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Gilteritinib-induced upregulation of S100A9 is mediated through BCL6 in Acute Myeloid Leukemia

ABSTRACT: Purpose: Compare transcriptional changes between drug treated (gilteritinib, TP-0903) and vehicle in acute myeloid leukemia xenografts. Methods: FLT3-ITD+ MOLM13-RES-Luc+ (MOLM13 cells with a D835Y mutation generating a resistant phenotype) AML cells were xenografted into NSG mice. Mice were randomized according to bioluminescence imaging, and treatment of FLT3 tyrosine kinase inhibitor (gilteritinib, 30 mg/kg, once daily for 5 days/week) was started on day 13 post-tail vein injection. At study end point, mice were humanely euthanized and bone marrow was collected. AML cells (human CD45+) were isolated, and ATAC-seq was performed on HiSeq 4000, total RNA. Sequencing reads were aligned and analyzed for differential gene expression of treatment vs vehicle cohorts. Results: The analysis revealed the chromatin accessibility changes induced by gilteritinib in MOLM13-RES AML xenograft model.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179421 | GEO | 2021/07/07

REPOSITORIES: GEO

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Gilteritinib-induced upregulation of S100A9 is mediated through BCL6 in Acute Myeloid Leukemia (RNA-Seq I)

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