Figure 1.
Figure 1. Molecular pattern of clonal interference of signaling mutations in CBF AML. (A) Pattern of gene mutations in cases with t(8;21) and inv(16) AML, presence of clonal interference in the 6 comprehensively analyzed signaling genes (KIT, NRAS, KRAS, FLT3, CBL, JAK2), and presence of ≥1 mutation in chromatin (ASXL1, ASXL2, BCOR, BCORL1, EZH2, KDM6A) or cohesin (RAD21, SMC1A, SMC3, STAG2) genes. (B) Scatter plot indicating the number of signaling genes (KIT, NRAS, KRAS, FLT3, CBL, JAK2) and the total number of clones in these 6 signaling genes. Patients with ≥2 signaling clones are assigned to the “clonal interference” group. (C) Volcano plot of the total VAF of signaling clones in patients with a single or multiple signaling clones, together with the P value of a linear regression adjusted on HTS platform. The number of patients with a total VAF > 60% is reported. The difference in the proportion of patients with total VAF > 60% was not statistically different (logistic regression adjusted for HTS platform; P = .16). (D) Circos plot showing the pattern of comutations in signaling genes in patients with ≥1 signaling clone. (E) Proportion of patients with a single signaling clone (n = 167) or with clonal interference (n = 126) with ≥1 clone displaying the genotype indicated on the x-axis (the error bar indicates the 95% CI). P values for logistic regression adjusted on HTS platform: **P < .01, ***P < .001. Unspecified P values are >.05. ex, exon; NA, not available.

Molecular pattern of clonal interference of signaling mutations in CBF AML. (A) Pattern of gene mutations in cases with t(8;21) and inv(16) AML, presence of clonal interference in the 6 comprehensively analyzed signaling genes (KIT, NRAS, KRAS, FLT3, CBL, JAK2), and presence of ≥1 mutation in chromatin (ASXL1, ASXL2, BCOR, BCORL1, EZH2, KDM6A) or cohesin (RAD21, SMC1A, SMC3, STAG2) genes. (B) Scatter plot indicating the number of signaling genes (KIT, NRAS, KRAS, FLT3, CBL, JAK2) and the total number of clones in these 6 signaling genes. Patients with ≥2 signaling clones are assigned to the “clonal interference” group. (C) Volcano plot of the total VAF of signaling clones in patients with a single or multiple signaling clones, together with the P value of a linear regression adjusted on HTS platform. The number of patients with a total VAF > 60% is reported. The difference in the proportion of patients with total VAF > 60% was not statistically different (logistic regression adjusted for HTS platform; P = .16). (D) Circos plot showing the pattern of comutations in signaling genes in patients with ≥1 signaling clone. (E) Proportion of patients with a single signaling clone (n = 167) or with clonal interference (n = 126) with ≥1 clone displaying the genotype indicated on the x-axis (the error bar indicates the 95% CI). P values for logistic regression adjusted on HTS platform: **P < .01, ***P < .001. Unspecified P values are >.05. ex, exon; NA, not available.

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