Fig. 5: Prolonged treatment with glucocorticoids induces phenotypic plasticity in vitro and in vivo.
From: Dasatinib overcomes glucocorticoid resistance in B-cell acute lymphoblastic leukemia

A Percentage of live cells (cPARP-/cCASP3-) in vehicle (ethanol), dexamethasone (dex, 1 µM), dasatinib (das, 100 nM), and dexamethasone + dasatinib (dex + das) conditions in two primary samples following 48 h and 6 days of treatment. B Median prpS6 and pCREB expression in live cells in Pt13R (top) and Pt14R (bottom) at Day 2 and Day 6. C Fold change of events classified into B-cell developmental populations in dexamethasone condition compared to vehicle after 48 h of treatment. D. Fold change versus vehicle of cells classified into B-cell developmental populations in dexamethasone condition after 6 days of treatment. E Experimental workflow of cohort analyzed by CyTOF at diagnosis and day 8 following prednisone monotherapy as per AEIOP-BFM 2009 protocol (Supplementary Table 1). F Mean percentage of classified leukemic cells in nine matched samples at diagnosis (gray line) and day 8 (blue line) of treatment with prednisone. Asterisks indicate populations differentially abundant at day 8 compared to diagnosis based on ANOVA analysis followed by Fisher’s LSD test (α = 0.05). Pre-BI: p < 0.0001; Pre-BII: p = 0.0081; Mature-B: p = 0.0463. G Mean (with 5th and 95th percentile) protein expression of nine primary samples at diagnosis (gray bars) and day 8 (blue bars). Asterisks indicate significance based on a two-tailed paired t-test. CD10: p = 0.0024; TdT: p = 0.0176; CD43: p = 0.0385; CD19: p = 0.0436; CD24: p = 0.0313; prpS6: p = 0.0038; pERK: p = 0.0081. *p ≤ 0.5 **p ≤ 0.01; ***p ≤ 0.001. Source data are provided as a Source Data file.