Fig. 6: APOBEC3B is required for APOBEC signature accumulation in Osi-treated human NSCLC cell line PC9.
From: The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance
a, Outline of WGS long-term TKI treatment experiment on APOBEC3B (A3B)-deficient and A3B-proficient PC9 single-cell clone lines. Figure created in BioRender.com. b, Focused plots showing APOBEC signature (SBS2 + SBS13) burden in the indicated A3B-deficient (A3B KO) and A3B-proficient (A3B WT) PC9 clones (A3B WT, n = 6 biological replicates; A3B KO, n = 6 biological replicates). c, Fraction of mutations in an APOBEC context (TCW C>T/G) of total mutations per replicate, of Osi-treated A3B WT and A3B KO cells (all data points shown, n = 6 biological replicates, mean ± s.d., two-tailed Mann–Whitney test, **P = 0.0043). d, Fraction of APOBEC mutations (RTCW C>T/G) of total mutations per replicate Osi-treated A3B WT and A3B KO cells (all data points shown, n = 6 biological replicates, two-tailed Mann–Whitney test, **P = 0.0022). e, Fraction of APOBEC mutations (YTCW C>T/G) of total mutations per replicate in Osi-treated A3B WT and A3B KO cells (all data points shown, n = 6 biological replicates, two-tailed Mann–Whitney test, P = 0.0931). f, Profiles of APOBEC-associated signatures SBS2 and SBS13 from the Catalogue of Somatic Mutations in Cancer (COSMIC) (cancer.sanger.ac.uk). g, Mutational profiles of A3B KO and A3B WT Osi-treated PC9 cell lines. Mutational profiles are plotted as the number of mutations (y axis) at cytosine or thymine bases classified into 96 possible trinucleotide sequence contexts (asterisk indicates cell lines that acquired APOBEC signature during TKI treatment timecourse (SBS2 + SBS13; A3B WT, n = 6 biological replicates; A3B KO, n = 6 biological replicates)).
