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TooManyPeaks identifies drug-resistant-specific regulatory elements from single-cell leukemic epigenomes [ChIP-seq]

ABSTRACT: Purpose: To investigate the impact of GSI resistance on epigenome of Notch-mutated T-ALL Methods: We generated scATAC-seq and H3K27ac ChIP-seq in parental and GSI-resistant cells Results: Using TooManyPeaks, a novel algorithm for scATAC-seq analysis, we identified subpopulation of epigenetically resistant-like parental cell.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171098 | GEO | 2023/08/07

REPOSITORIES: GEO

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TooManyPeaks identifies drug-resistant-specific regulatory elements from single-cell leukemic epigenomes [ATAC-seq]

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TooManyPeaks identifies drug-resistant-specific regulatory elements from single-cell leukemic epigenomes.

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| S-EPMC8409102 | biostudies-literature

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Project description:Purpose: To investigate the mechanisms of 3D genome organization in drug-resistant T-ALL Methods: We used multiple epigenomics, chromatin conformation, and transcriptomic assays to study the mechanisms of chromatin adaptation in GSI-sensitive and GSI-resistant T-ALL Results: We report here that T/B cell lineage determining transcription factors are differentially expressed in GSI-resistant T-ALL cells, driving enhancer switching and genome folding reorganization events to promote GSI-resistance. Conclusions: These observations suggest a general mechanism that diffenrential activity of pioneering factors can be exploited to evade addiction to oncogenic signals.

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