BCR-ABL1 b2a2/b3a2 Differentiation Kit

Chronic myeloid leukaemia (CML) is characterized by the consistent involvement of the Philadelphia chromosome (Ph) and the BCR-ABL1 fusion gene, which derives from the reciprocal translocation t(9;22)(q34;q11) between chromosome 9 and 22. In almost all CML patients, the breakpoint in the BCR gene involves the Major breakpoint cluster region (M-bcr). The position of the breakpoint within the M-bcr, after exon b2 (e13) or exon b3 (e14) determines two main types of the fused BCR-ABL1 mRNA defined as b2a2 (e13a2) and b3a2 (e14a2) transcripts differing by 75 nucleotides. These transcripts encode two 210-kDa tyrosine kinase proteins (p210 BCR-ABL1), which differ by 25 amino acids respectively. The impact of M-bcr breakpoint position on disease phenotype and its prognosis has been a subject of controversies for a long time. Several reports have suggested that the type of the chimeric mRNA (b2a2 or b3a2) is associated with differences in the clinical and haematological characteristics of CML patients and prognosis.