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. 2018 Nov 6;38(12):2042–2055. doi: 10.1038/s41388-018-0476-9

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© The Author(s) 2018

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — YAP is genetically hyperactivated and overexpressed in ESCC. a A visual summary of the alteration frequencies of major components involved in the Hippo/YAP pathway across the ESCC samples in the TCGA Esophageal Carcinoma dataset. Each row represents a gene, and each column corresponds to a sequenced case (n = 96). Note the frequent deletion and mutation of MST1/2 and LATS1/2 and amplification of YAP and WWTR1. b Representative staining of YAP expression in ESCC tissues, adjacent normal squamous epithelium, and intraepithelial neoplasia (IEN). c Statistical analysis of IHC-determined YAP expression in normal, IEN, and tumor tissues. ***P < 0.001 by Kruskal-Wallis with Dunn's post hoc test. d A proposed model for an unbalanced YAP–SOX9 regulatory circuit in promoting ESCC progression.