{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T18:52:39Z","timestamp":1787165559007,"version":"build-2736575974"},"reference-count":20,"publisher":"Scientific Scholar","issue":"Suppl 1","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2016,5]]},"abstract":"\n Background & objectives:<\/jats:title>\n \n Chronic myeloid leukaemia is (CML) characterized by the presence of a hallmark chromosomal translocation, the Philadelphia chromosome. Although there are many reports available regarding the different variants of\n BCR<\/jats:italic>\n -\n ABL<\/jats:italic>\n in CML, we studied the co-expression of e13a2 and e14a2 transcripts and a few polymorphisms in CML patients.\n <\/jats:p>\n <\/jats:sec>\n \n Methods:<\/jats:title>\n \n Molecular genetics approach was adapted to screen for polymorphisms, mutation and translocation in\n BCR<\/jats:italic>\n ,\n ABL<\/jats:italic>\n kinase domain and\n BCR<\/jats:italic>\n -\n ABL<\/jats:italic>\n breakpoint region in 73 CML patients.\n <\/jats:p>\n <\/jats:sec>\n \n Results:<\/jats:title>\n \n All eight patients with dual transcripts were found to harbour an exonic polymorphism (c.2700 T>C) and an intronic polymorphism (g.109366A>G) that were earlier reported to be associated with co-expression of both the transcripts. We also observed c.763G>A mutation in\n ABL<\/jats:italic>\n kinase domain and two polymorphisms, c.2387 A>G and c.2736A>G in the\n BCR<\/jats:italic>\n gene.\n <\/jats:p>\n <\/jats:sec>\n \n Interpretation & conclusions:<\/jats:title>\n \n Though our data support the previous findings that co-expression of\n BCR<\/jats:italic>\n -\n ABL<\/jats:italic>\n transcripts is due to the occurrence of exonic and intronic polymorphisms in the\n BCR<\/jats:italic>\n gene, it also shows that the intronic polymorphism can arise without the linked exonic polymorphism. The occurrence of\n ABL<\/jats:italic>\n kinase domain mutation is less frequent in Indian population.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.4103\/0971-5916.191816","type":"journal-article","created":{"date-parts":[[2016,10,10]],"date-time":"2016-10-10T04:36:33Z","timestamp":1476074193000},"page":"S136-S141","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":5,"title":["Dual transcripts of BCR-ABL & different polymorphisms in chronic myeloid leukaemia patients"],"prefix":"10.25259","volume":"143","author":[{"given":"S. Rajashree","family":"Nandagopalan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nivedita","family":"Kuila","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sutapa","family":"Biswas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naresh Chandra","family":"Pattnayak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gyanashyam","family":"Biswas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soumen","family":"Chakraborty","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"10894","reference":[{"key":"R1-18-20241212","doi-asserted-by":"crossref","first-page":"2375","DOI":"10.1182\/blood.V88.7.2375.bloodjournal8872375","article-title":"The diversity of BCR\u2013ABL fusion 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