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Background  The  BCR-ABL1  fusion gene underlying the pathogenesis of CML can arise from a variety of breakpoints. The e13a2 and e14a2 transcripts formed by breakpoints occurring around exon 13 and exon 14 of the  BCR  gene respectively are the most common.    Methods  We undertook a retrospective audit using local laboratory database and electronic patient care records of 69 CML patients with an e13a2 or e14a2 transcript type identified in our regional population.    Results  The e13a2 group was on average significantly younger (45.0 years v 54.5 years), had a higher average white cell count (189.8 × 10 9 /l v 92.40 × 10 9 /l) and lower platelet count (308 × 10 9 /l v 644 × 10 9 /l) in comparison to the e14a2 group suggesting that these are distinct biological entities. Over an average follow-up of 33.8 months and 27.2 months for the e13a2 and e14a2 groups we observed an inferior molecular response to imatinib in the e13a2 group. A significantly lower number of patients in the e13a2 arm met European Leukemia Net criteria for optimal response at 12 months therapy (17.64% v 50.0%) and were slower to obtain deep molecular responses MR 4  or MR 4.5 .    Conclusion  Patients with an e13a2 transcript demonstrate an inferior molecular response to imatinib in our regional population.

Response to Imatinib therapy is inferior for e13a2 BCR-ABL1 transcript type in comparison to e14a2 transcript type in chronic myeloid leukaemia