Anchoring Chromatin Loops to Cancer

descriptionPublicationkeyboard_double_arrow_right Article 01 Aug 2017 English Publisher:Elsevier BVJournal:Developmental Cell, volume 42, pages 209-211 (issn: 1534-5807,

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Authors: Faith, Fowler; Jessica K, Tyler;

doi: 10.1016/j.devcel.2017.07.013

pmid: 28787588

pmc: PMC5859922

Anchoring Chromatin Loops to Cancer

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Abstract

Although some genomic rearrangements are caused by replication or transcription, the etiology of others is unclear. Reporting in Cell, Canela et al. (2017) reveal that type II topoisomerase-mediated release of torsional strain at chromosomal loop anchors generates DNA double-strand breaks that drive multiple oncogenic translocations in a transcription-independent manner.

Related Organizations

Cornell University
United States
Weill Cornell Medicine
United States

Keywords

DNA Replication, Neoplasms, Humans, DNA Breaks, Double-Stranded, Chromatin, Translocation, Genetic

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