{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T17:32:24Z","timestamp":1791307944237,"version":"4.3.1"},"reference-count":28,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,4,10]],"date-time":"2014-04-10T00:00:00Z","timestamp":1397088000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objectives<\/jats:title><jats:p>Mature dendritic cells (<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s) may be derived from the BCR\/ABL1 expressing monocytes in chronic myeloid leukaemia. These cells have potential therapeutic applications, but are recognised to have defective function. In normal <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s, activation and maturation depend on ABL1 dependent signals. We therefore tested the hypothesis that in the <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s of chronic myeloid leukaemia, the presence of the BCR\/ABL1 molecule disrupts normal ABL1 signal pathways, and contributes to the observed functional defects of the cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We employed <jats:italic>in vitro<\/jats:italic> culture of clinical samples, combining microscopic and biochemical techniques with a phosphoproteomic approach to compare and characterise <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s from normal individuals and chronic myeloid leukaemia patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results and conclusions<\/jats:title><jats:p>We identified an altered intracellular localisation for ABL1 within <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s derived from the monocytes of chronic myeloid leukaemia. The protein was found in the perinuclear region co\u2010distributed with the adapter\u2010protein CRKL and the BCR\/ABL1 protein. This altered distribution was associated with defective generation of ABL1\u2010dependent maturation signals, and a dislocation of ABL1 from the F\u2010actin cytoskeleton. We suggest that abnormal ABL1\u2010dependent signals contribute to the recognised functional defects affecting chronic myeloid leukaemia <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ejh.12306","type":"journal-article","created":{"date-parts":[[2014,3,11]],"date-time":"2014-03-11T18:14:07Z","timestamp":1394561647000},"page":"96-102","source":"Crossref","is-referenced-by-count":16,"title":["Monocyte\u2010derived dendritic cells from chronic myeloid leukaemia have abnormal maturation and cytoskeletal function that is associated with defective localisation and signalling by normal ABL1 protein"],"prefix":"10.1111","volume":"93","author":[{"given":"Sarah","family":"Brown","sequence":"first","affiliation":[{"name":"Pharmacy Department University of Wolverhampton Wolverhampton UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claire 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