Fig. 2

The genomic landscape and clinicopathological features. S represents each patient’s identification number. A Top panel shows the number of somatic mutations of each sample, mutation signature (COSMIC version 2), BOR, etiology, the scores of PD-L1 CPS, AFP, and NLR. The middle panel shows the mutational landscape of non-synonymous mutation for frequently altered genes in HCC. Green, red, purple, blue, brown, orange, and gray tiles indicate missense, nonsense, frameshift-insertion, frameshift-deletion, inframe deletion, splice site mutation, and wild-type. The bottom panel displayed copy number alteration for frequently amplified/deleted genes in HCC. Tiles in red, salmon, sky blue, and blue indicate amplification (copy number (CN) ≥ 4), gain (CN ≥ 2.5), loss (CN ≤ 1.5), and deletion (CN ≤ 1), respectively. B GSEA plot representing CHIANG_LIVER_CANCER_SUBCLASS_PROLIFERATION_UP pathway was significantly enriched in responders (PR) (FDR = 0 and normalized enrichment score (NES) = 2.53). C GSEA plot representing CHIANG_LIVER_CANCER_SUBCLASS_CTNNB1_UP pathway was significantly enriched in non-responders (SD/PD) (FDR = 0 and NES = −2.76). D ssGSEA scores of Reactome MET receptor activation geneset were significantly higher in non-responders (SD/PD) than responders (PR) (Wilcoxon rank-sum p-value = 0.016). ssGSEA scores were calculated using GSVA package in R. BOR, best overall response; CPS, combined positive score; AFP, alpha-fetoprotein; NLR, neutrophil-to-lymphocyte ratio; PR, partial response; SD, stable disease; PD, progressive disease