ArticleMolecular and cellular biology1996
Spi-1/PU.1 transgenic mice develop multistep erythroleukemias.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 186 citations in OpenAlex.
- Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes.International journal of molecular sciences · 2024Review
- FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.Oncogene · 2023Article
- Vagal-mAChR4 signaling promotes Friend virus complex (FV)-induced acute erythroleukemia.Virologica Sinica · 2023Article
- HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependent gene repression in murine erythroleukaemia.Nucleic acids research · 2022Article
- HDAC1 is required for GATA-1 transcription activity, global chromatin occupancy and hematopoiesis.Nucleic acids research · 2021Article
- Molecular Landscapes and Models of Acute Erythroleukemia.HemaSphere · 2021Review
- Article
- Regulating the Regulators: The Role of Histone Deacetylase 1 (HDAC1) in Erythropoiesis.International journal of molecular sciences · 2020Review
- Nuclear interacting SET domain protein 1 inactivation impairs GATA1-regulated erythroid differentiation and causes erythroleukemia.Nature communications · 2020Article
- The ParaHox gene Cdx4 induces acute erythroid leukemia in mice.Blood advances · 2019Article
- The Effect of Bone Marrow Mesenchymal Stem Cells on the Granulocytic Differentiation of HL-60 Cells.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2018Article
- Erythroleukemia-historical perspectives and recent advances in diagnosis and management.Blood reviews · 2018Review
- Senescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells.Haematologica · 2017Article
- Histone deacetylase 1 activates PU.1 gene transcription through regulating TAF9 deacetylation and transcription factor IID assembly.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- The Spi1/PU.1 transcription factor accelerates replication fork progression by increasing PP1 phosphatase in leukemia.Oncotarget · 2017Article
- Transcription Factor GFI1B in Health and Disease.Frontiers in oncology · 2017Review
- Genome-Wide Approaches to Defining Macrophage Identity and Function.Microbiology spectrum · 2016Review
- Mouse models for radiation-induced cancers.Mutagenesis · 2016Review
- Genetically Engineered In Vitro Erythropoiesis.International journal of stem cells · 2016Article
- GATA-1 Inhibits PU.1 Gene via DNA and Histone H3K9 Methylation of Its Distal Enhancer in Erythroleukemia.PloS one · 2016Article
24 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insertional mutagenesis of the spi-1 gene is associated with the emergence of malignant proerythroblasts during Friend virus-induced acute erythroleukemia. To determine the role of spi-1/PU.1 in the genesis of leukemia, we generated spi-1 transgenic mice. In one founder line the transgene was overexpressed as an unexpected-size transcript in various mouse tissues. Homozygous transgenic animals gave rise to live-born offspring, but 50% of the animals developed a multistep erythroleukemia within 1.5 to 6 months of birth whereas the remainder survived without evidence of disease. At the onset of the disease, mice became severely anemic. Their hematopoietic tissues were massively invaded with nontumorigenic proerythroblasts that express a high level of Spi-1 protein. These transgenic proerythroblasts are partially blocked in differentiation and strictly dependent on erythropoietin for their proliferation both in vivo and in vitro. A complete but transient regression of the disease was observed after erythrocyte transfusion, suggesting that the constitutive expression of spi-1 is related to the block of the differentiation of erythroid precursors. At relapse, erythropoietin-independent malignant proerythroblasts arose. Growth factor autonomy could be partially explained by the autocrine secretion of erythropoietin; however, other genetic events appear to be necessary to confer the full malignant phenotype. These results reveal that overexpression of spi-1 is essential for malignant erythropoiesis and does not alter other hematopoietic lineages.
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