{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:06:09Z","timestamp":1791295569350,"version":"4.1.0"},"reference-count":29,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2003,10,10]],"date-time":"2003-10-10T00:00:00Z","timestamp":1065744000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100007391","name":"Association pour la Recherche sur le Cancer","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100007391","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp; Cancer"],"published-print":{"date-parts":[[2004,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Among cytogenetic studies of patients affected with myelofibrosis with myeloid metaplasia (MMM), a rare chronic myeloproliferative disorder, we found several reports of structural abnormalities of the long arm of chromosome 12. Two MMM patients had a balanced translocation involving 12q: t(4;12)(q32;q15) and t(5;12)(p14;q15), respectively. FISH (fluorescence in situ hybridization) analysis showed that BAC (bacterial artificial chromosome) RP11\u2010366L20 overlaps the breakpoint in both cases. A gene, <jats:italic>HMGA2<\/jats:italic>, most of which is included in that BAC, thus was identified as a potential candidate. Using reserves transcriptase\u2013polymerase chain reaction (RT\u2010PCR), we looked for expression of <jats:italic>HMGA2<\/jats:italic> in blood mononuclear cells from these 2 patients and demonstrated a transcript in both. Moreover, we found the gene expressed in the hematopoietic cells of 10 of 10 additional patients bearing no 12q anomalies. <jats:italic>HMGA2<\/jats:italic>, not expressed in normal subjects, is implicated in benign solid tumors such as lipomas, leiomyomas, and other rare tumors of mesenchymal origin. We postulate that its dysregulation and overexpression in myeloid progenitors contribute also to the pathogenesis of MMM. \u00a9 2003 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gcc.10297","type":"journal-article","created":{"date-parts":[[2003,10,31]],"date-time":"2003-10-31T20:21:08Z","timestamp":1067631668000},"page":"82-87","source":"Crossref","is-referenced-by-count":51,"title":["Dysregulation and overexpression of <i>HMGA2<\/i> in myelofibrosis with myeloid 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