{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T01:37:33Z","timestamp":1792892253267,"version":"4.5.0"},"reference-count":36,"publisher":"American Society of Hematology","issue":"1","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,12,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Myeloproliferative neoplasms (MPNs) are characterized by clonal myeloproliferation in 1 or more of the hematopoietic stem cell lineages. Primary myelofibrosis (MF), post\u2013polycythemia vera MF, and post\u2013essential thrombocythemia MF have the worst prognosis and are characterized by the presence of cytokine-mediated symptom complex, splenomegaly, progressive marrow failure, and clonal instability, leading to leukemic transformation. The key therapeutic aims encompass the management of symptoms, splenomegaly, and anemia and the improvement of survivals. These therapeutic aims have evolved with the availability of Jak inhibitors and novel agents, making disease modification potentially achievable. Novel agents may potentially target MPN stem cells, epigenetic alterations, signaling pathways, and apoptotic pathways. In this case-based review, we outline our approach to the management of MF and discuss the therapeutic landscape of MF, highlighting the utility of Jak inhibitors and novel Jak inhibitor\u2013based combinations.<\/jats:p>","DOI":"10.1182\/hematology.2023000452","type":"journal-article","created":{"date-parts":[[2023,12,8]],"date-time":"2023-12-08T15:14:17Z","timestamp":1702048457000},"page":"667-675","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":6,"title":["Evolving landscape of JAK inhibition in myelofibrosis: monotherapy and combinations"],"prefix":"10.1182","volume":"2023","author":[{"given":"Harinder","family":"Gill","sequence":"first","affiliation":[{"name":"Department of Medicine, School of Clinical Medicine, LKS Faculty of Medicine, University of Hong Kong, Hong Kong"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Garret M. K.","family":"Leung","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Clinical Medicine, LKS Faculty of Medicine, University of Hong Kong, Hong Kong"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yok-Lam","family":"Kwong","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Clinical Medicine, LKS Faculty of Medicine, University of Hong Kong, Hong Kong"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","published-online":{"date-parts":[[2023,12,8]]},"reference":[{"issue":"13","key":"2023120815083150200_hem2023000452C1","doi-asserted-by":"crossref","first-page":"2420","DOI":"10.1002\/cncr.34205","article-title":"Defining disease modification in myelofibrosis in the era of targeted 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