{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T09:49:56Z","timestamp":1760953796608},"reference-count":51,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,1,29]],"date-time":"2015-01-29T00:00:00Z","timestamp":1422489600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Umberto Veronesi Foundation"},{"name":"FP7, NGS-PTL"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2015,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:label \/><jats:p>The decrease of Chibby1 (CBY1) contributes to \u03b2 catenin constitutive activation associated with the presence of the <jats:italic>BCR\u2010ABL1<\/jats:italic> fusion gene of chronic myeloid leukemia (CML). This is mediated by transcriptional events and driven by DNA hyper\u2010methylation at promoter\u2010associated CpG islands of the CBY1\u2010encoding gene <jats:italic>C22orf2<\/jats:italic>. Moreover, CBY1 transcriptional induction proceeding from promoter de\u2010methylation is a component of <jats:italic>BCR\u2010ABL1<\/jats:italic>+ cell response to Imatinib (IM). Our study showed that DNA methyltransferase 1 (DNMT1) has a central role in the hyper\u2010methylation at the <jats:italic>C22orf2<\/jats:italic> promoter. Further investigation in leukemic hematopoietic progenitors from IM\u2010responsive and IM\u2010resistant CML patients at diagnosis failed to demonstrate any correlation between DNMT1\u2010driven hyper\u2010methylation of the <jats:italic>C22orf2<\/jats:italic> promoter and response to IM. Notably, the response to IM was neither predicted by DNMT1\u2010driven hyper\u2010methylation of <jats:italic>BCL2\u2010like11<\/jats:italic> at diagnosis. In conclusion, the hypermethylation of <jats:italic>C22orf2<\/jats:italic> and <jats:italic>BCL2\u2010like11 promoters<\/jats:italic> proceeding from DNMT1 is a crucial component of their reduced expression, but it is not directly involved in CML resistance to IM. It might rather contribute to the disease evolution towards a drug\u2010resistant phenotype in more advanced phases or blast crisis. J. Cell. Biochem. 116: 589\u2013597, 2015. \u00a9 2014 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.25010","type":"journal-article","created":{"date-parts":[[2014,11,11]],"date-time":"2014-11-11T20:24:17Z","timestamp":1415737457000},"page":"589-597","source":"Crossref","is-referenced-by-count":7,"title":["DNA Methyltransferase 1 Drives Transcriptional Down\u2010Modulation of \u03b2 Catenin Antagonist Chibby1 Associated With the <i>BCR\u2010ABL1<\/i> Gene of Chronic Myeloid Leukemia"],"prefix":"10.1002","volume":"116","author":[{"given":"Elisa","family":"Leo","sequence":"first","affiliation":[{"name":"Dipartimento di Medicina Specialistica Diagnostica a Sperimentale\u2010DIMES Istituto di Ematologia \u201cL. e A. 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