{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:33:56Z","timestamp":1790746436673,"version":"4.1.0"},"reference-count":144,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2020,8,23]],"date-time":"2020-08-23T00:00:00Z","timestamp":1598140800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancers"],"abstract":"<jats:p>Myelofibrosis (MF) is subtype of myeloproliferative neoplasm (MPN) characterized by a relatively poor prognosis in patients. Understanding the factors that drive MF pathogenesis is crucial to identifying novel therapeutic approaches with the potential to improve patient care. Driver mutations in three main genes (janus kinase 2 (JAK2), calreticulin (CALR), and myeloproliferative leukemia virus oncogene (MPL)) are recurrently mutated in MPN and are sufficient to engender MPN using animal models. Interestingly, animal studies have shown that the underlying molecular mutation and the acquisition of additional genetic lesions is associated with MF outcome and transition from early stage MPN such as essential thrombocythemia (ET) and polycythemia vera (PV) to secondary MF. In this issue, we review murine models that have contributed to a better characterization of MF pathobiology and identification of new therapeutic opportunities in MPN.<\/jats:p>","DOI":"10.3390\/cancers12092381","type":"journal-article","created":{"date-parts":[[2020,8,23]],"date-time":"2020-08-23T21:28:06Z","timestamp":1598218086000},"page":"2381","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Murine Models of Myelofibrosis"],"prefix":"10.3390","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5087-3641","authenticated-orcid":false,"given":"Sebastien","family":"Jacquelin","sequence":"first","affiliation":[{"name":"Cancer program QIMR Berghofer Medical Research Institute, Brisbane, Queensland 4006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7615-9291","authenticated-orcid":false,"given":"Frederike","family":"Kramer","sequence":"additional","affiliation":[{"name":"Division of Hematology, Department of Medicine, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA 02115, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ann","family":"Mullally","sequence":"additional","affiliation":[{"name":"Division of Hematology, Department of Medicine, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA 02115, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven W.","family":"Lane","sequence":"additional","affiliation":[{"name":"Cancer program QIMR Berghofer Medical Research Institute, Brisbane, Queensland 4006, Australia"},{"name":"Cancer Care Services, The Royal Brisbane and Women\u2019s Hospital, Brisbane 4029, Australia"},{"name":"University of Queensland, St Lucia, QLD 4072, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2020,8,23]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1144","DOI":"10.1038\/nature03546","article-title":"A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera","volume":"434","author":"James","year":"2005","journal-title":"Nature"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"5258","DOI":"10.1074\/jbc.M707125200","article-title":"Dimerization by a cytokine receptor is necessary for constitutive activation of JAK2V617F","volume":"283","author":"Lu","year":"2008","journal-title":"J. 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