American Society of Hematology

Figure 1.

$Figure 1. Clonal architecture of non-del(5q) MDS CD34+ CD38− HSPCs. (A) Tracking of mutations initially detected in the bone marrow of 17 MDS patients in CD34+CD38− single cell–derived colonies by the Sanger method. For each patient sample, the proportions of mutated subclone to the total number of sequenced colonies are indicated as percentages and 95% CI. Each subclone is represented as a circle. Filled circles with bold type represent the dominant or codominant subclones statistically identified using the Fisher exact test. Dominant subclones in linear architecture and in complex architecture are indicated in light and dark blue, respectively. (B) Distribution of the different mutation categories according to their respective occurrence in CD34+CD38−–derived clones. Shown are the percent of unique first events, multiple first events, and second events. (C) Mutations of different gene categories detected or not in the CD19+ cells sorted from the CD34− fraction.$

Clonal architecture of non-del(5q) MDS CD34⁺CD38⁻HSPCs. (A) Tracking of mutations initially detected in the bone marrow of 17 MDS patients in CD34⁺CD38⁻ single cell–derived colonies by the Sanger method. For each patient sample, the proportions of mutated subclone to the total number of sequenced colonies are indicated as percentages and 95% CI. Each subclone is represented as a circle. Filled circles with bold type represent the dominant or codominant subclones statistically identified using the Fisher exact test. Dominant subclones in linear architecture and in complex architecture are indicated in light and dark blue, respectively. (B) Distribution of the different mutation categories according to their respective occurrence in CD34⁺CD38⁻–derived clones. Shown are the percent of unique first events, multiple first events, and second events. (C) Mutations of different gene categories detected or not in the CD19⁺ cells sorted from the CD34⁻ fraction.

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