ArticleCell2014
A single oncogenic enhancer rearrangement causes concomitant EVI1 and GATA2 deregulation in leukemia.
Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 419 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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Who cites it
419 citing papers in PubMed, 705 citations in OpenAlex.
- Identification of Genome-Wide Chromatin Structural Aberration in Cancer by Hi-C Analysis.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Origins and consequences of oncogenic 3D chromatin remodelling.Nature reviews. Cancer · 2026Review
- Tumor-specific super-enhancer drives overexpression of EVI1/MECOM in ovarian cancer.Neoplasia (New York, N.Y.) · 2026Article
- The Runx1-Gata2 axis: epigenetic architecture of lineage fate.Molecular biology reports · 2026Review
- Tandem Double Inversion Resolves the Structural Paradox Underlying Recurrent KAT6A::NCOA2 Fusion in Acute Myeloid Leukemia.Genes, chromosomes & cancer · 2026Article
- Optical genome mapping refines diagnosis of high-grade myeloid neoplasms through detection of MECOM rearrangements cryptic to conventional karyotype.American journal of clinical pathology · 2026Article
- 3D chromatin structure remodelling in cancer.Cell communication and signaling : CCS · 2026Review
- MECOM promotes leukemia progression and inhibits mast cell differentiation through functional competition with GATA2.Leukemia · 2026Article
- ZEB1 drives terminal erythroid maturation by controlling the GATA2-KLF1 regulatory switch.Nucleic acids research · 2026Article
- Optimized post-GWAS analysis identifies therapeutic targets for essential thrombocythemia and polycythemia vera.Communications medicine · 2026Article
- 3D chromatin architecture in cancer: mechanisms of dysregulation and emerging therapeutic strategies.Experimental & molecular medicine · 2026Review
- Hi-C for genome-wide detection of enhancer-hijacking rearrangements in routine lymphoid cancer biopsies.Cell genomics · 2026Article
- A specific stem cell program and CD112 immunological axis dysfunctions underpinning monosomy 7-associated myeloid neoplasms.Signal transduction and targeted therapy · 2026Article
- TCF3::HLF orchestrates an enhancer-promoter network with activation of MEF2C to promote immature HSC gene expression in leukemia.Science advances · 2026Article
- BCR::ABL1-Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B-ALL Cells to Enhancer-Targeting Drugs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Connecting multiway enhancer-promoter interactions to changes in gene expression in cancer.bioRxiv : the preprint server for biology · 2026Article
- Redistribution of super-enhancers promotes malignancy in human hepatocellular carcinoma.Journal of advanced research · 2026Article
- Crosstalk BetweenCancers · 2026Review
- Review
- BET inhibitor-based combinations targeting novel dependencies in MECOM-rearranged (r) AML.Leukemia · 2026Article
359 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosomal rearrangements without gene fusions have been implicated in leukemogenesis by causing deregulation of proto-oncogenes via relocation of cryptic regulatory DNA elements. AML with inv(3)/t(3;3) is associated with aberrant expression of the stem-cell regulator EVI1. Applying functional genomics and genome-engineering, we demonstrate that both 3q rearrangements reposition a distal GATA2 enhancer to ectopically activate EVI1 and simultaneously confer GATA2 functional haploinsufficiency, previously identified as the cause of sporadic familial AML/MDS and MonoMac/Emberger syndromes. Genomic excision of the ectopic enhancer restored EVI1 silencing and led to growth inhibition and differentiation of AML cells, which could be replicated by pharmacologic BET inhibition. Our data show that structural rearrangements involving the chromosomal repositioning of a single enhancer can cause deregulation of two unrelated distal genes, with cancer as the outcome.
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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.