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Fig. 3 | Genome Medicine

Fig. 3

From: Mechanistic insights into the interactions between cancer drivers and the tumour immune microenvironment

Fig. 3

Immune profiles and TIME driver alterations of HNSC. A HNSC extended cohort. HNSCs collected from TCGA and CPTAC were divided in HPV+, HPV− CNAlow and HPV− CNAhigh samples based on HPV infection and level of aneuploidy [41]. Kaplan–Meier survival curves between HPV+ and HPV− (B) or HPV− CNAlow and HPV− CNAhigh (C) HNSC patients. Overall survivals were compared using the log-rank test. Comparison of CIBERSORTx absolute score medians between HPV+ and HPV− (D); HPV− CNAlow and HPV− CNAhigh (E); or HPV+ and HPV− CNAlow (F) HNSCs. Only immune cell types enriched in at least one HNSC subtype are shown. Comparison of sample proportion in the five TIME features between HPV+ and HPV− (G) or HPV− CNAlow and HPV− CNAhigh (H) HNSCs (see Methods). TIME drivers more frequently damaged in HPV+ HNSCs (I), HPV− CNAlow (J), or HPV− CNAhigh HNSC samples (K). For HPV− CNAhigh HNSCs only the top 13 TIME drivers are shown (full list in Additional File 2: Table S4). CPI = cancer-promoting inflammation; CYS, cytotoxicity score; CPTAC, Clinical Proteomic Tumour Analysis Consortium; FDR, false discovery rate; HPV, human papillomavirus; ICR, immunologic constant of rejection; IS, immune score; TIS, tumour inflammation signature. Proportions were compared using Fisher’s exact test (D–F, I–K) or Mantel–Haenszel chi-square test (G, H). Distributions (M, N) were compared using Kruskal − Wallis test. In D–K, Benjamini–Hochberg correction for multiple testing was applied

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