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. 2020 Dec 1;20:1175. doi: 10.1186/s12885-020-07676-6

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© The Author(s) 2020

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. 3 — Clinical verification of ANXA1 and HSPD1 by Dot blot assay. Scatter plot showing relative levels of autoantibodies in controls (Healthy individuals, n = 34; GSD, n = 48) and cases (GBC stage I and II, n = 12; GBC Stage IIIA (n = 11); GBC Stage IIIB (n = 6); GBC stage IVB, n = 23). (a) The analysis showed a significant difference (p value ≤0.05) in autoantibody levels for ANXA1 in GBC stage I and II or IIIA (b) early stage GBC cases and (c) lymph node negative GBC cases (c) in comparison to both the controls. No significant difference in autoantibody levels for HSPD1 was observed in any of the GBC stages (d), early or advanced stage GBC cases (e) and lymph node negative or positive cases (f) in comparison to controls