Fig. 5: Molecular subtypes of FH-deficient RCC exhibit distinct genomic, transcriptomic and clinical features. | Nature Communications

Fig. 5: Molecular subtypes of FH-deficient RCC exhibit distinct genomic, transcriptomic and clinical features.

From: Comprehensive molecular profiling of FH-deficient renal cell carcinoma identifies molecular subtypes and potential therapeutic targets

Fig. 5

a Heatmap shows the genomic, transcriptomic and clinicopathological features for each molecular clusters (C1, n = 27; C2, n = 23; C3, n = 6). b Bar chart depicts the proportions of patients who achieved ORR when receiving first-line ICB + TKI combination therapy or TKI monotherapy in each molecular cluster. C1: ICB + TKI (n = 18), TKI (n = 3); C2: ICB + TKI (n = 8), TKI (n = 5); C3: ICB + TKI (n = 2), TKI (n = 3). c Kaplan-Meier curves show PFS of patients in different clusters when receiving first-line ICB + TKI (C1, n = 18; C2, n = 8; C3, n = 2). d Kaplan-Meier curves show PFS of patients in different clusters when receiving first-line TKI monotherapy (C1, n = 3; C2, n = 5; C3, n = 3). P-values were determined by two-sided log-rank test (c, d). RCC renal cell carcinoma, ORR objective response rate, ICB immune checkpoint blockade, TKI tyrosine kinase inhibitor, PFS progression-free survival. Source data are provided as a Source Data file.

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