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The Retinal Determination Gene Network can confer chemoresistant properties to AML

GSE287893 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2025/12/03 Platform GPL34328
Summary
HoxA9, Six1 and Eya1 are targets of MOZ-TIF2 and MLL-AF9 fusion proteins in murine models. Hoxa9 overexpression can induce AML in murine HSPCs with a latency of ~6-9 months. Co-overexpression of RDGN members Six1 or Eya1 with Hoxa9 can enhance the differentiation block and colony forming potential of HoxA9 alone in vitro. RNA-seq was carried out on these lines to establish genetic pathways responsible for these chages in leukemogenicity. Benzarone is a potent EYA1 inhibitor. We wanted to assess if this drug was able to reverse the leukemogenic properties that EYA1 adds to HOXA9.
Published in
Retinal determination network reactivation drives chemoresistance and blocks myeloid differentiation in acute myeloid leukemia
Clayfield L, Malik D, Whittle J et al. · Cell reports 2026 · PMID 41575857 · doi:10.1016/j.celrep.2025.116875
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Also filed as BioProject PRJNA1214873 and SRA study SRP559519. Searching any of these in the dataset finder brings you back here.

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