Fig. 5
From: A subset of diffuse-type gastric cancer is susceptible to mTOR inhibitors and checkpoint inhibitors
Features of mutations in primary GCs in TCGA cohort and PDX cells. a Overview of mutations in diffuse-type GCs in clusters I and II, and intestinal-type GCs in TCGA cohort. Top 15 most frequently mutated genes are shown. b Mutation frequencies of the top 15 genes in diffuse-type GCs in clusters I and II, and intestinal-type GCs in TCGA cohort. * P < 0.05, ** P < 0.01 by Chi-square test between two populations. In the case of PIK3CA, mutation frequency in diffuse-type GCs in cluster II (7/27) was significantly greater than that in intestinal-type GCs (7/76; P = 0.029), or than that in non-diffuse-type GCs in cluster II (diffuse-type GCs in cluster I + intestinal-type GCs; 11/110; P = 0.028). In the case of CDH1, mutation frequency in diffuse-type GCs in cluster I (8/34) was significantly greater than that in intestinal-type GCs (2/76; P < 0.001), or than that in diffuse-type GCs in cluster II (1/27; P = 0.030). c Expression of MLH1 in diffuse-type GCs in cluster I and II in TCGA cohort. *** P < 0.001 by two sample t-test. d Western blot analysis of CDH1, MLH1, and MSH2 in HGC-3, − 18, and − 20 PDXs. GAPDH was used as a loading control. e Methylation-specific polymerase chain reaction analysis of MLH1 promoter region in HGC-3, − 18, and − 20 PDXs. PCR products recognizing methylated (lanes M) and unmethylated (lanes U) CpG sites were loaded in 2.5% agarose gels. f Mutation numbers/Mb in HGC-3, − 18, and − 20 cells, and in CIN, MSI, EBV, and GS subtype GCs in TCGA cohort