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. 2022 Feb 10;17:27. doi: 10.1186/s13000-022-01212-9

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© The Author(s) 2022

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Pathological examination and schematic diagram of ALK rearrangement of case 1. (A) Hematoxylin and eosin (H&E) staining of the left upper lobe revealed adenocarcinoma (× 400). (B) A breakpoint within ALK (shown in blue) intron 19 at chromosome 2 was fused within SSH2 (shown in red) intron 2 at chromosome 17, giving rise to the ALK-SSH2 fusion gene. (C) A breakpoint within ALK (shown in blue) intron 19 at chromosome 2 was fused within EML4 (shown in red) intron 6 at chromosome 2, but have opposite orientations, giving rise to the EML4-ALK fusion gene