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. 2018 Oct 5;51:36. doi: 10.1186/s40659-018-0185-4

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© The Author(s) 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

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Fig. 2 — UTRs from the BRCA TCGA cohort show increased editing variants associated to ADAR1 activity. a Workflow for ADAR1-target selection, based on the intersection of three independent studies with complementary RNA editing study approaches. b Cumulative parameter count across the different possible variants across the UTRs analyzed. c Correlation of ADAR expression isoforms (RSEM, Log10) and the number of A to G(I) variants for each tumor (Log10). d A to G(I) counts in the 571 evaluated UTRs from BRCA TCGA cohort in normal and tumor breast samples. Box and Whiskers plot with Tukey distribution, ****: Kolmogorov–Smirnov p < 0.001. Pearson Correlation analysis for figure (c) r = 0.679 p < 0.0001 (ADAR1); r = − 0.077 p < 0.01 (ADAR2); r = − 0.028 p < 0.3765 (ADAR3)