ArticleOncogene2005
Myeloid maturation block by AML1-MTG16 is associated with Csf1r epigenetic downregulation.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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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.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- UBC9 inhibits myeloid differentiation in collaboration with AML1-MTG8.International journal of hematology · 2022Article
- High Expression of CSF-1R Predicts Poor Prognosis and CSF-1RFrontiers in oncology · 2022Article
- Homology modeling and molecular dynamics studies of Wilms' tumor gene 1 frameshift mutations in exon 7.Biomedical reports · 2013Article
- RUNX1: A microRNA hub in normal and malignant hematopoiesis.International journal of molecular sciences · 2013Review
- Opposing effects of Runx2 and estradiol on breast cancer cell proliferation: in vitro identification of reciprocally regulated gene signature related to clinical letrozole responsiveness.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Down-regulation of microRNAs 222/221 in acute myelogenous leukemia with deranged core-binding factor subunits.Neoplasia (New York, N.Y.) · 2010Article
- Runx2 transcriptome of prostate cancer cells: insights into invasiveness and bone metastasis.Molecular cancer · 2010Article
- Loss of MTG16a (CBFA2T3), a novel rDNA repressor, leads to increased ribogenesis and disruption of breast acinar morphogenesis.Journal of cellular and molecular medicine · 2010Article
- Novel RNA-binding properties of the MTG chromatin regulatory proteins.BMC molecular biology · 2008Article
- A distinct epigenetic signature at targets of a leukemia protein.BMC genomics · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
De novo epigenetic changes at histone and DNA level that affect gene transcription in cancer may be less random than we originally thought. Leukemia fusion proteins associated with specific chromosome translocations could mechanistically determine the epigenetic fate of specific target genes critical for normal hematopoiesis. This seems to be the case with AML1-MTG16, a fusion protein resulting from the t(16;21) translocation, a hallmark of therapy-related leukemia and myelodysplastic syndrome. Here we show that AML1-MTG16 blocks both myeloid differentiation and proliferation in the 32D/WT1-mouse myeloid cell line. These biological effects can be traced to the AML1 and MTG16 moieties of the fusion protein, respectively. Further, we show that AML1-MTG16 can induce epigenetic repressive changes at the histone and DNA level of the AML1 target gene Csf1r (c-fms), encoding the macrophage colony stimulating factor receptor. We observed that, concomitant with Csf1r downregulation, 32D/WT1 cells lost the ability to undergo myeloid differentiation in response to the granulocyte macrophage colony-stimulating factor (GM-CSF). Thus, there seems to be an association between AML1-MTG16-induced myeloid maturation block and epigenetic changes of a myeloid master gene.
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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.