{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,28]],"date-time":"2025-09-28T08:26:56Z","timestamp":1759048016390},"reference-count":37,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,7,14]],"date-time":"2006-07-14T00:00:00Z","timestamp":1152835200000},"content-version":"vor","delay-in-days":5492,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp; Cancer"],"published-print":{"date-parts":[[1991,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Chromosome in situ hybridization studies showed that the normal karyotype of leukemic cells from a patient with Ph<jats:sup>1<\/jats:sup>\u2010 negative, <jats:italic>BCR<\/jats:italic>\u2010positive chronic myeloid leukemia (CML) concealed a complex t(9;22;20)(q34;q 11;p13). The close association of <jats:italic>5\u2032\u2010BCR<\/jats:italic> and <jats:italic>3\u2032\u2010ABL<\/jats:italic> was demonstrated by field inversion gel electrophoresis, and in situ hybridization showed that <jats:italic>BCR\u2010ABL<\/jats:italic> was located on the short arm of chromosome 20. Our findings further indicate that chromosome rearrangement is the cause of <jats:italic>BCR\u2010ABL<\/jats:italic> gene fusion in leukemic cells that show a normal karyotype. Results from in situ hybridization studies were consistent with formation of the t(9;22;20) by a two step chromosomal rearrangement, but field inversion gel electrophoresis results indicated a more complex rearrangement.<\/jats:p>","DOI":"10.1002\/gcc.2870030405","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T22:50:20Z","timestamp":1172098220000},"page":"263-271","source":"Crossref","is-referenced-by-count":20,"title":["A complex chromosome rearrangement forms the <i>BCR\u2010ABL<\/i> fusion gene in leukemic cells with a normal 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