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. 2021 Jun 5;13:122. doi: 10.1186/s13148-021-01105-6

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© The Author(s) 2021

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. 1 — Correlation of ATAC-seq chromatin accessibility profiles across ovarian cancer cell lines. Heatmaps of ATAC-seq coverage in regions showing differential accessibility between the cisplatin-sensitive and cisplatin-resistant line in each pair. Each row is a 1-Kb window showing log2FC > ± 2 and FDR < 0.001. Dendrograms show similarity between samples as defined by unsupervised hierarchical clustering a A2780/CP70, b PEA1/PEA2, c PEO1/PEO4. d Heatmap of Spearman’s correlation coefficients for each experimental replicate for each cell line analyzed, based on all windows passing filter