Chronic myeloid leukemia (CML) is characterised by the consistent involvement of the Philadelphia chromosome (Ph) and the BCR-ABL 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-ABL mRNA defined as b2a2 and b3a2 transcripts differing by 75 nucleotides. These transcripts encode two 210-kDa tyrosine kinase proteins (p210 BCR-ABL), 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 hematological characteristics of CML patients and prognosis.
The TRUPCR BCR-ABL1 b2a2/b3a2 kit is a real time PCR assay which detects BCR-ABL1 fusion gene transcripts P210 (e13a2, e14a2), P190 (e1a2), P230 (e19a2) and also differentiates between e13a2 (b2a2) and e14a2 (b3a2) transcript in bone marrow or peripheral blood samples of chronic myeloid leukemia (CML) or acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML).