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. 2018 Oct 3;10:121. doi: 10.1186/s13148-018-0554-4

Fig. 5.

Fig. 5

EPZ-6438/lenalidomide combination targets key B cell transcription factors and induces MMCs quiescence. a The expression of Ikaros (IKZF1), c-Myc, and IRF4 of HMCLs was evaluated by flow cytometry in XG7 after EPZ-6438 (1 μM) and/or lenalidomide (2 μM) treatment using PE-conjugated anti-IKZF1, anti-MYC and anti-IRF4 mAb, and isotype matched PE-conjugated mAb. Data are mean values ± standard deviation of three experiments. b Heatmap presenting RNA-seq GEP expression of E2F1, PRDM1, IRF4, MYC, BCL6, CDKN1A, BACH2, and PAX5 in XG7 HMCL treated with EPZ-6438 (1 μM) and/or lenalidomide (2 μM). c XG7 cell cycle was analyzed, after EPZ-6438 (1 μM) and/or lenalidomide (2 μM) treatment, by flow cytometry using DAPI, BrdU incorporation, and labeling with an anti-BrdU antibody. Results are representative of four independent experiments. * indicates a significant difference compared to control cells using a paired t test (P ≤ 0.05). d The percentage of Ki67 negative cells of EPZ-6438 and/or lenalidomide-treated XG7 HMCL was analyzed by flow cytometry using anti-Ki67 antibody. Data are the mean values ± SD of three separate experiments. * indicates a significant difference compared to control cells using a paired t test (P ≤ 0.05). e Model of EPZ-6438/lenalidomide combination action in MMCs