ArticleOncogene2010
ETV6/RUNX1 abrogates mitotic checkpoint function and targets its key player MAD2L1.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Trial
- The overexpression of HOXC6 in LUSC and pan-squamous cell carcinomas indicates the coexistence of nuclear division regulatory mechanisms.Cancer biomarkers : section A of Disease markers · 2025Article
- PIGN spatiotemporally regulates the spindle assembly checkpoint proteins in leukemia transformation and progression.Scientific reports · 2021Article
- Identifying functions and prognostic biomarkers of network motifs marked by diverse chromatin states in human cell lines.Oncogene · 2020Article
- Examining the biomarkers and molecular mechanisms of medulloblastoma based on bioinformatics analysis.Oncology letters · 2019Article
- Chromosome integrity checkpoints in stem and progenitor cells: transitions upon differentiation, pathogenesis, and aging.Cellular and molecular life sciences : CMLS · 2018Review
- Pathogenesis of ETV6/RUNX1-positive childhood acute lymphoblastic leukemia and mechanisms underlying its relapse.Oncotarget · 2017Review
- Predicting interactome network perturbations in human cancer: application to gene fusions in acute lymphoblastic leukemia.Molecular biology of the cell · 2014Article
- Blocking ETV6/RUNX1-induced MDM2 overexpression by Nutlin-3 reactivates p53 signaling in childhood leukemia.Leukemia · 2014Article
- ETV6/RUNX1 induces reactive oxygen species and drives the accumulation of DNA damage in B cells.Neoplasia (New York, N.Y.) · 2013Article
- Silencing of ETV6/RUNX1 abrogates PI3K/AKT/mTOR signaling and impairs reconstitution of leukemia in xenografts.Leukemia · 2012Article
- Cell cycle control in acute myeloid leukemia.American journal of cancer research · 2012Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Approximately 25% of childhood B-cell precursor acute lymphoblastic leukemia have an ETV6/RUNX1 (E/R) gene fusion that results from a t(12;21). This genetic subgroup of leukemia is associated with near-triploidy, near-tetraploidy, and trisomy 21 as rather specific types of secondary changes. Here, we show that, unlike various controls, E/R-expressing Ba/F3 clones acquire a tetraploid karyotype on prolonged culture, corroborating the assumption that E/R may attenuate the mitotic checkpoint (MC). Consistent with this notion, E/R-expressing diploid murine and human cell lines have decreased proportions of cells with 4N DNA content and a lower mitotic index when treated with spindle toxins. Moreover, both RUNX1 and E/R regulate mitotic arrest-deficient 2 L1 (MAD2L1), an essential MC component, by binding to promoter-inherent RUNX1 sites, which results in down-regulation of MAD2L1 mRNA and protein in E/R-expressing cells. Forced expression of E/R also abolishes RUNX1-induced reporter activation, whereas E/R with a mutant DNA-binding site leads to only minor effects. Our data link for the first time E/R, MC, and MAD2L1 and provide new insights into the function of the E/R fusion gene product. Although tetraploidy is an almost exclusive feature of E/R-positive leukemias, its rarity within this particular subgroup implies that further yet unknown factors are required for its manifestation.
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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.