{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T11:17:50Z","timestamp":1790248670912,"version":"4.1.0"},"reference-count":43,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2015,7,14]],"date-time":"2015-07-14T00:00:00Z","timestamp":1436832000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2015,7,14]],"date-time":"2015-07-14T00:00:00Z","timestamp":1436832000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001677","name":"Institut national de la sant\u00e9 et de la recherche m\u00e9dicale","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001677","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006364","name":"Institut National Du Cancer","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100006364","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006431","name":"Canc\u00e9rop\u00f4le \u00cele-de-France","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100006431","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    2 inhibition therapy is used to treat patients suffering from myeloproliferative neoplasms (\n                    <jats:styled-content style=\"fixed-case\">MPN<\/jats:styled-content>\n                    ). Conflicting data on this therapy are reported possibly linked to the types of inhibitors or disease type. Therefore, we decided to compare in mice the effect of a\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    2 inhibitor, Fedratinib, in\n                    <jats:styled-content style=\"fixed-case\">MPN<\/jats:styled-content>\n                    models of increasing severity: polycythemia vera (\n                    <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n                    ), post\u2010\n                    <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n                    myelofibrosis (\n                    <jats:styled-content style=\"fixed-case\">PPMF<\/jats:styled-content>\n                    ) and rapid post\u2010essential thrombocythemia\n                    <jats:styled-content style=\"fixed-case\">MF<\/jats:styled-content>\n                    (\n                    <jats:styled-content style=\"fixed-case\">PTMF<\/jats:styled-content>\n                    ). The models were generated through\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    2 activation by the\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    2\n                    <jats:sup>V617F<\/jats:sup>\n                    mutation or\n                    <jats:styled-content style=\"fixed-case\">MPL<\/jats:styled-content>\n                    constant stimulation.\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    2 inhibition induced a correction of splenomegaly, leucocytosis and microcytosis in all three\n                    <jats:styled-content style=\"fixed-case\">MPN<\/jats:styled-content>\n                    models. However, the effects on fibrosis, osteosclerosis, granulocytosis, erythropoiesis or platelet counts varied according to the disease severity stage. Strikingly, complete blockade of fibrosis and osteosclerosis was observed in the\n                    <jats:styled-content style=\"fixed-case\">PPMF<\/jats:styled-content>\n                    model, linked to correction of\n                    <jats:styled-content style=\"fixed-case\">MK<\/jats:styled-content>\n                    hyper\/dysplasia, but not in the\n                    <jats:styled-content style=\"fixed-case\">PTMF<\/jats:styled-content>\n                    model, suggesting that\n                    <jats:styled-content style=\"fixed-case\">MF<\/jats:styled-content>\n                    development may also become\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    2\u2010independent. Interestingly, we originally found a decreased in the\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    2\n                    <jats:sup>V617F<\/jats:sup>\n                    allele burden in progenitor cells from the spleen but not in other cell types. Overall, this study shows that\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    2 inhibition has different effects according to disease phenotypes and can (\n                    <jats:italic>i<\/jats:italic>\n                    ) normalize platelet counts, (\n                    <jats:italic>ii<\/jats:italic>\n                    ) prevent the development of marrow fibrosis\/osteosclerosis at an early stage and (\n                    <jats:italic>iii<\/jats:italic>\n                    ) reduce splenomegaly through blockage of stem cell mobilization in the spleen.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.12608","type":"journal-article","created":{"date-parts":[[2015,7,14]],"date-time":"2015-07-14T16:16:17Z","timestamp":1436890577000},"page":"2564-2574","source":"Crossref","is-referenced-by-count":9,"title":["JAK2 inhibition has different therapeutic effects according to myeloproliferative neoplasm development in mice"],"prefix":"10.1111","volume":"19","author":[{"given":"Franck","family":"Debeurme","sequence":"first","affiliation":[{"name":"Inserm, U.1009, Institut Gustave Roussy (IGR) Universit\u00e9 Paris XI Villejuif France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine","family":"Lacout","sequence":"additional","affiliation":[{"name":"Inserm, U.1009, Institut Gustave Roussy (IGR) Universit\u00e9 Paris XI Villejuif France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudine","family":"Moratal","sequence":"additional","affiliation":[{"name":"iBV, CNRS UMR7277, INSERM U1091 Universit\u00e9 Nice\u2010Sophia Antipolis Nice France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca G.","family":"Bagley","sequence":"additional","affiliation":[{"name":"Sanofi Oncology Cambridge MA 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