Figure 5.
AZA-mediated modulations of IL-6–induced STAT3 phosphorylation in Tcons are not linked to the mutation number and profile of HR-MDS patients. (A) Spectrum of recurrent mutations and cytogenetic abnormalities in patients who downregulated (green) or upregulated (purple) the IL-6/STAT3 signaling axis in Tcons. Each column represents an individual patient sample. (Β) Comparable number of oncogenic mutations before AZA initiation between IL-6/STAT3 downregulators and upregulators. (C) No associations of any functional pathway of oncogenic mutations with the AZA-induced IL6/STAT3 signaling alterations in Tcons. (D) Frequency of driver mutations or karyotypic abnormalities in the IL-6/pSTAT3_down (green) and IL-6/pSTA3_up (blue) groups. No statistically significant associations of single mutations with IL-6/STAT3 modifications were found.

AZA-mediated modulations of IL-6–induced STAT3 phosphorylation in Tcons are not linked to the mutation number and profile of HR-MDS patients. (A) Spectrum of recurrent mutations and cytogenetic abnormalities in patients who downregulated (green) or upregulated (purple) the IL-6/STAT3 signaling axis in Tcons. Each column represents an individual patient sample. (Β) Comparable number of oncogenic mutations before AZA initiation between IL-6/STAT3 downregulators and upregulators. (C) No associations of any functional pathway of oncogenic mutations with the AZA-induced IL6/STAT3 signaling alterations in Tcons. (D) Frequency of driver mutations or karyotypic abnormalities in the IL-6/pSTAT3_down (green) and IL-6/pSTA3_up (blue) groups. No statistically significant associations of single mutations with IL-6/STAT3 modifications were found.

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