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Several chromosomal rearrangements can lead to this: the most common (inv(3)\/t(3;3)) results in a hijacked\n                    <jats:italic>GATA2<\/jats:italic>\n                    enhancer, and there are several atypical\n                    <jats:italic>MECOM<\/jats:italic>\n                    rearrangements involving enhancers from other hematopoietic genes. The set of enhancers which can be hijacked by\n                    <jats:italic>MECOM<\/jats:italic>\n                    can also be hijacked by\n                    <jats:italic>BCL11B<\/jats:italic>\n                    . Enhancer deregulation is also a driver of oncogenesis in a range of other malignancies. The mechanisms of enhancer deregulation observed in other cancer types, including TAD boundary disruptions and the creation of de novo (super\u2010) enhancers, may explain overexpression of\n                    <jats:italic>MECOM<\/jats:italic>\n                    or other oncogenes in AML without enhancer hijacking upon translocation. Gaining mechanistic insight in both enhancer deregulation and super\u2010enhancer activity is critical to pave the way for new treatments for AML and other cancers that are the result of enhancer deregulation.\n                  <\/jats:p>","DOI":"10.1002\/ijc.35330","type":"journal-article","created":{"date-parts":[[2025,1,24]],"date-time":"2025-01-24T05:15:36Z","timestamp":1737695736000},"page":"333-341","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Mechanisms of enhancer\u2010driven oncogene activation"],"prefix":"10.1002","volume":"158","author":[{"given":"Joyce","family":"Vriend","sequence":"first","affiliation":[{"name":"Department of Hematology Erasmus MC Cancer Institute, University Medical Center Rotterdam  Rotterdam The Netherlands"},{"name":"Oncode Institute  Utrecht The 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