Figure 4.
Figure 4. Graphs showing changes to genetic mutation profile variant at diagnosis, post-IC/pre–allo-SCT, and relapse posttransplant in AML patients. The key shown in (A) applies to (A-C). (A) Patients (61 and 62) where genetic mutations are present at diagnosis were detected at CR and recurred at relapse. (B) Patients (35 and 68) who acquired new mutations at relapse that were not detected at diagnosis or CR. (C) Patients (65 and 92) who acquired new mutations at relapse that were detected pre–allo-SCT. (D) The changes to clonal structure in patients 65 and 92 from diagnosis (Dx) (blue shading), pre–allo-SCT (green shading), and relapse (pink shading) inferred from changes of VAF. Two possible examples of clonal structure of 65 and the most likely structure for 92 are depicted. Letters represent mutations (shown in key) that cooccur in the same clone/ subclone. Red X, elimination of subclone.

Graphs showing changes to genetic mutation profile variant at diagnosis, post-IC/pre–allo-SCT, and relapse posttransplant in AML patients. The key shown in (A) applies to (A-C). (A) Patients (61 and 62) where genetic mutations are present at diagnosis were detected at CR and recurred at relapse. (B) Patients (35 and 68) who acquired new mutations at relapse that were not detected at diagnosis or CR. (C) Patients (65 and 92) who acquired new mutations at relapse that were detected pre–allo-SCT. (D) The changes to clonal structure in patients 65 and 92 from diagnosis (Dx) (blue shading), pre–allo-SCT (green shading), and relapse (pink shading) inferred from changes of VAF. Two possible examples of clonal structure of 65 and the most likely structure for 92 are depicted. Letters represent mutations (shown in key) that cooccur in the same clone/ subclone. Red X, elimination of subclone.

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