{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T02:22:55Z","timestamp":1778725375767,"version":"3.51.4"},"reference-count":39,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2011,6,16]],"date-time":"2011-06-16T00:00:00Z","timestamp":1308182400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2011,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Juvenile Myelomonocytic Leukemia (JMML) is a relentlessly progressive myeloproliferative\/myelodysplastic (MPD\/MDS) hematopoietic disorder more common in patients with any one of at least three distinct genetic lesions, specifically <jats:italic>NF1<\/jats:italic> gene loss and <jats:italic>PTPN11<\/jats:italic> and <jats:italic>NRAS<\/jats:italic> mutations. <jats:italic>NF1<\/jats:italic> and <jats:italic>PTPN11<\/jats:italic> are molecular lesions associated with Neurofibromatosis Syndrome Type I (NF1 Syndrome) and Noonan's Syndrome, respectively. The occurrence of JMML is rare; even among those predisposed with these syndromes to development of disease, and secondary genetic events likely contribute to the development and progression of disease. In NF1 syndrome, loss of p53 function is a common event in solid tumors, but uncommon in JMML, suggesting that the p53 pathway may be modified by other events in this hematopoietic disorder. The work presented here investigates the possible role of the <jats:italic>p19<\/jats:italic><jats:sup><jats:italic>Arf<\/jats:italic><\/jats:sup> (<jats:italic>p19<\/jats:italic>) tumor suppressor in development of MPD associated with <jats:italic>Nf1<\/jats:italic> gene loss in mice. We find that <jats:italic>Nf1<\/jats:italic> mutant hematopoietic cells with loss of <jats:italic>p19<\/jats:italic> develop accelerated hematopoietic disease similar to acute leukemia with a variable phenotype. This suggests that <jats:italic>p19<\/jats:italic> may play a role in development of JMML and evaluation of the human <jats:italic>p19<\/jats:italic> homolog (<jats:italic>p14<\/jats:italic><jats:sup><jats:italic>ARF<\/jats:italic><\/jats:sup>) in JMML may be informative. Am. J. Hematol. 86:579\u2013585, 2011. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ajh.22035","type":"journal-article","created":{"date-parts":[[2011,3,21]],"date-time":"2011-03-21T16:07:37Z","timestamp":1300723657000},"page":"579-585","source":"Crossref","is-referenced-by-count":4,"title":["<i>Nf1<\/i> mutant mice with <i>p19ARF<\/i> gene loss develop accelerated hematopoietic disease resembling acute leukemia with a variable phenotype"],"prefix":"10.1002","volume":"86","author":[{"given":"Stephen M.","family":"Wiesner","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jennifer L.","family":"Geurts","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miechaleen D.","family":"Diers","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rachel 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