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A polymorphism in exon b2 of the major breakpoint cluster region (M‐bcr) identified in chronic myeloid leukaemia patients
Author(s) -
Meissner Rosely De V.,
Dias Paula M. B.,
Covas Dimas T.,
Job Fani,
Leite Márcia,
Nardi Nance B.
Publication year - 1998
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1998.00945.x
Subject(s) - exon , breakpoint cluster region , biology , breakpoint , genetics , complementary dna , philadelphia chromosome , cytosine , microbiology and biotechnology , coding region , allele , cancer research , gene , chromosome , chromosomal translocation
The BCR/ABL junctional region and the b3 exon from chronic myeloid leukaemia (CML) patients were sequenced. In all 21 samples analysed the junctional region, as well as the b3 exon of 8 b3a2 mRNA molecules, presented no differences to the already described sequences. However, we identified a polymorphic base in the b2 exon in two out of seven b3a2 samples, four out of 10 b2a2 samples and all four b3a2/b2a2 samples analysed. In the eighth position before the junctional region of BCR/ABL cDNA, a cytosine replaces thymine in these cases. The polymorphism described here could be a useful marker for the differentiation of normal and rearranged BCR alleles in heterozygotes.