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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 1]

ABSTRACT: To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

ORGANISM(S): Mus musculus

PROVIDER: GSE281856 | GEO | 2025/11/12

REPOSITORIES: GEO

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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 3]

Project description:To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 2]

Project description:To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

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Project description:Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 2]

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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 1]

Project description:Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 1]

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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 3]

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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia.

Project description:Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia.

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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia.

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:Tyrosine kinase inhibitors (TKIs) targeting the BCR-ABL1 fusion tyrosine kinase have revolutionized the treatment of chronic myeloid leukemia (CML). However, the development of TKI resistance and the subsequent transition from the chronic phase (CP) to blast crisis (BC) threaten CML patients. Accumulating evidence suggests that translational control is crucial for cancer development and progression. Here, we performed high throughput CRISPR/Cas9 screening and identified poly(A) binding protein cytoplasmic 1 (PABPC1) as a driver for CML-BC progression. PABPC1 preferentially improved the translation efficiency of multiple leukemogenic mRNAs with long and highly structured 5' untranslated regions, including BCR-ABL1 and its TKI-resistant mutants, through forming biomolecular condensates. Inhibiting PABPC1 significantly suppressed CML cell proliferation and attenuated disease progression, but did not affect normal hematopoiesis seriously. More importantly, we identified two novel PABPC1 inhibitors, 1,10-Phen and ML324, which inhibited BC progression and overcame TKI resistance in murine and human CML. Overall, our work identified PABPC1 as a selective translation enhancing factor in CML-BC, the genetic or pharmacological inhibition of which overcame TKI resistance and suppressed BC progression in CML.

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