{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T18:13:50Z","timestamp":1790360030309,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,2,21]],"date-time":"2013-02-21T00:00:00Z","timestamp":1361404800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Br J Haematol"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Although <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ABL<\/jats:styled-content>1 tyrosine kinase inhibitors reliably induce disease remission for patients with chronic myeloid leukaemia (<jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>), unlimited extension of therapy is necessary to prevent relapse from persistent leukaemic cells. Here, we analysed model cell lines and primary <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> cells for the expression and functions of the <jats:styled-content style=\"fixed-case\">ABC<\/jats:styled-content> transporter A3 (<jats:styled-content style=\"fixed-case\">ABCA<\/jats:styled-content>3) as well as the embryonic stem cell\u2010associated transcription factor <jats:styled-content style=\"fixed-case\">SALL<\/jats:styled-content>4. <jats:styled-content style=\"fixed-case\">ABCA<\/jats:styled-content>3 protected leukaemic cells from the cytotoxic effects of the tyrosine kinase inhibitors imatinib, dasatinib, and nilotinib. In the surviving cells, exposure to tyrosine kinase inhibitors significantly enhanced <jats:italic><jats:styled-content style=\"fixed-case\">ABCA<\/jats:styled-content>3<\/jats:italic> expression <jats:italic>in vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic>, and was associated with increased expression of <jats:styled-content style=\"fixed-case\">SALL<\/jats:styled-content>4, which binds the <jats:italic><jats:styled-content style=\"fixed-case\">ABCA<\/jats:styled-content>3<\/jats:italic> promoter. Inhibition of <jats:styled-content style=\"fixed-case\">ABCA<\/jats:styled-content>3 or <jats:styled-content style=\"fixed-case\">SALL<\/jats:styled-content>4 by genetic silencing or indomethacin, but not interferon gamma, interrupted <jats:styled-content style=\"fixed-case\">SALL<\/jats:styled-content>4\u2010dependent regulation of <jats:italic><jats:styled-content style=\"fixed-case\">ABCA<\/jats:styled-content>3<\/jats:italic> and restored susceptibility of leukaemic cells to tyrosine kinase inhibition. Tyrosine kinase inhibitor exposure facilitates a protective loop of <jats:styled-content style=\"fixed-case\">SALL<\/jats:styled-content>4 and <jats:styled-content style=\"fixed-case\">ABCA<\/jats:styled-content>3 cooperation in persistent leukaemic cells.<\/jats:p>","DOI":"10.1111\/bjh.12246","type":"journal-article","created":{"date-parts":[[2013,2,21]],"date-time":"2013-02-21T17:58:36Z","timestamp":1361469516000},"page":"204-213","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Tyrosinekinase inhibition facilitates cooperation of transcription factor <scp>SALL<\/scp>4 and <scp>ABC<\/scp> transporter A3 towards intrinsic <scp>CML<\/scp> cell drug resistance"],"prefix":"10.1111","volume":"161","author":[{"given":"Timo","family":"Hupfeld","sequence":"first","affiliation":[{"name":"Department of Haematology and Oncology Georg\u2010August\u2010University Goettingen Goettingen 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