Skip to main content
[Preprint]. 2024 May 17:2024.05.15.24307318. [Version 1] doi: 10.1101/2024.05.15.24307318

Fig. 3. Passive smoking influence in the genomic landscape of LCINS.

Fig. 3.

a-d, Differences in base substitution burden and tumor-to-normal telomere length ratio using univariate comparisons (a and b) as well as multivariable linear regressions considering clinical and epidemiological covariates (c and d), including age, sex, genetic ancestry, histology, and tumor purity. e, Volcano plot indicating enrichment of mutational signatures derived from SBS mutations in passive vs. non-passive smokers. Horizontal lines marking statistically significant thresholds were included at 0.05 (dashed orange line) and 0.01 FDR levels (dashed red line). f, Comparison of the mutations belonging to each of the six main SBS mutation subtypes in passive vs. non-passive smokers. g, Volcano plot indicating enrichment of mutations in driver genes affecting specific LCINS tumors.