ArticleOncogene2005
Mutations of the PU.1 Ets domain are specifically associated with murine radiation-induced, but not human therapy-related, acute myeloid leukaemia.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- Review
- Article
- Hyper-radiosensitivity affects low-dose acute myeloid leukemia incidence in a mathematical model.Radiation and environmental biophysics · 2022Article
- Oxidative Stress and X-ray Exposure Levels-Dependent Survival and Metabolic Changes in Murine HSPCs.Antioxidants (Basel, Switzerland) · 2021Article
- Modeling low-dose radiation-induced acute myeloid leukemia in male CBA/H mice.Radiation and environmental biophysics · 2021Article
- Kras mutations and PU.1 promoter methylation are new pathways in murine radiation-induced AML.Carcinogenesis · 2020Article
- Article
- Low-dose radiation accelerates aging of the T-cell receptor repertoire in CBA/Ca mice.Cellular and molecular life sciences : CMLS · 2017Article
- PML/RARa inhibits PTEN expression in hematopoietic cells by competing with PU.1 transcriptional activity.Oncotarget · 2016Article
- Mouse models for radiation-induced cancers.Mutagenesis · 2016Review
- Transcriptomic and proteomic analysis of mouse radiation-induced acute myeloid leukaemia (AML).Oncotarget · 2016Article
- RAG-mediated DNA double-strand breaks activate a cell type-specific checkpoint to inhibit pre-B cell receptor signals.The Journal of experimental medicine · 2016Article
- Genome-scale definition of the transcriptional programme associated with compromised PU.1 activity in acute myeloid leukaemia.Leukemia · 2016Article
- PU.1 affects proliferation of the human acute myeloid leukemia U937 cell line by directly regulating MEIS1.Oncology letters · 2015Article
- PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML.Carcinogenesis · 2015Review
- Radiation-induced myeloid leukemia in murine models.Human genomics · 2014Review
- Live cell detection of chromosome 2 deletion and Sfpi1/PU1 loss in radiation-induced mouse acute myeloid leukaemia.Leukemia research · 2013Article
- Frequency of acute myeloid leukaemia-associated mouse chromosome 2 deletions in X-ray exposed immature haematopoietic progenitors and stem cells.Mutation research · 2013Article
- Molecular characterisation of murine acute myeloid leukaemia induced by 56Fe ion and 137Cs gamma ray irradiation.Mutagenesis · 2013Article
- Mouse models for efficacy testing of agents against radiation carcinogenesis—a literature review.International journal of environmental research and public health · 2012Review
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Murine radiation-induced acute myeloid leukaemia (AML) is characterized by loss of one copy of chromosome 2. Previously, we positioned the critical haematopoietic-specific transcription factor PU.1 within a minimally deleted region. We now report a high frequency (>65%) of missense mutation at codon 235 in the DNA-binding Ets domain of PU.1 in murine AML. Earlier studies, outside the context of malignancy, determined that conversion of arginine 235 (R235) to any other amino-acid residue leads to ablation of DNA-binding function and loss of expression of downstream targets. We show that mutation of R235 does not lead to protein loss, and occurs specifically in those AMLs showing loss of one copy of PU.1 (P=0.001, Fisher's exact test). PU.1 mutations were not found in the coding region, UTRs or promoter of human therapy-related AMLs. Potentially regulatory elements upstream of PU.1 were located but no mutations found. In conclusion, we have identified the cause of murine radiation-induced AML and have shown that loss of one copy of PU.1, as a consequence of flanking radiation-sensitive fragile domains on chromosome 2, and subsequent R235 conversion are highly specific to this mouse model. Such a mechanism does not operate, or is extremely rare, in human AML.
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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.