Figures and data
![](https://prod--epp.elifesciences.org/iiif/2/96951%2Fv1%2Fcontent%2F573827v1_fig1.tif/full/max/0/default.jpg)
Profile of CH in NSCLC patients treated with ICI. (A) Overall study design. (B) Frequency of CH variant detection in each gene in NSCLC samples before (light blue) and after (blue) ICI treatment. (C) Comparison of variant allele frequency before and after ICI treatment, divided by pathology type (LUAD, LUSC, other). (D) Effect of ICI treatment on the clonal landscape of all genes (left) and frequently detected CH genes.
![](https://prod--epp.elifesciences.org/iiif/2/96951%2Fv1%2Fcontent%2F573827v1_fig2.tif/full/max/0/default.jpg)
Prevalence of CH in relation to various parameters. (A)-(D): discovery cohort (n = 100), (E)-(G): replication cohort (n = 180; see Methods for description). (A, E) CH prevalence by pathology (LUSC and LUAD). (B) Effect of ICI treatment on CH. (C, F) Effect of post-ICI prognosis to ICI on CH. (D, G) Age distribution of the cohort, stratified by CHIP allele frequency and pathology status.
![](https://prod--epp.elifesciences.org/iiif/2/96951%2Fv1%2Fcontent%2F573827v1_fig3.tif/full/max/0/default.jpg)
scRNA-seq analysis detected myeloid-specific inflammatory signatures in patients with high CH burden. (A) UMAP plot of scRNA-seq data from the discovery cohort (n = 63). (B) Effect of pathology (left) and VAF (right) on cell composition. (C) GSEA of DEGs from myeloid populations. Color represents normalized effect score (NES) and dot size represents adjusted P-values. (D) Expression of selected genes in the NF-ĸB pathway from the scRNA-seq data. (E) GSEA plots of selected pathways from (C).