December 8, 2025Blood

Clonal timing of FLT3-ITD dictates evolutionary trajectory and phenotypic heterogeneity in acute myeloid leukemia

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Observational analysis reveals FLT3-ITD mutation timing drives clonal evolution and phenotypic heterogeneity in acute myeloid leukemia.

Initiating FLT3-ITD mutations reprogram leukemic cells to a quiescent state, promoting a linear evolutionary pattern.
In acute myeloid leukemia patients, 78% of signaling mutations were terminal subclonal events, with significant differences in white blood cell counts.
Analysis using single-cell RNA sequencing confirmed that leukemic transformation preceded FLT3-ITD acquisition in subclonal events.
Upregulation of leukemia stem cell markers and emergence of uniparental disomy in initiating mutations suggest new therapeutic vulnerabilities in AML.

He et al. (2025) studied this question.

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December 8, 2025Blood

View Full Paper

Ask AI

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Authors

Observational analysis reveals FLT3-ITD mutation timing drives clonal evolution and phenotypic heterogeneity in acute myeloid leukemia.

Initiating FLT3-ITD mutations reprogram leukemic cells to a quiescent state, promoting a linear evolutionary pattern.
In acute myeloid leukemia patients, 78% of signaling mutations were terminal subclonal events, with significant differences in white blood cell counts.
Analysis using single-cell RNA sequencing confirmed that leukemic transformation preceded FLT3-ITD acquisition in subclonal events.
Upregulation of leukemia stem cell markers and emergence of uniparental disomy in initiating mutations suggest new therapeutic vulnerabilities in AML.

He et al. (2025) studied this question.

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