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Abstract RUNX1 is a critical regulator of hematopoiesis. In CML, somatic RUNX1 mutations and RUNX1::MECOM/EVI1, are associated with TKI resistance and progression to BP-CML. To examine post-transcriptional dysregulation downstream of RUNX1 aberrations, we used orthogonal organic phase separation to characterise the RNA-binding proteome of RUNX1 deficient BP-CML cells.
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