{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T03:33:15Z","timestamp":1791343995944,"version":"4.3.1"},"reference-count":19,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2016,6,15]],"date-time":"2016-06-15T00:00:00Z","timestamp":1465948800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Gesellschaft zur Erforschung der Biologie und Behandlung von Tumorkrankheiten"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2016,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>In chronic myelomonocytic leukemia (<jats:styled-content style=\"fixed-case\">CMML<\/jats:styled-content>), colony\u2010forming units granulocyte\/macrophage (<jats:styled-content style=\"fixed-case\">CFU<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">GM<\/jats:styled-content>), which grow <jats:italic>in vitro<\/jats:italic> in the absence of exogenous growth factors, arise from the abnormal clone that is responsible for the overproduction of granulomonocytic cells. Previous <jats:italic>in vitro<\/jats:italic> findings including ours suggest that divergent molecular aberrations in <jats:styled-content style=\"fixed-case\">CMML<\/jats:styled-content> seem to converge within the <jats:styled-content style=\"fixed-case\">GM<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> signaling pathway. As <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2 is a sentinel kinase in this pathway, <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2 inhibition may be an attractive treatment approach in <jats:styled-content style=\"fixed-case\">CMML<\/jats:styled-content>. We investigated the <jats:italic>in vitro<\/jats:italic> effects of the specific <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2 inhibitor <jats:styled-content style=\"fixed-case\">TG<\/jats:styled-content>101209 on the autonomous <jats:styled-content style=\"fixed-case\">CFU<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">GM<\/jats:styled-content> formation from peripheral blood mononuclear cells of patients with <jats:styled-content style=\"fixed-case\">CMML<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">TG<\/jats:styled-content>101209 was found to either block or strongly inhibit spontaneous <jats:styled-content style=\"fixed-case\">CFU<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">GM<\/jats:styled-content> growth in all 10 patients tested. This inhibitory effect was dose dependent and significantly more pronounced as compared to the inhibitory effect on stimulated <jats:styled-content style=\"fixed-case\">CFU<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">GM<\/jats:styled-content> growth from normal individuals. In a <jats:styled-content style=\"fixed-case\">CMML<\/jats:styled-content> patient with splenomegaly, who was treated with the <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>1\/2 inhibitor ruxolitinib off label, we can demonstrate a spleen response and the disappearance of constitutional symptoms which was associated with a decrease in autonomous <jats:styled-content style=\"fixed-case\">CFU<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">GM<\/jats:styled-content> formation <jats:italic>ex vivo<\/jats:italic>. Pharmacological <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2 inhibition may be an interesting approach to be systematically studied in patients with <jats:styled-content style=\"fixed-case\">CMML<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/ejh.12773","type":"journal-article","created":{"date-parts":[[2016,5,9]],"date-time":"2016-05-09T11:27:09Z","timestamp":1462793229000},"page":"562-567","source":"Crossref","is-referenced-by-count":13,"title":["<i>In vitro<\/i> and <i>in vivo<\/i> effects of <scp>JAK<\/scp>2 inhibition in chronic myelomonocytic leukemia"],"prefix":"10.1111","volume":"97","author":[{"given":"Klaus","family":"Geissler","sequence":"first","affiliation":[{"name":"5th Medical Department with Hematology, Oncology and Palliative Medicine Hospital Hietzing Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"J\u00e4ger","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Medical University of Vienna Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agnes","family":"Barna","sequence":"additional","affiliation":[{"name":"Blood Transfusion Service for Upper Austria Austrian Red Cross Linz Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thamer","family":"Sliwa","sequence":"additional","affiliation":[{"name":"3rd Medical Department Hanusch Hospital Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Kn\u00f6bl","sequence":"additional","affiliation":[{"name":"Division of Hematology and Hemostaseology Department of Internal Medicine I Medical University of Vienna Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilse","family":"Schwarzinger","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Medical University of Vienna Vienna 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