{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T20:58:47Z","timestamp":1791061127561,"version":"4.1.0"},"reference-count":27,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2014,5,15]],"date-time":"2014-05-15T00:00:00Z","timestamp":1400112000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp; Cancer"],"published-print":{"date-parts":[[2014,9]]},"abstract":"<jats:p>To outline further genetic mechanisms of transformation from follicular lymphoma (FL) to diffuse large B\u2010cell lymphoma (DLBCL), we have performed whole genome array\u2010CGH in 81 tumors from 60 patients [29 de novo DLBCL (dnDLBCL), 31 transformed DLBCL (tDLBCL), and 21 antecedent FL]. In 15 patients, paired tumor samples (primary FL and a subsequent tDLBCL) were available, among which three possessed more than two subsequent tumors, allowing us to follow specific genetic alterations acquired before, during, and after the transformation. Gain of 2p15\u201316.1 encompassing, among others, the <jats:italic>REL<\/jats:italic>, <jats:italic>BCL11A<\/jats:italic>, <jats:italic>USP34<\/jats:italic>, <jats:italic>COMMD1<\/jats:italic>, and <jats:italic>OTX1<\/jats:italic> genes was found to be more common in the tDLBCL compared with dnDLBCL (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001). Furthermore, a high\u2010level amplification of 2p15\u201316.1 was also detected in the FL stage prior to transformation, indicating its importance during the transformation event. Quantitative real\u2010time PCR showed a higher level of amplification of <jats:italic>REL<\/jats:italic>, <jats:italic>USP34<\/jats:italic>, and <jats:italic>COMMD1<\/jats:italic> (all involved in the NF\u03ba\u0392\u2010pathway) compared with <jats:italic>BCL11A<\/jats:italic>, which indicates that the altered genes disrupting the NF\u03ba\u0392 pathway may be the driver genes of transformation rather than the previously suggested <jats:italic>BCL11A<\/jats:italic>. Moreover, a 17q21.33 amplification was exclusively found in tDLBCL, never in FL (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.04) or dnDLBCL, indicating an upregulation of genes of importance during the later phase of transformation. Taken together, our study demonstrates potential genomic markers for disease progression to clinically more aggressive forms. We also confirm the importance of the TP53\u2010, CDKN2A\u2010, and NF\u03ba\u0392\u2010pathways for the transformation from FL to DLBCL. \u00a9 2014 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/gcc.22184","type":"journal-article","created":{"date-parts":[[2014,5,15]],"date-time":"2014-05-15T13:19:07Z","timestamp":1400159947000},"page":"750-768","source":"Crossref","is-referenced-by-count":31,"title":["Amplification of 2p as a genomic marker for transformation in lymphoma"],"prefix":"10.1002","volume":"53","author":[{"given":"Anna","family":"Kwiecinska","sequence":"first","affiliation":[{"name":"Department of Oncology\u2010Pathology Karolinska Institutet, CCK Karolinska University Hospital  Solna Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koichi","family":"Ichimura","sequence":"additional","affiliation":[{"name":"Department of Pathology and Cytology Addenbrooke's Hospital Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mattias","family":"Berglund","sequence":"additional","affiliation":[{"name":"Department of Radiology Oncology, and Radiation Science, Rudbeck Laboratory, Uppsala University  Uppsala Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrii","family":"Dinets","sequence":"additional","affiliation":[{"name":"Department of Oncology\u2010Pathology Karolinska Institutet, CCK Karolinska University Hospital  Solna Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luqman","family":"Sulaiman","sequence":"additional","affiliation":[{"name":"Department of Oncology\u2010Pathology Karolinska Institutet, CCK Karolinska University Hospital  Solna Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V. 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