{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T08:55:03Z","timestamp":1792054503206,"version":"4.4.0"},"reference-count":103,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,7,16]],"date-time":"2007-07-16T00:00:00Z","timestamp":1184544000000},"content-version":"vor","delay-in-days":45,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:sc>Abstract:\u2002<\/jats:sc>\n                    <\/jats:bold>\n                    <jats:bold>\n                      Nucleoporin 98 (NUP98) is a component of the nuclear pore complex that facilitates mRNA export from the nucleus. It is mapped to 11p15.5 and is fused to a number of distinct partners, including nine members of the homeobox family as a consequence of leukemia\u2010associated chromosomal translocations. NUP98\u2010HOXA9 is associated with the t(7;11)(p15;p15) translocation in acute myeloid leukemia (AML), myelodysplastic syndrome, and blastic crisis of chronic myeloid leukemia. Expression of NUP98\u2010HOXA9 in murine bone marrow resulted in a myeloproliferative disease progressing to AML by 7\u20138 months. Transduction of NUP98 fusion genes into human CD34\n                      <jats:sup>+<\/jats:sup>\n                      cells confers a proliferative advantage in long\u2010term cytokine\u2010stimulated and stromal cocultures and in NOD\u2010SCID engrafted mice, associated with a five\u2010 to eight\u2010fold increase in hematopoietic stem cells. NUP98\u2010HOXA9 expression inhibited erythroid and myeloid differentiation but enhanced serial progenitor replating. NUP98\u2010HOXA9 upregulated a number of homeobox genes of the A and B cluster as well as MEIS1 and Pim\u20101, and downmodulated globin genes and C\/EBP\u03b1. The HOXA9 component of the NUP98\u2010HOXA9 fusion protein was protected from cullin\u20104A\u2013mediated ubiquitination and subsequent proteasome\u2010dependent degradation. In NUP98\u2010HOX\u2013transduced CD34\n                      <jats:sup>+<\/jats:sup>\n                      cells and cells from AML patients with t(7;11)(p15;p15) NUP98 was no longer associated with the nuclear pore complex but formed intranuclear aggregation bodies. Analysis of NUP98 allelic expression in AML and myelodysplastic syndrome showed loss of heterozygosity observed in 29% of the former and 8% of the latter. This was associated with poor prognosis.\n                    <\/jats:bold>\n                  <\/jats:p>","DOI":"10.1196\/annals.1392.019","type":"journal-article","created":{"date-parts":[[2007,7,19]],"date-time":"2007-07-19T15:28:24Z","timestamp":1184858904000},"page":"114-142","source":"Crossref","is-referenced-by-count":68,"title":["NUP98 Dysregulation in Myeloid Leukemogenesis"],"prefix":"10.1111","volume":"1106","author":[{"given":"M. A. S.","family":"MOORE","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K. Y.","family":"CHUNG","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"PLASILOVA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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