ArticleLeukemia2014
Aberrant TAL1 activation is mediated by an interchromosomal interaction in human T-cell acute lymphoblastic leukemia.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- Mechanisms of enhancer-driven oncogene activation.International journal of cancer · 2026Review
- iceDP: identifying inter-chromatin engagement via density peaks clustering algorithm.Briefings in bioinformatics · 2026Article
- The METTL3-YTHDC1 axis mediates architectural RNA mMolecular cancer · 2025Article
- Noncoding RNA,Molecular and cellular biology · 2025Article
- The effect of trisomic chromosomes on spatial genome organization and global transcription in embryonic stem cells.Cell proliferation · 2024Article
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- Interchromosomal Colocalization with Parental Genes Is Linked to the Function and Evolution of Mammalian Retrocopies.Molecular biology and evolution · 2023Article
- A Variant in theJournal of dental research · 2023Article
- Computational methods for identifying enhancer-promoter interactions.Quantitative biology (Beijing, China) · 2023Review
- rDNA Transcription in Developmental Diseases and Stem Cells.Stem cell reviews and reports · 2023Review
- HOTTIP-dependent R-loop formation regulates CTCF boundary activity and TAD integrity in leukemia.Molecular cell · 2022Article
- HDAC1 is required for GATA-1 transcription activity, global chromatin occupancy and hematopoiesis.Nucleic acids research · 2021Article
- RNA Biogenesis Instructs Functional Inter-Chromosomal Genome Architecture.Frontiers in genetics · 2021Article
- CTCF-mediated genome organization and leukemogenesis.Leukemia · 2020Review
- Architectural proteins for the formation and maintenance of the 3D genome.Science China. Life sciences · 2020Review
- Alteration of CTCF-associated chromatin neighborhood inhibits TAL1-driven oncogenic transcription program and leukemogenesis.Nucleic acids research · 2020Article
- The prostate cancer risk variant rs55958994 regulates multiple gene expression through extreme long-range chromatin interaction to control tumor progression.Science advances · 2019Article
- HOX Loci Focused CRISPR/sgRNA Library Screening Identifying Critical CTCF Boundaries.Journal of visualized experiments : JoVE · 2019Article
- Article
- Molecular mechanisms underlying noncoding risk variations in psychiatric genetic studies.Molecular psychiatry · 2017Review
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Long-range chromatin interactions control metazoan gene transcription. However, the involvement of intra- and interchromosomal interactions in development and oncogenesis remains unclear. TAL1/SCL is a critical transcription factor required for the development of all hematopoietic lineages; yet, aberrant TAL1 transcription often occurs in T-cell acute lymphoblastic leukemia (T-ALL). Here, we report that oncogenic TAL1 expression is regulated by different intra- and interchromosomal loops in normal hematopoietic and leukemic cells, respectively. These intra- and interchromosomal loops alter the cell-type-specific enhancers that interact with the TAL1 promoter. We show that human SET1 (hSET1)-mediated H3K4 methylations promote a long-range chromatin loop, which brings the +51 enhancer in close proximity to TAL1 promoter 1 in erythroid cells. The CCCTC-binding factor (CTCF) facilitates this long-range enhancer/promoter interaction of the TAL1 locus in erythroid cells while blocking the same enhancer/promoter interaction of the TAL1 locus in human T-cell leukemia. In human T-ALL, a T-cell-specific transcription factor c-Maf-mediated interchromosomal interaction brings the TAL1 promoter into close proximity with a T-cell-specific regulatory element located on chromosome 16, activating aberrant TAL1 oncogene expression. Thus, our study reveals a novel molecular mechanism involving changes in three-dimensional chromatin interactions that activate the TAL1 oncogene in human T-cell leukemia.
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