ArticleProceedings of the National Academy of Sciences of the United States of America2006
Inactivation of PU.1 in adult mice leads to the development of myeloid leukemia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
50 citing papers in PubMed, 96 citations in OpenAlex.
- Emerging insights into epigenetics and hematopoietic stem cell trafficking in age-related hematological malignancies.Stem cell research & therapy · 2024Review
- Aging is associated with functional and molecular changes in distinct hematopoietic stem cell subsets.Nature communications · 2024Article
- Article
- PU.1-c-Jun interaction is crucial for PU.1 function in myeloid development.Communications biology · 2022Article
- Hyper-radiosensitivity affects low-dose acute myeloid leukemia incidence in a mathematical model.Radiation and environmental biophysics · 2022Article
- Combined Approach to Leukemic Differentiation Using Transcription Factor PU.1-Enhancing Agents.International journal of molecular sciences · 2022Article
- E3 ubiquitin ligases in the acute leukemic signaling pathways.Frontiers in physiology · 2022Review
- Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia.Nature communications · 2021Article
- Ubiquitin-Mediated Control of ETS Transcription Factors: Roles in Cancer and Development.International journal of molecular sciences · 2021Review
- Modeling low-dose radiation-induced acute myeloid leukemia in male CBA/H mice.Radiation and environmental biophysics · 2021Article
- PRDM16s transforms megakaryocyte-erythroid progenitors into myeloid leukemia-initiating cells.Blood · 2019Article
- Down-Regulation ofInternational journal of hematology-oncology and stem cell research · 2019Article
- PU.1 regulates Alzheimer's disease-associated genes in primary human microglia.Molecular neurodegeneration · 2018Article
- Article
- Tracking preleukemic cells in vivo to reveal the sequence of molecular events in radiation leukemogenesis.Leukemia · 2018Article
- Senescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells.Haematologica · 2017Article
- Systemic inoculation of Escherichia coli causes emergency myelopoiesis in zebrafish larval caudal hematopoietic tissue.Scientific reports · 2016Article
- Mouse models for radiation-induced cancers.Mutagenesis · 2016Review
- Article
- Genome-scale definition of the transcriptional programme associated with compromised PU.1 activity in acute myeloid leukaemia.Leukemia · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Genetically primed adult C57BL mice were deleted of exon 5 of the gene encoding the transcription factor PU.1 by IFN activation of Cre recombinase. After a 13-week delay, conditionally deleted (PU.1(-/-)) mice began dying of myeloid leukemia, and 95% of the mice surviving from early postinduction death developed transplantable myeloid leukemia whose cells were deleted of PU.1 and uniformly Gr-1 positive. The leukemic cells formed autonomous colonies in semisolid culture with varying clonal efficiency, but colony formation was enhanced by IL-3 and sometimes by granulocyte-macrophage colony-stimulating factor. Nine of 13 tumors analyzed had developed a capacity for autocrine IL-3 or granulocyte-macrophage colony-stimulating factor production, and there was evidence of rearrangement of the IL-3 gene. Acquisition of autocrine growth-factor production and autonomous growth appeared to be major events in the transformation of conditionally deleted PU.1(-/-) cells to fully developed myeloid leukemic populations.
Indexed as
Identifiers
What OpenQuestion holds
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.