gsk1210151a and Leukemia--Biphenotypic--Acute

In 2015, as part of the Reproducibility Project: Cancer Biology, we published a Registered Report (Fung et al., 2015), that described how we intended to replicate selected experiments from the paper "Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia" (Dawson et al., 2011). Here, we report the results of those experiments. We found treatment of MLL-fusion leukaemia cells (MV4;11 cell line) with the BET bromodomain inhibitor I-BET151 resulted in selective growth inhibition, whereas treatment of leukaemia cells harboring a different oncogenic driver (K-562 cell line) did not result in selective growth inhibition; this is similar to the findings reported in the original study (Figure 2A and Supplementary Figure 11A,B; Dawson et al., 2011). Further, I-BET151 resulted in a statistically significant decrease in

Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Chromatin; Disease Models, Animal; Heterocyclic Compounds, 4 or More Rings; Heterografts; Humans; Leukemia, Biphenotypic, Acute; Mice; Nerve Tissue Proteins; Protein Binding; Receptors, Cell Surface; Treatment Outcome