Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Sep 1;33(17-18):1265–1279. doi: 10.1101/gad.327593.119

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2019 Hurtz et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

PMC Copyright notice

Figure 7. — Dual targeting of BCL2 and BCL6 in MLL-rearranged B-ALL. (A) Human MLL-rearranged B-ALL cells were treated with Dex, RI-BPI, or a combination of both. CI values for ED50 are shown. Relative viability was assessed. n = 3. (B) Human MLL-rearranged B-ALL cells were treated with Dex, FX1, or a combination of both. Relative viability and CI were assessed. n = 3. (C) Relative viability (n = 3) was assessed upon treatment with increasing concentrations of ABT-199 in pre-B cells expressing MLL-ENL following 4-OHT Cre-mediated deletion of Bcl6. (D) Human MLL-rearranged B-ALL cells were treated with ABT-199, RI-BPI, or ABT-199 in combination with RI-BPI. Relative viability and CI were assessed. (E) Relative viability and CI were examined following treatment of human MLL-rearranged B-ALL cells with ABT-199, FX1, or a combination of both. (F) MLL-rearranged fusion proteins induce aberrant expression of BCL6, which contributes to MLL-rearranged-driven leukemogenesis by restricting expression of BIM, a proapoptotic molecule. The BCL2 inhibitor ABT-199 disrupts the interaction between BCL2 and BIM. Pharmacological inhibition of BCL6 (RI-BPI or FX1) synergizes with ABT-199 in eradicating MLL-rearranged B-ALL cells. (G,H) Relative viability was determined upon treatment with increasing concentrations of ABT-199, RI-BPI (G), FX1 (H), or a combination of ABT-199 with RI-BPI (G) or FX1 (H) in ETV6-RUNX1 B-ALL cells.