{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T20:01:33Z","timestamp":1790712093049,"version":"4.1.0"},"reference-count":33,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2015,8,7]],"date-time":"2015-08-07T00:00:00Z","timestamp":1438905600000},"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; Cancer"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:p>\n                    We report five chronic myeloid leukaemia (CML) patients in whom we identified and characterized undescribed\n                    <jats:italic>BCR\u2013ABL1<\/jats:italic>\n                    fusion transcripts. We investigated the precise features of the molecular rearrangements and the minimal residual disease follow\u2010up for these five patients. Three resulted from new rearrangements between the\n                    <jats:italic>BCR<\/jats:italic>\n                    and\n                    <jats:italic>ABL1<\/jats:italic>\n                    sequences (the breakpoints being located within\n                    <jats:italic>BCR<\/jats:italic>\n                    exon 13 in two cases and within\n                    <jats:italic>BCR<\/jats:italic>\n                    exon 18 in one case). The other two cases revealed a complex e8\u2010[ins]\u2010a2 fusion transcript involving a third partner gene,\n                    <jats:italic>PRDM12<\/jats:italic>\n                    and\n                    <jats:italic>SPECC1L<\/jats:italic>\n                    , respectively. Moreover, single nucleotide polymorphism\u2010array analysis performed in the latter two cases showed copy number alterations shared by the two patients, thus identifying genes that were deleted during rearrangement and suggesting their potential role in CML pathogenesis. Interestingly, we highlight that the prognosis of alterations, such as the presence of an e8a2 transcript or the deletion of various genes, which have been controversial, may be definitively erased by the introduction of tyrosine kinase inhibitors (TKIs). \u00a9 2015 Wiley Periodicals, Inc.\n                  <\/jats:p>","DOI":"10.1002\/gcc.22263","type":"journal-article","created":{"date-parts":[[2015,8,7]],"date-time":"2015-08-07T10:23:16Z","timestamp":1438942996000},"page":"595-605","source":"Crossref","is-referenced-by-count":21,"title":["Molecular characterization and follow\u2010up of five\n                    <scp>CML<\/scp>\n                    patients with new\n                    <scp>BCR\u2013ABL<\/scp>\n                    1 fusion transcripts"],"prefix":"10.1002","volume":"54","author":[{"given":"Sarah","family":"Huet","sequence":"first","affiliation":[{"name":"Laboratoire D'h\u00e9matologie Centre De Biologie Sud, Hospices Civils De Lyon, Pierre\u2010B\u00e9nite  France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"St\u00e9phanie","family":"Dulucq","sequence":"additional","affiliation":[{"name":"Laboratoire D'h\u00e9matologie Centre Hospitalo\u2010Universitaire De Bordeaux Bordeaux France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aur\u00e9lie","family":"Chauveau","sequence":"additional","affiliation":[{"name":"Laboratoire D'h\u00e9matologie Centre Hospitalo\u2010Universitaire R\u00e9gional De Brest Brest France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Audrey","family":"M\u00e9nard","sequence":"additional","affiliation":[{"name":"Laboratoire D'h\u00e9matologie Institut De Biologie, Centre Hospitalo\u2010Universitaire De Nantes Nantes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean\u2010Claude","family":"Chomel","sequence":"additional","affiliation":[{"name":"Service De Canc\u00e9rologie Biologique Centre Hospitalo\u2010Universitaire De Poitiers 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