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. 2019 Jun 6;69(1):18–31. doi: 10.1136/gutjnl-2018-318070

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Increased ploidy and chromosomal instability in peritoneal carcinomatosis (PC) specimens with advanced stage and aggressive histological phenotypes. (A) Density plot showing the distribution of tumour ploidy by histopathological subtypes. (B, C) Composite of copy number profiles for ascites with diffuse or intestinal (B), signet-ring cell (SRC) or NOS subtypes (C), with gains in red and losses in blue. The regions that showed a difference in the frequency of copy number alterations between two subtypes were shaded in light gray rectangles, and within which the names of cancer-related or biologically important genes are labelled.