ReviewCarcinogenesis2015
PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML.
Review in Carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Computational Analysis of SPI1 Missense Mutations and ADMET-Guided Molecular Docking of Cinnamic Acid Targeting the PU.1 ETS Domain: Implications for Hematopoietic Dysregulation and Leukemogenesis.International journal of molecular sciences · 2026Article
- Spi-1 proto-oncogene regulates mRNA hypertranscription and malignant progression in head and neck cancer.Signal transduction and targeted therapy · 2026Article
- Review
- The role of SPI1/VSIG4/THBS1 on glioblastoma progression through modulation of the PI3K/AKT pathway.Journal of advanced research · 2025Article
- The role of long noncoding RNAs in the diagnosis, prognosis and therapeutic biomarkers of acute myeloid leukemia.Annals of hematology · 2024Review
- Article
- Article
- Identifying differentially expressed genes and miRNAs in Kawasaki disease by bioinformatics analysis.Scientific reports · 2022Article
- Hyper-radiosensitivity affects low-dose acute myeloid leukemia incidence in a mathematical model.Radiation and environmental biophysics · 2022Article
- Protection of the hematopoietic system against radiation-induced damage: drugs, mechanisms, and developments.Archives of pharmacal research · 2022Review
- Study on the role of transcription factor SPI1 in the development of glioma.Chinese neurosurgical journal · 2022Article
- Oxidative Stress and X-ray Exposure Levels-Dependent Survival and Metabolic Changes in Murine HSPCs.Antioxidants (Basel, Switzerland) · 2021Article
- DNA damage response of haematopoietic stem and progenitor cells to high-LET neutron irradiation.Scientific reports · 2021Article
- Modeling low-dose radiation-induced acute myeloid leukemia in male CBA/H mice.Radiation and environmental biophysics · 2021Article
- PTEN in Regulating Hematopoiesis and Leukemogenesis.Cold Spring Harbor perspectives in medicine · 2020Review
- Kras mutations and PU.1 promoter methylation are new pathways in murine radiation-induced AML.Carcinogenesis · 2020Article
- Clinical significance of PI3 and HLA-DOB as potential prognostic predicators for ovarian cancer.Translational cancer research · 2020Article
- No equal opportunity for leukemia initiating cells.Oncotarget · 2018Article
- Tracking preleukemic cells in vivo to reveal the sequence of molecular events in radiation leukemogenesis.Leukemia · 2018Article
- Transcription factor PU.1 is involved in the progression of glioma.Oncology letters · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor PU.1, encoded by the murine Sfpi1 gene (SPI1 in humans), is a member of the Ets transcription factor family and plays a vital role in commitment and maturation of the myeloid and lymphoid lineages. Murine studies directly link primary acute myeloid leukaemia (AML) and decreased PU.1 expression in specifically modified strains. Similarly, a radiation-induced chromosome 2 deletion and subsequent Sfpi1 point mutation in the remaining allele lead to murine radiation-induced AML. Consistent with murine data, heterozygous deletion of the SPI1 locus and mutation of the -14kb SPI1 upstream regulatory element were described previously in human primary AML, although they are rare events. Other mechanisms linked to PU.1 downregulation in human AML include TP53 deletion, FLT3-ITD mutation and the recurrent AML1-ETO [t(8;21)] and PML-RARA [t(15;17)] translocations. This review provides an up-to-date overview on our current understanding of the involvement of PU.1 in the initiation and development of radiation-induced AML, together with recommendations for future murine and human studies.
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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.