ArticleBlood2008
Loss of TLE1 and TLE4 from the del(9q) commonly deleted region in AML cooperates with AML1-ETO to affect myeloid cell proliferation and survival.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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
52 citing papers in PubMed, 89 citations in OpenAlex.
- Trial
- A novel knockout mouse model to assess the impact of one-copy loss of Hnrnpk in CD4 + T cells in chronically inflamed skin as a prelude to CTCL.Scientific reports · 2025Article
- Extrachromosomal circular DNA (eccDNA) characteristics in the bile and plasma of advanced perihilar cholangiocarcinoma patients and the construction of an eccDNA-related gene prognosis model.Frontiers in cell and developmental biology · 2024Article
- c-Myc-induced long noncoding RNA MIRE cooperates with hnRNPK to stabilize ELF2 mRNA and promotes clear cell renal cell carcinogenesis.Cancer gene therapy · 2023Article
- Zebrafish-based platform for emerging bio-contaminants and virus inactivation research.The Science of the total environment · 2023Review
- The Role of RNA-Binding Proteins in Hematological Malignancies.International journal of molecular sciences · 2022Review
- The Zebrafish model in dermatology: an update for clinicians.Discover oncology · 2022Review
- Roles of transducin-like enhancer of split (TLE) family proteins in tumorigenesis and immune regulation.Frontiers in cell and developmental biology · 2022Review
- Gene-Based Variant Analysis of Whole-Exome Sequencing in Relation to Eosinophil Count.Frontiers in immunology · 2022Article
- Enhancer recruitment of transcription repressors RUNX1 and TLE3 by mis-expressed FOXC1 blocks differentiation in acute myeloid leukemia.Cell reports · 2021Article
- The prognostic role of the Transducin-like Enhancer of split protein family in lung adenocarcinoma.Translational lung cancer research · 2021Article
- TLE4 Is a Critical Mediator of Osteoblast and Runx2-Dependent Bone Development.Frontiers in cell and developmental biology · 2021Article
- Article
- Pathway and network analysis of more than 2500 whole cancer genomes.Nature communications · 2020Article
- Zebrafish Models of Cancer-New Insights on Modeling Human Cancer in a Non-Mammalian Vertebrate.Genes · 2019Review
- Impact of 9q deletions on the classification of patients with acute myeloid leukemia.Journal of cancer research and clinical oncology · 2019Article
- Cancer the'RBP'eutics-RNA-binding proteins as therapeutic targets for cancer.Pharmacology & therapeutics · 2019Review
- RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia.International journal of molecular sciences · 2019Review
- Transducin-like enhancer of split 3 regulates proliferation of melanoma cells via histone deacetylase activity.Oncotarget · 2019Article
- Genome-wide Scan Identifies Role for AOX1 in Prostate Cancer Survival.European urology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Deletions on chromosome 9q are seen in a subset of acute myeloid leukemia (AML) cases and are specifically associated with t(8;21) AML. We previously defined the commonly deleted region in del(9q) AML and characterized the genes in this interval. To determine the critical lost gene(s) that might cooperate with the AML1-ETO fusion gene produced by t(8;21), we developed a set of shRNAs directed against each gene in this region. Within this library, shRNAs to TLE1 and TLE4 were the only shRNAs capable of rescuing AML1-ETO expressing U937T-A/E cells from AML1-ETO-induced cell-cycle arrest and apoptosis. Knockdown of TLE1 or TLE4 levels increased the rate of cell division of the AML1-ETO-expressing Kasumi-1 cell line, whereas forced expression of either TLE1 or TLE4 caused apoptosis and cell death. Knockdown of Gro3, a TLE homolog in zebrafish, cooperated with AML1-ETO to cause an accumulation of noncirculating hematopoietic blast cells. Our data are consistent with a model in which haploinsufficiency of these TLEs overcomes the negative survival and antiproliferative effects of AML1-ETO on myeloid progenitors, allowing preleukemic stem cells to expand into AML. This study is the first to implicate the TLEs as potential tumor suppressor genes in myeloid leukemia.
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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.