ArticleProceedings of the National Academy of Sciences of the United States of America2005
Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 82 citations in OpenAlex.
- PML::RARA and GATA2 proteins interact via DNA templates to induce aberrant self-renewal in mouse and human hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Gut microbiome as therapeutic target for diabesity management: opportunity for nanonutraceuticals and associated challenges.Drug delivery and translational research · 2024Review
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- PU.1-Dependent Enhancer Inhibition Separates Tet2-Deficient Hematopoiesis from Malignant Transformation.Blood cancer discovery · 2022Article
- Article
- CircSPI1 acts as an oncogene in acute myeloid leukemia through antagonizing SPI1 and interacting with microRNAs.Cell death & disease · 2021Article
- CITED2 and the modulation of the hypoxic response in cancer.World journal of clinical oncology · 2020Review
- Senescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells.Haematologica · 2017Article
- Haploinsufficiency for DNA methyltransferase 3A predisposes hematopoietic cells to myeloid malignancies.The Journal of clinical investigation · 2017Article
- Mouse models for radiation-induced cancers.Mutagenesis · 2016Review
- 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
- JNK-dependent gene regulatory circuitry governs mesenchymal fate.The EMBO journal · 2015Article
- PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML.Carcinogenesis · 2015Review
- CITED2-mediated human hematopoietic stem cell maintenance is critical for acute myeloid leukemia.Leukemia · 2015Article
- Article
- MIR125B1 represses the degradation of the PML-RARA oncoprotein by an autophagy-lysosomal pathway in acute promyelocytic leukemia.Autophagy · 2014Article
- Radiation-induced myeloid leukemia in murine models.Human genomics · 2014Review
- Positive feedback between PU.1 and the cell cycle controls myeloid differentiation.Science (New York, N.Y.) · 2013Article
- Notch signaling in acute promyelocytic leukemia.Leukemia · 2013Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
PU.1 is a member of the ETS family of transcription factors that is known to be important for hematopoietic development. Recently, haploinsufficiency for PU.1 has been shown to cause a shift in myelomonocytic progenitor fate toward the myeloid lineage. We have previously shown that transgenic mice expressing PML-RARalpha (PR) and RARalpha-PML frequently develop acute promyelocytic leukemia (APL) in association with a large (>20 Mb) interstitial deletion of chromosome 2 that includes PU.1. To directly assess the relevance of levels of expression of PU.1 for leukemia progression, we bred hCG-PR mice with PU.1+/- mice and assessed their phenotype. Young, nonleukemic hCG-PR x PU.1+/- mice developed splenomegaly because of the abnormal expansion of myeloid cells in their spleens. hCG-PR x PU.1+/- mice developed a typical APL syndrome after a long latent period, but the penetrance of disease was 84%, compared with 7% in hCG-PR x PU.1+/+ mice (P < 0.0001). The residual PU.1 allele in hCG-PR x PU.1+/- APL cells was expressed, and complete exonic resequencing revealed no detectable mutations in nine of nine samples. However, PR expression in U937 myelomonocytic cells and primary murine myeloid bone marrow cells caused a reduction in PU.1 mRNA levels. Therefore, the loss of one copy of PU.1 through a deletional mechanism, plus down-regulation of the residual allele caused by PR expression, may synergize to expand the pool of myeloid progenitors that are susceptible to transformation, increasing the penetrance of APL.
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