ArticleCarcinogenesis2020
Kras mutations and PU.1 promoter methylation are new pathways in murine radiation-induced AML.
Article in Carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed, 17 citations in OpenAlex.
- ARID1A deficiency promotes malignant proliferation of hepatocellular carcinoma by activating HDAC7/ENO1 signaling pathway.Hepatology communications · 2025Article
- Review
- Identification and interaction analysis of hubgenes related to neutrophil ferroptosis in intracranial atherosclerotic stenosis.Genetics and molecular biology · 2025Article
- PU.1 upregulation is linked to improved prognosis in non-small cell lung cancer.Frontiers in immunology · 2025Article
- The roles of ubiquitination in AML.Annals of hematology · 2024Review
- Article
- Circ_DLEU2 knockdown represses cell proliferation, migration and invasion, and induces cell apoptosis through the miR-582-5p/COX2 pathway in acute myeloid leukemia.Histology and histopathology · 2023Article
- Protection of the hematopoietic system against radiation-induced damage: drugs, mechanisms, and developments.Archives of pharmacal research · 2022Review
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Therapy-related and more specifically radiotherapy-associated acute myeloid leukaemia (AML) is a well-recognized potential complication of cytotoxic therapy for the treatment of a primary cancer. The CBA mouse model is used to study radiation leukaemogenesis mechanisms with Sfpi1/PU.1 deletion and point mutation already identified as driving events during AML development. To identify new pathways, we analysed 123 mouse radiation-induced AML (rAML) samples for the presence of mutations identified previously in human AML and found three genes to be mutated; Sfpi1 R235 (68%), Flt3-ITD (4%) and Kras G12 (3%), of which G12R was previously unreported. Importantly, a significant decrease in Sfpi1 gene expression is found almost exclusively in rAML samples without an Sfpi1 R235 mutation and is specifically associated with up-regulation of mir-1983 and mir-582-5p. Moreover, this down-regulation of Sfpi1 mRNA is negatively correlated with DNA methylation levels at specific CpG sites upstream of the Sfpi1 transcriptional start site. The down regulation of Sfpi1/PU.1 has also been reported in human AML cases revealing one common pathway of myeloid disruption between mouse and human AML where dysregulation of Sfpi1/PU.1 is a necessary step in AML development.
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