ArticleNature communications2019
MLL-AF9 initiates transformation from fast-proliferating myeloid progenitors.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.
What it found
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
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- Research Progress on the KMT2A-AFF3 Fusion Gene in Childhood Acute Lymphoblastic Leukemia: Mechanisms, Clinical Implications, and Therapeutic Strategies.Current issues in molecular biology · 2025Review
- Involvement of membrane palmitoylated protein 6 (MPP6) in synapses of mouse cerebrum.Histochemistry and cell biology · 2025Article
- Context and timing matters in acute myeloid leukemia: females are the superior hosts.Haematologica · 2025Article
- Fine-tuning plant valuable secondary metabolite biosynthesis via small RNA manipulation: strategies and potential.Planta · 2024Review
- Trained and ready - the case for an inflammatory memory for hematopoietic stem and progenitor cells in the AML niche.Oncotarget · 2024Review
- The Role of Epithelial-to-Mesenchymal Transition Transcription Factors (EMT-TFs) in Acute Myeloid Leukemia Progression.Biomedicines · 2024Review
- Inflammatory recruitment of healthy hematopoietic stem and progenitor cells in the acute myeloid leukemia niche.Leukemia · 2024Article
- Low doses of IFN-γ maintain self-renewal of leukemia stem cells in acute myeloid leukemia.Oncogene · 2023Article
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- Serum Response Factor Reduces Gene Expression Noise and Confers Cell State Stability.Stem cells (Dayton, Ohio) · 2023Article
- EVI1 exerts distinct roles in AML via ERG and cyclin D1 promoting a chemoresistant and immune-suppressive environment.Blood advances · 2023Article
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- Vascular endothelial cell development and diversity.Nature reviews. Cardiology · 2023Review
- Krüppel-like Factor 4 Supports the Expansion of Leukemia Stem Cells in MLL-AF9-driven Acute Myeloid Leukemia.Stem cells (Dayton, Ohio) · 2022Article
- Connecting Calcium-Based Nanomaterials and Cancer: From Diagnosis to Therapy.Nano-micro letters · 2022Article
- Loss of IRF7 accelerates acute myeloid leukemia progression and induces VCAM1-VLA-4 mediated intracerebral invasion.Oncogene · 2022Article
- Epigenetic changes in human model KMT2A leukemias highlight early events during leukemogenesis.Haematologica · 2022Article
- Metabolic syndrome related gene signature predicts the prognosis of patients with pancreatic ductal carcinoma. A novel link between metabolic dysregulation and pancreatic ductal carcinoma.Cancer cell international · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Cancer is a hyper-proliferative disease. Whether the proliferative state originates from the cell-of-origin or emerges later remains difficult to resolve. By tracking de novo transformation from normal hematopoietic progenitors expressing an acute myeloid leukemia (AML) oncogene MLL-AF9, we reveal that the cell cycle rate heterogeneity among granulocyte-macrophage progenitors (GMPs) determines their probability of transformation. A fast cell cycle intrinsic to these progenitors provide permissiveness for transformation, with the fastest cycling 3% GMPs acquiring malignancy with near certainty. Molecularly, we propose that MLL-AF9 preserves gene expression of the cellular states in which it is expressed. As such, when expressed in the naturally-existing, rapidly-cycling immature myeloid progenitors, this cell state becomes perpetuated, yielding malignancy. In humans, high CCND1 expression predicts worse prognosis for MLL fusion AMLs. Our work elucidates one of the earliest steps toward malignancy and suggests that modifying the cycling state of the cell-of-origin could be a preventative approach against malignancy.
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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.