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High-density cultures (3D-cultures) associated therapy resistance in AML THP-1 cells

GSE298747 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2025/06/09 Platform GPL18460
Summary
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by the rapid proliferation of immature myeloid cells in the bone marrow, leading to impaired hematopoiesis and life-threatening complications. Despite advances in chemotherapy, targeted therapy, and stem cell transplantation, treatment resistance remains a major clinical challenge, contributing to high relapse rates and poor survival outcomes. Understanding the mechanisms of resistance — including genetic mutations, epigenetic alterations, and microenvironmental interactions — is crucial for developing more effective therapies. Investigating how AML cells develop treatment resistance, particularly under pro-inflammatory conditions, may reveal novel therapeutic targets and improve patient prognosis. Our study focuses on resistance mechanisms in AML cells under density-induced sterile pro-inflammatory conditions (modelled via high-density culture, HDC). This approach aims to identify key molecular pathways associated with therapy resistance in AML.
Published in
Studying Signaling Pathway Activation in TRAIL-Resistant Macrophage-Like Acute Myeloid Leukemia Cells
Lomovskaya YV, Krasnov KS, Kobyakova MI et al. · Acta naturae 2024 · PMID 38698963 · doi:10.32607/actanaturae.27317
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Direct links to NCBI, no account and no request form: the whole study as GSE298747_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 9 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1271049 and SRA study SRP589293. Searching any of these in the dataset finder brings you back here.

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