Fig. 8: In silico analysis suggests the underlying mechanism of gemcitabine sensitivity in TP53-mutated NSCLC. | Cell Death Discovery

Fig. 8: In silico analysis suggests the underlying mechanism of gemcitabine sensitivity in TP53-mutated NSCLC.

From: Utilizing TP53 hotspot mutations as effective predictors of gemcitabine treatment outcome in non-small-cell lung cancer

Fig. 8

A Gene Set Enrichment Analysis (GSEA) of the TCGA-LUAD dataset comparing TP53-mutant and wild-type patients. Enriched pathways are categorized into three major groups: cell growth and division, DNA damage repair, and Rho GTPase signaling. Dot colors represent the normalized enrichment score (NES), while dot sizes indicate the number of genes in each gene set. B Perturbational classes (PCLs) strongly linked to gemcitabine, retrieved via the CLUE platform. Red indicates inhibitory PCLs, while blue indicates activating PCLs. C Gene knockdown (KD) signatures highly associated with gemcitabine, also retrieved via CLUE. In the chord diagram, chords connect genes to their corresponding pathways, as defined in (A). Chord transparency reflects the CLUE connectivity score, with higher visibility indicating stronger similarity between gemcitabine treatment and gene KD effects. Connections with a connectivity score >90 are considered strong.

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