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. 2023 Oct 4;37(11):2150–2167. doi: 10.1038/s41375-023-02048-y

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — The genomic configurations of the ABL1 (11 exons) and BCR genes (23 exons) are shown at the top. In the great majority of CML patients the genomic breakpoints fall in the regions indicated by the two horizontal double blue arrows, i.e. 5’ of ABL1 exon 2 and between exons 13 and 15 of BCR, giving rise to e13a2 and/or e14a2 BCR::ABL1 mRNA fusions. The approximate positions of recurrent variant breakpoints are indicated by the red vertical arrows giving rise to mRNA fusions that involve different BCR exons and/or ABL1 exon 3. Some of these atypical variants are illustrated (e1a2, e6a2, e8a2, e19a2, e13a3, e14a3) but other variants are seen in occasional cases. BCR exon 8 is out of frame with ABL1 exon 2; e8a2 fusions typically break within BCR exon 8 or additional intron-derived sequences are retained to maintain the reading frame. Diagrams are illustrative and not to scale.