241 The role of the MR 7 ◀ Supplemental Figure 4. Transcriptional steroid response of two primary patient samples (PS25 and PS26) and one PDX sample, all harboring ETV6-RUNX1 fusion gene. Cells were treated with 0.05µM prednisolone, 0.05µM dexamethasone or 2µM hydrocortisone, with or without addition of 4µM RU28318. Expression of NR3C1, NR3C2, BIM, GILZ and FKBP5 was measured. (B) Transcriptional steroid response of two primary patient samples (PS25 and PS26), one PDX sample and doxycycline-induced RehNR3C2. Patient and PDX cells were treated with 0.05µM prednisolone, 0.05µM dexamethasone or 2µM hydrocortisone, RehNR3C2 cells were treated with 0.032µM prednisolone, 0.16µM dexamethasone or 0.0028µM hydrocortisone, all in presence or absence of MR antagonist RU28318. Absolute NR3C1 (upper panel) and NR3C2 (lower panel) expression was measured. Supplemental Figure 5. Event free survival for the 131 ALL patients with either high or low NR3C1 or NR3C2 expression.
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