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. 2023 Jun 27;80(7):191. doi: 10.1007/s00018-023-04838-0

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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 — Hallmarks of eccDNA profile in gastric cancer. A Workflow of the study. B The absolute eccDNA number in the paired samples of gastric cancer patients. C GCT group contained significantly more eccDNAs than that of NAT group. D The eccDNA count per million reads mapped (EPM) of GCT group was significantly higher than that of NAT group. E Length distibutions of GCT- and NAT-eccDNAs. F Comparision of eccDNA within different length-intervals between NAT and GCT groups. G Guanine-cytosine content distribution of GCT, NAT, in silico eccDNAs and their upstream and downstream regions with equivalent length. H The genome-wide scale distributions of GCT- and NAT-eccDNAs (pool of 13 samples for each group). The red and blue dots represent the GCT derived and NAT derived eccDNAs, respectively. I The normalized eccDNA density (percentage of eccDNA EPM) in 24 chromosomes of GCT and NAT group