Extended Data Figure 4: Resistant MLL–AF9;NrasG12D AML cells generated through Suz12 suppression are not enriched for LSC-associated surface markers or expression signatures. | Nature

Extended Data Figure 4: Resistant MLL–AF9;NrasG12D AML cells generated through Suz12 suppression are not enriched for LSC-associated surface markers or expression signatures.

From: Transcriptional plasticity promotes primary and acquired resistance to BET inhibition

Extended Data Figure 4

a, Immunophenotyping of JQ1-resistant mouse AML cells expressing two independent Suz12 shRNAs stably cultured in 50 nM JQ1 for more than 4 weeks (LT) compared to cells expressing Ren.713 control shRNA. Data are representative of two independent biological replicates. b, Percentage of c-Kit+ cells in CD45.2+ bone marrow cells isolated from terminally diseased CD45.1+ mice following transplantation with MLL–AF9;NrasG12D cells expressing Ren.713 or Suz12.1676 and in vivo treatment with DMSO carrier or JQ1 (50 mg kg−1 per day) (n = 5, mean ± s.e.m.). c, Gene set enrichment analysis evaluating changes in macrophage and LSC gene signatures in resistant MLL–AF9;NrasG12D AML expressing three PRC2 shRNAs compared to cells expressing Ren.713 shRNA (n = 2) or empty vector (see also Fig. 2e, f).

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