Clinicopathological significance of histological diversity in gastric adenocarcinoma with primitive enterocyte phenotype: A methylation-driven aggressive entity

Figure 4 Distinct genomic landscapes across gastric cancer subtypes. A: Somatic mutation analysis identifying the top 10 most frequently mutated genes in gastric adenocarcinoma with primitive enterocyte phenotype (blue), conventional gastric cancer (CGC) (orange) cohorts and CGC expressing primitive phenotypic markers (purple), with mutation frequencies expressed as percentages; B: Somatic mutation analysis revealing the top 10 most frequently mutated genes in hepatoid adenocarcinoma (brown) and gastric adenocarcinoma with enteroblastic differentiation (black) cohorts, with both groups exhibiting notably high TP53 mutation frequencies; C: Copy number alteration analysis highlighting the top 10 genes with the highest alteration frequencies in gastric adenocarcinoma with primitive enterocyte phenotype (blue), CGC expressing primitive phenotypic markers (purple), and CGC (orange) cohorts; D: Copy number alteration analysis showcasing the top 10 genes with the highest alteration frequencies in hepatoid adenocarcinoma (brown) and gastric adenocarcinoma with enteroblastic differentiation (black) cohorts. GAPEP: Gastric adenocarcinoma with primitive enterocyte phenotype; CGC: Conventional gastric cancer; CGC-P: Conventional gastric cancer expressing primitive phenotypic markers; HAC: Hepatoid adenocarcinoma; GAED: Gastric adenocarcinoma with enteroblastic differentiation.