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. 2017 May 22;45(13):7786–7795. doi: 10.1093/nar/gkx463

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© The Author(s) 2017. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — Mutation hotspots in cancer driver genes in POLE-mutant tumors. (A) Contingency table and significance from Fisher's exact test of Polymerase epsilon exonuclease domain mutant (POLE-mutant) and microsatellite stable (MSS) colorectal cancer samples which are wild-type or mutant at tumor protein p53 (TP53) R213 and adenomatous polyposis coli (APC) R1114 codons. (B) Methylation status in normal colon tissue for each CpG site within coding exons of TP53 and APC, together with significance by one-sample t-test against methylation at R213 and R1114 codons respectively. Mean and standard deviation are shown. ** denotes P < 0.01.