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RNA-Seq quantitative analysis of the regulation of imatinib-resistant cell-derived exosomes on CML cell transcriptomes

GSE318329 Homo sapiens Expression profiling by high throughput sequencing 4 samples Submitted 2026/02/11 Platform GPL16791
Summary
Drug resistance frequently results in treatment failure for leukemia and leads to the progression of chronic myeloid leukemia (CML) into an accelerated or blast phase. Although new tyrosine kinase inhibitors (TKIs) and combined TKI therapies have been developed to address BCR-ABL1 mutation-induced drug resistance in CML patients, an increasing number of primitive CML cases exhibit reduced responsiveness or are unresponsive to TKIs. Herein, we discovered that drug-resistant CML cell-derived exosomes (R-Exo) promote resistance to imatinib (IM) in CML compared to drug-sensitive CML cell-derived exosomes (S-Exo). To shed light on the mechanism underlying R-Exo-induced CML drug resistance, we performed high throughput RNA-Seq analyses to reveal the differentially expressed genes in CML cells treated with or without R-Exo. We observed that there was a significant overlap in the expression of drug resistance-related genes that were altered in K562 upon R-Exo treatment. Of these, ATP-binding cassette subfamily B member 1 (ABCB1) exhibited the most obvious upregulation.
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Direct links to NCBI, no account and no request form: the whole study as GSE318329_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1418594 and SRA study SRP674683. Searching any of these in the dataset finder brings you back here.

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