ArticleZhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi2016
[Discovery of a novel spliceosome of ABL gene (ABL(Δexon7+35INS)) and its association with TKIs resistance in chronic myeloid leukemia].
Article in Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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13 authors at 1 institution in 1 country.
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Abstract
objectiveTo explore whether the ABL(Δexon7) and ABL(35INS) spliceosome contributed to TKIs resistance.
methodsScreening ABL(Δexon7) and ABL(35INS) in 74 normal people and 76 CML patients (53 patients in remission and 23 patients with TKIs resistance) by using polyacrylamide gel electrophoresis combined with cloning sequencing.
resultsA novel spliceosome ABL(Δexon7+ 35INS) (ABL(Δexon7) and ABL(3)5INS existed at the same time) was identified and the mutation was detected in 8 (10.8%) of 74 normal people, 4 (7.5%) of 53 remission patients and 2 (8.7%) of 23 resistant patients. While 47 (63.5%) cases expressed ABL(Δexon7) and 8 (10.8% ) cases expressed ABL(35INS) in 74 healthy people, 30 (56.6%) cases expressed ABL(Δexon7) and 5 (9.4% ) cases expressed ABL(35INS) in 53 remission patients, 12 (52.2%) cases expressed ABL(Δexon7) and 3(13.0%) cases expressed ABL(35INS) in 23 resistant patients. Three kinds of spliceosome in all groups had no statistical difference.
conclusionABL(Δexon7+ 35INS), ABL(Δexon7) and ABL(35INS) may be not uncommon in ABL gene and were unrelated to resistance in CML with TKIs treatment. ABL(35INS) were often accompanying with exon 7 deletion.
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