic Stem Cell Niche.Advanced healthcare materials · 2019Article
- The Landscape ofHemaSphere · 2019Article
- Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes.Cancer discovery · 2018Article
- Article
- PU.1 is essential for MLL leukemia partially via crosstalk with the MEIS/HOX pathway.Leukemia · 2014Article
- Downregulation of RUNX1/CBFβ by MLL fusion proteins enhances hematopoietic stem cell self-renewal.Blood · 2014Article
- Identification of functional cooperative mutations of SETD2 in human acute leukemia.Nature genetics · 2014Article
- Article
- Article
- Stem cell enrichment with selectin receptors: mimicking the pH environment of trauma.Sensors (Basel, Switzerland) · 2013Article
- Review
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
Abstract
One mechanism for disrupting the MLL gene in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) is through partial tandem duplication (MLL-PTD); however, the mechanism by which MLL-PTD contributes to MDS and AML development and maintenance is currently unknown. Herein, we investigated hematopoietic stem/progenitor cell (HSPC) phenotypes of Mll-PTD knock-in mice. Although HSPCs (Lin(-)Sca1(+)Kit(+) (LSK)/SLAM(+) and LSK) in Mll(PTD/WT) mice are reduced in absolute number in steady state because of increased apoptosis, they have a proliferative advantage in colony replating assays, CFU-spleen assays, and competitive transplantation assays over wild-type HSPCs. The Mll(PTD/WT)-derived phenotypic short-term (ST)-HSCs/multipotent progenitors and granulocyte/macrophage progenitors have self-renewal capability, rescuing hematopoiesis by giving rise to long-term repopulating cells in recipient mice with an unexpected myeloid differentiation blockade and lymphoid-lineage bias. However, Mll(PTD/WT) HSPCs never develop leukemia in primary or recipient mice, suggesting that additional genetic and/or epigenetic defects are necessary for full leukemogenic transformation. Thus, the Mll-PTD aberrantly alters HSPCs, enhances self-renewal, causes lineage bias, and blocks myeloid differentiation. These findings provide a framework by which we can ascertain the underlying pathogenic role of MLL-PTD in the clonal evolution of human leukemia, which should facilitate improved therapies and patient outcomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.