Figure 1
Figure 1. TET2 alterations and clinical outcome. (A) Schematic representation of the TET2 protein. The 2 conserved domains are colored in grey. TET2 mutations reported in the study by Abdel-Wahab et al8 and found in our cohort of de novo AML are represented, respectively, with broken and straight lines (dark gray background represents frameshift and nonsense mutations; light gray background, missense mutations; and white background, polymorphisms). Kaplan-Meier estimates of disease-free survival (B) and overall survival (C) according to TET2 mutational status in cytogenetically normal AML patients (N = 54, 3-year DFS, 0% for patients with TET2 mutations, 95% CI, 1%-66% vs 57%, 95% CI, 41%-73%, P = .17; 3-year OS, 51% for patients with TET2 mutations, 95% CI, 19%-83% vs 54%, 95% CI, 37%-72%, P = .63).

TET2 alterations and clinical outcome. (A) Schematic representation of the TET2 protein. The 2 conserved domains are colored in grey. TET2 mutations reported in the study by Abdel-Wahab et al and found in our cohort of de novo AML are represented, respectively, with broken and straight lines (dark gray background represents frameshift and nonsense mutations; light gray background, missense mutations; and white background, polymorphisms). Kaplan-Meier estimates of disease-free survival (B) and overall survival (C) according to TET2 mutational status in cytogenetically normal AML patients (N = 54, 3-year DFS, 0% for patients with TET2 mutations, 95% CI, 1%-66% vs 57%, 95% CI, 41%-73%, P = .17; 3-year OS, 51% for patients with TET2 mutations, 95% CI, 19%-83% vs 54%, 95% CI, 37%-72%, P = .63).

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