Abstract
Acute myeloid leukemia (AML) is a heterogeneous disease caused by a variety of mutations in transcription factors, epigenetic regulators and signaling molecules. To determine how different mutant regulators establish AML subtype-specific transcriptional networks we performed a comprehensive global analysis of cis-regulatory element activity and interaction, transcription factor occupancy and gene expression patterns in purified leukemic blast cells. Here, we focussed on specific sub-groups of patients carrying mutations in genes encoding transcription factors (RUNX1, CEBPα) and signaling molecules (FTL3-ITD, RAS, NPM1). Integrated analysis of these data demonstrates that each mutant regulator establishes a specific transcriptional and signaling network unrelated to normal cells sustaining the expression of unique sets of genes required for AML growth and maintenance.
Original language | English |
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Pages (from-to) | 151-162 |
Number of pages | 12 |
Journal | Nature Genetics |
Volume | 51 |
Issue number | 1 |
Early online date | 12 Nov 2018 |
DOIs | |
Publication status | Published - Jan 2019 |
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Birmingham Environment for Academic Research (BEAR)
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Research brings personalised medicine to treat leukaemia one step closer
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