ArticleOncogene2014
Aggressive acute myeloid leukemia in PU.1/p53 double-mutant mice.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Review
- The synergistic effect of c-Myb hyperactivation and Pu.1 deficiency induces Pelger-Huët anomaly and promotes sAML.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Combined Approach to Leukemic Differentiation Using Transcription Factor PU.1-Enhancing Agents.International journal of molecular sciences · 2022Article
- BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.Blood advances · 2022Article
- Review
- Intricate crosstalk between MYB and noncoding RNAs in cancer.Cancer cell international · 2021Review
- Aberrant chromatin landscape following loss of the H3.3 chaperone Daxx in haematopoietic precursors leads to Pu.1-mediated neutrophilia and inflammation.Nature cell biology · 2021Article
- Kras mutations and PU.1 promoter methylation are new pathways in murine radiation-induced AML.Carcinogenesis · 2020Article
- The role of TP53 in acute myeloid leukemia: Challenges and opportunities.Genes, chromosomes & cancer · 2019Review
- [Advances in the mouse models of myeloid leukemia].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2019Review
- MicroRNAs as New Biomarkers for Diagnosis and Prognosis, and as Potential Therapeutic Targets in Acute Myeloid Leukemia.International journal of molecular sciences · 2018Review
- Dynamical Analysis of the Regulatory Network Controlling Natural Killer Cells Differentiation.Frontiers in physiology · 2018Article
- Overview of the Use of Murine Models in Leukemia and Lymphoma Research.Frontiers in oncology · 2017Review
- Article
- GATA-1 Inhibits PU.1 Gene via DNA and Histone H3K9 Methylation of Its Distal Enhancer in Erythroleukemia.PloS one · 2016Article
- Digging deep into "dirty" drugs - modulation of the methylation machinery.Drug metabolism reviews · 2015Review
- PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML.Carcinogenesis · 2015Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PU.1 downregulation within hematopoietic stem and progenitor cells (HSPCs) is the primary mechanism for the development of acute myeloid leukemia (AML) in mice with homozygous deletion of the upstream regulatory element (URE) of PU.1 gene. p53 is a well-known tumor suppressor that is often mutated in human hematologic malignancies including AML and adds to their aggressiveness; however, its genetic deletion does not cause AML in mouse. Deletion of p53 in the PU.1(ure/ure) mice (PU.1(ure/ure)p53(-/-)) results in more aggressive AML with shortened overall survival. PU.1(ure/ure)p53(-/-) progenitors express significantly lower PU.1 levels. In addition to URE deletion we searched for other mechanisms that in the absence of p53 contribute to decreased PU.1 levels in PU.1(ure/ure)p53(-/-) mice. We found involvement of Myb and miR-155 in downregulation of PU.1 in aggressive murine AML. Upon inhibition of either Myb or miR-155 in vitro the AML progenitors restore PU.1 levels and lose leukemic cell growth similarly to PU.1 rescue. The MYB/miR-155/PU.1 axis is a target of p53 and is activated early after p53 loss as indicated by transient p53 knockdown. Furthermore, deregulation of both MYB and miR-155 coupled with PU.1 downregulation was observed in human AML, suggesting that MYB/miR-155/PU.1 mechanism may be involved in the pathogenesis of AML and its aggressiveness characterized by p53 mutation.
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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.