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. 2023 Apr 18;29(12):2310–2323. doi: 10.1158/1078-0432.CCR-22-2242

Figure 2.

Figure 2. Landscape of sequence alterations in plasma. The type and origin of variants detected across plasma samples analyzed for this study are shown. Alteration frequencies for each gene across plasma samples analyzed are shown on the right and per-sample mutation counts are displayed in the bar plot on top. Panels indicating sampling time point, treatment type, PA scores, combined molecular response, OS, and PFS are shown below. Germline variants (filled circles) were observed in a total of 8 genes (FLT3, FGFR1, CDK6, ALK, POLE, BRAF, PTCH1, and BRCA2) on a patient-specific basis. Variants attributed to CH (crosses) were identified in canonical CH genes (DNMT3A, TP53, and ATM) in >50% (18/33) of patients analyzed for the study and across 14 additional genes at a lower prevalence. Overall, tumor-derived sequence alterations (solid border) were detected in plasma from 30 of the 33 patients analyzed and were most frequently detected in the TP53 gene, which was mutated in 26 patients. Of these 26 patients, 3 shared a mutation in RB1.

Landscape of sequence alterations in plasma. The type and origin of variants detected across plasma samples analyzed for this study are shown. Alteration frequencies for each gene across plasma samples analyzed are shown on the right and per-sample mutation counts are displayed in the bar plot on top. Panels indicating sampling time point, treatment type, PA scores, combined molecular response, OS, and PFS are shown below. Germline variants (filled circles) were observed in a total of 8 genes (FLT3, FGFR1, CDK6, ALK, POLE, BRAF, PTCH1, and BRCA2) on a patient-specific basis. Variants attributed to CH (crosses) were identified in canonical CH genes (DNMT3A, TP53, and ATM) in >50% (18/33) of patients analyzed for the study and across 14 additional genes at a lower prevalence. Overall, tumor-derived sequence alterations (solid border) were detected in plasma from 30 of the 33 patients analyzed and were most frequently detected in the TP53 gene, which was mutated in 26 patients. Of these 26 patients, 3 shared a mutation in RB1.