Fig. 6
- ID
- ZDB-FIG-150629-5
- Publication
- Blackburn et al., 2014 - Clonal evolution enhances leukemia-propagating cell frequency in T cell acute lymphoblastic leukemia through Akt/mTORC1 pathway activation
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Dexamethasone Resistance Is Acquired following Akt Pathway Activation in Clonally Evolved Cells and Can Be Overcome by Combined Treatment with MK2206 (A) Primary monoclonal T-ALL that were pAkt-negative (red) and tertiary transplanted T-ALL that were pAkt-positive (green) were treated ex vivo as indicated and assessed for viability (n = 6 replicates per clone). Error bars are ± SE. (B) Human cell lines with (green) or without (red) active Akt signaling were treated in vitro as indicated. Each point is the average viability after 24 hr of drug treatment (n = 3 replicates per cell line). Error bars ± SE. (C) Representative images of leukemic fish prior to or 4 days after drug treatment with DMSO, 350 mg/l dexamethasone, 3.5 µM MK2206, or 350 mg/l dexamethasone + 3.5 µM MK2206. Clone name and pAkt status are shown to the left. Waterfall plots at the bottom summarize the in vivo T-ALL responses. Each bar denotes the percent change in T-ALL burden within a single animal, those with diagonal lines indicate >50% reduction in T-ALL burden. See also Figure S6. |
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| Stage: | Adult |
Reprinted from Cancer Cell, 25, Blackburn, J.S., Liu, S., Wilder, J.L., Dobrinski, K.P., Lobbardi, R., Moore, F.E., Martinez, S.A., Chen, E.Y., Lee, C., Langenau, D.M., Clonal evolution enhances leukemia-propagating cell frequency in T cell acute lymphoblastic leukemia through Akt/mTORC1 pathway activation, 366-78, Copyright (2014) with permission from Elsevier. Full text @ Cancer Cell