{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T01:00:18Z","timestamp":1790384418378,"version":"4.1.0"},"posted":{"date-parts":[[2026,9,22]]},"group-title":"Cancer Biology","reference-count":53,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T00:00:00Z","timestamp":1790035200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"award":["R35GM144131"],"award-info":[{"award-number":["R35GM144131"]}],"id":[{"id":"https:\/\/ror.org\/04q48ey07","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,9,22]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  <jats:italic>MLL\/KMT2A<\/jats:italic>\n                  amplifications and rearrangements are prevalent in infant, adult, and therapy-induced leukemia; however, the molecular contributors controlling these alterations remain elusive. Here, we reveal that rapid CTCF degradation generates local genome structure alterations at\n                  <jats:italic>KMT2A<\/jats:italic>\n                  and copy gains and rearrangements. We then established a conserved, coordinated interplay between DNA and histone methylation pathways that control CTCF occupancy, and in turn,\n                  <jats:italic>KMT2A<\/jats:italic>\n                  locus stability. For example, DNMT1 overexpression promotes increased H3K9 methylation, reduced CTCF occupancy, and causes\n                  <jats:italic>KMT2A<\/jats:italic>\n                  alterations. However, DNMT1 inhibition suppresses these events and\n                  <jats:italic>KMT2A<\/jats:italic>\n                  alterations caused by topoisomerase II inhibition. Locus-specific epigenome targeting demonstrated that DNA or H3K9 methylation promotes\n                  <jats:italic>KMT2A<\/jats:italic>\n                  copy gains and rearrangement, whereas targeted TET activity suppresses these events upon methylation perturbation or doxorubicin treatment. These findings identify a conserved, coordinated DNA\u2013histone methylation axis governing\n                  <jats:italic>KMT2A<\/jats:italic>\n                  amplifications and rearrangement susceptibility, revealing biomarkers and therapeutic targets to predict and intercept these events in cancer.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>STATEMENT OF SIGNIFICANCE<\/jats:title>\n                  <jats:p>\n                    This study reveals a conserved DNA-histone methylation mechanism controlling the susceptibility of the\n                    <jats:italic>KMT2A<\/jats:italic>\n                    locus to copy gain and rearrange. These events can be generated or prevented by genetic, therapeutic or epigenome editing. Furthermore, DNMT1 inhibition blocks chemotherapy-induced\n                    <jats:italic>KMT2A<\/jats:italic>\n                    disruption, identifying a therapeutic strategy to intercept these oncogenic genomic alterations.\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.09.21.753283","type":"posted-content","created":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T01:50:12Z","timestamp":1790128212000},"source":"Crossref","is-referenced-by-count":0,"title":["DNMT1-Mediated Epigenetic Reprogramming Drives\n                  <i>KMT2A<\/i>\n                  Amplifications and Rearrangements"],"prefix":"10.64898","author":[{"given":"Madison A.","family":"Lineberger","sequence":"first","affiliation":[{"name":"Cancer Epigenetics Institute, Fox Chase Cancer Center, Philadelphia PA 19111"},{"name":"Nuclear Dynamics and Cancer Program, Fox Chase Cancer Center, Philadelphia PA 19111"},{"name":"Institute for Cancer Research, Fox Chase Cancer Center, 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