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In this study, we generated a <jats:styled-content style=\"fixed-case\">TKI<\/jats:styled-content>\u2010resistant <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> cell line, K562R, that lacks a mutation in <jats:italic><jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content>\u2013<jats:styled-content style=\"fixed-case\">ABL<\/jats:styled-content><\/jats:italic>. Interleukin\u20101\u03b2 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2) was more highly expressed in K562R than in the parental cell line K562S, and higher levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 contributed to the imatinib resistance of K562R. In addition, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 secreted from K562R cells affected stromal cell production of <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>11, which in turn promoted migration of K562R cells into the stroma. Thus, elevated <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 production from <jats:styled-content style=\"fixed-case\">TKI<\/jats:styled-content>\u2010resistant K562R cells may contribute to <jats:styled-content style=\"fixed-case\">TKI<\/jats:styled-content> resistance by increasing cell viability and promoting cell migration.<\/jats:p>","DOI":"10.1002\/1873-3468.12057","type":"journal-article","created":{"date-parts":[[2016,1,7]],"date-time":"2016-01-07T13:23:20Z","timestamp":1452173000000},"page":"358-368","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Secretion of <scp>IL<\/scp>\u20101\u03b2 from imatinib\u2010resistant chronic myeloid leukemia cells contributes to <i>BCR<\/i>\u2013<i>ABL<\/i> mutation\u2010independent imatinib resistance"],"prefix":"10.1002","volume":"590","author":[{"given":"Cho\u2010Rong","family":"Lee","sequence":"first","affiliation":[{"name":"School 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