Fig. 6: Demethylating treatment restores Gata2 expression and prolongs survival in TET2-deficient Cebpa-mutant AML. | Nature Communications

Fig. 6: Demethylating treatment restores Gata2 expression and prolongs survival in TET2-deficient Cebpa-mutant AML.

From: TET2 lesions enhance the aggressiveness of CEBPA-mutant acute myeloid leukemia by rebalancing GATA2 expression

Fig. 6: Demethylating treatment restores Gata2 expression and prolongs survival in TET2-deficient Cebpa-mutant AML.The alt text for this image may have been generated using AI.

a Experimental setup for evaluating the effect of short-term 5-azacytidine (5-AZA) treatment in vivo. Recipient mice were sub-lethally irradiated and transplanted with leukemic BM from moribund secondary recipient mice. Three individual CebpaΔ/p30Tet2Δ/Δ clones (A–C) and two CebpaΔ/p30Tet2+/+ clones (A–B) were used, respectively. The illustration was created with BioRender.com. b Expansion of myeloid (Mac1+) donor-derived cells in bone marrow (BM) assessed by flow cytometry, and c Gata2 mRNA expression in sorted leukemic blasts by qPCR assessed 24 hours after the last of three injections of 5-AZA or vehicle (samples from 3 mice per clone and 6 and 9 mice per group, for CebpaΔ/p30Tet2+/+ and CebpaΔ/p30Tet2Δ/Δ, respectively). Dot plots showing individual mice for separate clones and bar graphs shows mean ± SEM for each group. Data were analyzed by Kruskal–Wallis test followed by Dunn’s correction for multiple comparisons. d Experimental setup for evaluating the effect of 5-AZA treatment on AML progression in vivo. The illustration was created with BioRender.com. e Survival of sub-lethally irradiated tertiary recipient mice after transplantation of leukemic BM from moribund secondary recipient mice (clone A from both genotypes) in response to intermittent 5-AZA treatment (5-AZA treated groups 8 mice and vehicle-treated groups 4 mice). The data were analyzed by Mantel–Cox Log-rank test. Source data are provided as a Source Data file.

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