ArticleCancer science2007
RUNX1/EVI1, which blocks myeloid differentiation, inhibits CCAAT-enhancer binding protein alpha function.
Article in Cancer science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- SPINK2 in hematopoiesis and cancer: Biology and clinical implications.Cell death discovery · 2026Review
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Significance of Somatic Mutation Profiling in CML Beyond BCR-ABL: A Retrospective Study of the Indian Population.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025Article
- 3q26.2/Cancers · 2023Article
- Review
- C/EBPα overrides epigenetic reprogramming by oncogenic transcription factors in acute myeloid leukemia.Blood advances · 2018Article
- Acute myeloid leukemia with t(3;21)(q26.2;q22) developing following low-dose methotrexate therapy for rheumatoid arthritis and expressing two AML1/MDS1/EVI1 fusion proteins: A case report.Oncology letters · 2017Article
- RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.Cell reports · 2017Article
- EVI1 Interferes with Myeloid Maturation via Transcriptional Repression of Cebpa, via Binding to Two Far Downstream Regulatory Elements.The Journal of biological chemistry · 2016Article
- The trithorax protein partner menin acts in tandem with EZH2 to suppress C/EBPα and differentiation in MLL-AF9 leukemia.Haematologica · 2013Article
- Fadd and Skp2 are possible downstream targets of RUNX1-EVI1.International journal of hematology · 2013Article
- Hierarchical differentiation of myeloid progenitors is encoded in the transcription factor network.PloS one · 2011Article
- Regulation of clock-controlled genes in mammals.PloS one · 2009Article
- Role of the RUNX1-EVI1 fusion gene in leukemogenesis.Cancer science · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RUNX1/EVI1 chimeric transcription factor produced by t(3;21) causes leukemic transformation in hematopoietic stem cell tumors, possibly through a differentiation block of malignant myeloid progenitors. A dominant negative effect over wild-type RUNX1 has been shown to constitute one of the underlying molecular mechanisms. We introduced RUNX1/EVI1 cDNA into LG-3 cells that differentiate along the myeloid lineage upon exposure to granulocyte colony stimulating factor, and confirmed that RUNX1/EVI1 suppressed the differentiation. To further investigate the molecular mechanisms of RUNX1/EVI1-mediated differentiation block, we analyzed RUNX1/EVI1's effect on the functions of CCAAT-enhancer binding protein alpha (C/EBPalpha), a key transcriptional regulator that induces granulocytic differentiation. RUNX1/EVI1 was found to associate with C/EBPalpha. By using a reporter assay with the CEBPA promoter, we observed a dominant negative effect of RUNX1/EVI1 over C/EBPalpha-mediated transcriptional activation via the carboxyl terminal-binding protein (CtBP)-binding site in the EVI1 portion. In a gel-shift assay, RUNX1/EVI1 downregulated the DNA-binding activity of C/EBPalpha. Therefore, recruitment of histone deacetylase via CtBP and disruption of DNA binding could be likely scenarios for the RUNX1/EVI1-induced dominant repression on C/EBPalpha. Importantly, coexpression of C/EBPalpha restored the differentiation ability of the RUNX1/EVI1-expressing LG-3 cells. All of these data argue that inhibition of C/EBPalpha function may be causatively related to the leukemogenic potential of RUNX1/EVI1.
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.