دورية أكاديمية
أعرض في EDS

Elevated enhancer-oncogene contacts and higher oncogene expression levels by recurrent CTCF inactivating mutations in acute T cell leukemia.

التفاصيل البيبلوغرافية
العنوان: Elevated enhancer-oncogene contacts and higher oncogene expression levels by recurrent CTCF inactivating mutations in acute T cell leukemia.
المؤلفون: Smits WK; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands., Vermeulen C; Oncode Institute, Utrecht, the Netherlands; Hubrecht Institute-KNAW, Utrecht, the Netherlands; Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, the Netherlands., Hagelaar R; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands; Oncode Institute, Utrecht, the Netherlands., Kimura S; Laboratory of Pathology, St. Jude's Children's Research Hospital, Memphis TN, USA., Vroegindeweij EM; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands., Buijs-Gladdines JGCAM; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands., van de Geer E; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands., Verstegen MJAM; Oncode Institute, Utrecht, the Netherlands; Hubrecht Institute-KNAW, Utrecht, the Netherlands., Splinter E; Cergentis BV, Utrecht, the Netherlands., van Reijmersdal SV; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands., Buijs A; Department of Genetics, University Medical Center Utrecht, Utrecht, the Netherlands., Galjart N; Department of Cell Biology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands., van Eyndhoven W; Diagnostics and Genomics Group, Agilent Technologies, Amstelveen, the Netherlands., van Min M; Cergentis BV, Utrecht, the Netherlands., Kuiper R; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands; Department of Genetics, University Medical Center Utrecht, Utrecht, the Netherlands., Kemmeren P; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands., Mullighan CG; Laboratory of Pathology, St. Jude's Children's Research Hospital, Memphis TN, USA., de Laat W; Oncode Institute, Utrecht, the Netherlands; Hubrecht Institute-KNAW, Utrecht, the Netherlands., Meijerink JPP; Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands. Electronic address: jules.meijerink@acerta-pharma.com.
المصدر: Cell reports [Cell Rep] 2023 Apr 25; Vol. 42 (4), pp. 112373. Date of Electronic Publication: 2023 Apr 14.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101573691 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2211-1247 (Electronic) NLM ISO Abbreviation: Cell Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, c 2012-
مواضيع طبية MeSH: Precursor T-Cell Lymphoblastic Leukemia-Lymphoma*/genetics, Humans ; CCCTC-Binding Factor/genetics ; CCCTC-Binding Factor/metabolism ; Chromatin ; Enhancer Elements, Genetic/genetics ; Mutation ; Oncogenes ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Transcription Factors/metabolism ; Tumor Suppressor Proteins/metabolism
مستخلص: 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.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)
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معلومات مُعتمدة: R35 CA197695 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: BCL11B; CP: Cancer; CTCF mutation; T cell acute lymphoblastic leukemia; TLX3; competitive chromatin looping; enhancer insulation; oncogene regulation
المشرفين على المادة: 0 (BCL11B protein, human)
0 (CCCTC-Binding Factor)
0 (Chromatin)
0 (Repressor Proteins)
0 (Transcription Factors)
0 (Tumor Suppressor Proteins)
0 (CTCF protein, human)
تواريخ الأحداث: Date Created: 20230415 Date Completed: 20231010 Latest Revision: 20231227
رمز التحديث: 20231227
مُعرف محوري في PubMed: PMC10750298
DOI: 10.1016/j.celrep.2023.112373
PMID: 37060567
قاعدة البيانات: MEDLINE
الوصف
تدمد:2211-1247
DOI:10.1016/j.celrep.2023.112373