{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T14:42:07Z","timestamp":1770993727393,"version":"3.50.1"},"reference-count":49,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2003,1,30]],"date-time":"2003-01-30T00:00:00Z","timestamp":1043884800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp;amp; Cancer"],"published-print":{"date-parts":[[2003,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Aberrations of chromosomal bands 1p36 and 1q11\u2013q23 are among the most common chromosomal alterations in non\u2010Hodgkin lymphoma (NHL). In this study, 16 cases of NHL showing recurrent unbalanced translocation t(1;1)(p36;q11\u201323) by G\u2010band analysis were selected for further analysis. To delineate the exact breakpoints, multicolor band analysis for chromosome 1 (M\u2010BAND1), and locus\u2010specific fluorescence in situ hybridization (LS\u2010FISH) using human genome designated BAC clones were performed. In all but one dicentric case, the breakpoint was determined to involve chromosomal bands 1p36.3 and 1q21.1\u20132. LS\u2010FISH analysis for the <jats:italic>TP73<\/jats:italic>, <jats:italic>MEL1<\/jats:italic>, <jats:italic>SKI<\/jats:italic>, and <jats:italic>CASP9<\/jats:italic> loci at 1p36, and the loci <jats:italic>IRTA1<\/jats:italic>, <jats:italic>IRTA2<\/jats:italic>, <jats:italic>BCL9<\/jats:italic>, <jats:italic>AF1Q<\/jats:italic>, <jats:italic>JTB<\/jats:italic>, and <jats:italic>MUC1<\/jats:italic> at 1q21, verified the MBAND1 results and further delineated the breakpoints. In band 1p36, two hybridization patterns were observed, one involving deletions of <jats:italic>MEL1<\/jats:italic>, <jats:italic>TP73<\/jats:italic>, and <jats:italic>SKI<\/jats:italic>, but not <jats:italic>CASP9<\/jats:italic>, and the second involving a breakpoint telomeric to <jats:italic>TP73<\/jats:italic>. In region 1q21, four hybridization patterns were observed, the first involving duplication\/translocation of all five genes; the second involving duplication\/translocation of <jats:italic>BCL9<\/jats:italic>, <jats:italic>AF1Q<\/jats:italic>, <jats:italic>JTB<\/jats:italic>, and <jats:italic>MUC1<\/jats:italic>; the third involving duplication\/translocation of <jats:italic>AF1Q<\/jats:italic>, <jats:italic>JTB<\/jats:italic>, and <jats:italic>MUC1<\/jats:italic>; and the fourth with a breakpoint telomeric to <jats:italic>MUC1<\/jats:italic>. Using an \u03b1\u2010satellite probe for chromosome 1 (D1Z5), centromeric involvement in the unbalanced translocation t(1;1)(p36.3;q21.1\u20132) was excluded in all but the one dicentric case, that is, dic(1;1)(p36.3;q10). In conclusion, deletion of 1p36 and duplication of 1q21 through formation of an unbalanced translocation t(1;1)(p36.3;q21.1\u20132) is a non\u2010random event in NHL, suggesting a deletion\u2013duplication mechanism involved in lymphoma progression and justifying further systematic research. \u00a9 2003 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gcc.10181","type":"journal-article","created":{"date-parts":[[2003,3,18]],"date-time":"2003-03-18T22:54:05Z","timestamp":1048028045000},"page":"375-381","source":"Crossref","is-referenced-by-count":23,"title":["Characterization of the recurrent translocation t(1;1)(p36.3;q21.1\u20132) in non\u2010Hodgkin lymphoma by multicolor banding and fluorescence in situ hybridization analysis"],"prefix":"10.1002","volume":"36","author":[{"given":"Valia 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