Elevated enhancer-oncogene contacts and higher oncogene expression levels by recurrent CTCF inactivating mutations in acute T cell leukemia
Cell Reports, ISSN: 2211-1247, Vol: 42, Issue: 4, Page: 112373
2023
- 3Citations
- 13Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations3
- Citation Indexes3
- CrossRef2
- Captures13
- Readers13
- 13
Article Description
Monoallelic inactivation of CCCTC-binding factor (CTCF) in human cancer drives altered methylated genomic states, altered CTCF occupancy at promoter and enhancer regions, and deregulated global gene expression. In patients with T cell acute lymphoblastic leukemia (T-ALL), we find that acquired monoallelic CTCF-inactivating events drive subtle and local genomic effects in nearly half of t(5; 14) (q35; q32.2) rearranged patients, especially when CTCF-binding sites are preserved in between the BCL11B enhancer and the TLX3 oncogene. These solitary intervening sites insulate TLX3 from the enhancer by inducing competitive looping to multiple binding sites near the TLX3 promoter. Reduced CTCF levels or deletion of the intervening CTCF site abrogates enhancer insulation by weakening competitive looping while favoring TLX3 promoter to BCL11B enhancer looping, which elevates oncogene expression levels and leukemia burden.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2211124723003844; http://dx.doi.org/10.1016/j.celrep.2023.112373; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85152703129&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/37060567; https://linkinghub.elsevier.com/retrieve/pii/S2211124723003844; https://dx.doi.org/10.1016/j.celrep.2023.112373
Elsevier BV
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