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. Author manuscript; available in PMC: 2025 Dec 24.
Published in final edited form as: Blood. 2025 Feb 13;145(7):748–764. doi: 10.1182/blood.2022019306

Figure 5. p300i is invariably effective during early stages of resistance to BET inhibition.

Figure 5

A. Graphical schema of the experimental approach to induce and store cells at all stages of resistance to BETi in SKNO1 and OCI-AML3 cells.

B. Experimental approach to the assessment of transcriptional changes via RNASeq during the longitudinal scale of establishment of resistance to BETi. To avoid putative sequencing-related batch effects, these experiments were directly performed in conjunction with matched p300i-treated (24h) samples (shown with lower opacity). All RNASeq experiments were performed on 3 biological replicates that were raised from individual wells (altogether 24 RNASeq samples per model).

C.-D. Variance by non-supervised hierarchical clustering of the 100 most variable genes in DMSO, BETi_72h, IC50_r and IC90_r isogenic SKNO1 (5C) and OCI-AML3 (5D) cells.

E.-F. Assessment of cell proliferation of the indicated isogenic SKNO1 (5E) and OCI-AML3 (5F) cell lines after 72h (for SKNO1) and 120h (for OCI-AML3) of p300i treatment. Shown are mean percentages normalized to DMSO-treated controls and SD from 3 biological replicates.