ArticleBlood cancer discovery2026
Rapid Transcription Dynamics Confers Cytarabine Resistance in Acute Myeloid Leukemia.
Article in Blood cancer discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chemotherapy resistance remains a critical challenge in the treatment of patients with cancer, including acute myeloid leukemia (AML). Although genetic alterations can contribute to resistance, the role of rapid-adaptive nongenetic mechanisms, particularly transcription dynamics, remains poorly understood. In this article, we demonstrate that short-term treatment of AML cells with the widely used chemotherapeutic cytarabine (AraC) leads to the rapid emergence of a cell population with significant RNA induction and increased AraC resistance in cell lines and primary patient samples. Mechanistically, transcriptomic and targeted high-resolution analysis of transcription dynamics using single-molecule RNA FISH revealed rapid induction of transcriptional dynamics and upregulation of key transcription factors (TF)-which we term "AraC rapid response TFs." Functionally, short-term pre- and cotreatment with RNA transcription inhibitors suppressed chemotherapy-induced RNA induction and prevented resistance acquisition in vitro and in vivo. Furthermore, CRISPR-mediated suppression of TFs PU.1 and GATA1 significantly attenuated AraC resistance. Our findings reveal a role of rapid-adaptive transcriptional dynamics in AML chemotherapy resistance. SIGNIFICANCE: This study reveals a role of rapid-adaptive transcriptional dynamics in AML chemotherapy resistance, highlighting master TFs as key regulators. These insights offer a pharmacologically accessible approach to potentially alleviate the major clinical problem of chemotherapy resistance.
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