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. Author manuscript; available in PMC: 2009 Jul 1.
Published in final edited form as: Nat Med. 2008 Dec 21;15(1):50–58. doi: 10.1038/nm.1900

Figure 1.

Figure 1

GSIs reverse glucocorticoid resistance in T-ALL cells. (a) Viability assays in the glucocorticoid-resistant T-ALL cell lines CUTLL1 (72 h), KOPTK1 (48 h) and TALL1 (72 h) treated with 100nM CompE (black squares) or vehicle only (open circles) plus increasing concentrations of dexamethasone. (b) Analysis of T-ALL cell lines sensitive to glucocorticoids (DND41, P12 ICHIKAWA) or B-lineage cell lines (Raji and Ramos). (c) Analysis of in primary T-ALL samples resistant to glucocorticoids. (d) Analysis of CUTLL1 cells treated with glucocorticoid receptor antagonist RU486 (1 µM). (e) Analysis of CUTLL1 cells expressing constitutively active intracellular NOTCH1 (ICN1). (f) Percentage of apoptotic cells (annexinV positive/PI negative) in CUTLL1 (72 h), KOPTK1 (48 h) and TALL1 cells (72 h) treated with DMSO (control), CompE (100 nM), dexamethasone (1 µM) and dexamethasone ( 1 µM) plus CompE (100 nM). (g,h) Inhibition of apoptosis induction by dexamethatosone plus CompE cotreatment by the Z-VAD caspase inhibitor as demonstrated by inhibition of PARP cleavage by Western blot (g) and decreased annexinV positive/PI negative cells by flow cytometry (h). Data in a-f and h are means ± SD of triplicate experiments. Statistical significance was assessed with Student’s t-test.

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