ArticleNature communications2015
Site- and allele-specific polycomb dysregulation in T-cell leukaemia.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A systematic review of recent trends in research on therapeutically significant L-asparaginase and acute lymphoblastic leukemia.Molecular biology reports · 2022Pooled it
- Enhancer-dependent gene regulation in space, time, and malignancies.International journal of cancer · 2026Review
- Towards methylation-based redefinition of TAL1 positive T-cell acute lymphoblastic leukaemia (T-ALL).Leukemia · 2025Article
- The Clinicogenomic Landscape of Induction Failure in Childhood and Young Adult T-Cell Acute Lymphoblastic Leukemia.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023Article
- TAL1 activation in T-cell acute lymphoblastic leukemia: a novel oncogenic 3' neo-enhancer.Haematologica · 2023Article
- Harnessing the MYB-dependent TAL1 5'super-enhancer for targeted therapy in T-ALL.Molecular cancer · 2023Article
- Unveiling the complexity of transcription factor networks in hematopoietic stem cells: implications for cell therapy and hematological malignancies.Frontiers in oncology · 2023Review
- Epigenomic translocation of H3K4me3 broad domains over oncogenes following hijacking of super-enhancers.Genome research · 2022Article
- Deregulation of enhancer structure, function, and dynamics in acute lymphoblastic leukemia.Trends in immunology · 2021Review
- The Genetics and Mechanisms of T-Cell Acute Lymphoblastic Leukemia.Cold Spring Harbor perspectives in medicine · 2020Review
- Epigenetic Control of a Local Chromatin Landscape.International journal of molecular sciences · 2020Review
- The role of noncoding mutations in blood cancers.Disease models & mechanisms · 2019Review
- An integrated transcriptome analysis in T-cell acute lymphoblastic leukemia links DNA methylation subgroups to dysregulated TAL1 and ANTP homeobox gene expression.Cancer medicine · 2019Article
- Oncogenic transcriptional program driven by TAL1 in T-cell acute lymphoblastic leukemia.International journal of hematology · 2019Review
- Targeted genome editing in acute lymphoblastic leukemia: a review.BMC biotechnology · 2018Review
- Enhancer reprogramming in tumor progression: a new route towards cancer cell plasticity.Cellular and molecular life sciences : CMLS · 2018Review
- Concise Review: Epigenetic Regulation of Hematopoiesis: Biological Insights and Therapeutic Applications.Stem cells translational medicine · 2017Review
- APOBEC signature mutation generates an oncogenic enhancer that drives LMO1 expression in T-ALL.Leukemia · 2017Article
- The genomic landscape of pediatric and young adult T-lineage acute lymphoblastic leukemia.Nature genetics · 2017Article
- PGBD5 promotes site-specific oncogenic mutations in human tumors.Nature genetics · 2017Article
Corrections and comments
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Authors and funding
28 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cell acute lymphoblastic leukaemias (T-ALL) are aggressive malignant proliferations characterized by high relapse rates and great genetic heterogeneity. TAL1 is amongst the most frequently deregulated oncogenes. Yet, over half of the TAL1(+) cases lack TAL1 lesions, suggesting unrecognized (epi)genetic deregulation mechanisms. Here we show that TAL1 is normally silenced in the T-cell lineage, and that the polycomb H3K27me3-repressive mark is focally diminished in TAL1(+) T-ALLs. Sequencing reveals that >20% of monoallelic TAL1(+) patients without previously known alterations display microinsertions or RAG1/2-mediated episomal reintegration in a single site 5' to TAL1. Using 'allelic-ChIP' and CrispR assays, we demonstrate that such insertions induce a selective switch from H3K27me3 to H3K27ac at the inserted but not the germline allele. We also show that, despite a considerable mechanistic diversity, the mode of oncogenic TAL1 activation, rather than expression levels, impact on clinical outcome. Altogether, these studies establish site-specific epigenetic desilencing as a mechanism of oncogenic activation.
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