Fig. 4: Co-targeting the ancillary survival factor improves the in vivo treatment responses of tumors. | Cell Death & Differentiation

Fig. 4: Co-targeting the ancillary survival factor improves the in vivo treatment responses of tumors.

From: Re-appraising assays on permeabilized blood cancer cells testing venetoclax or other BH3 mimetic agents selectively targeting pro-survival BCL2 proteins

Fig. 4: Co-targeting the ancillary survival factor improves the in vivo treatment responses of tumors.

A Genetic deletion of BCL2 prolonged survival of AMO1 myeloma bearing mice treated with MCL1i. NSG mice (n = 6–15 mice/group) were inoculated i.v. with wild-type (BCL2+/+; left) or BCL2–/– (right) AMO1 cells. B Venetoclax enhances the activity of MCL1i in AMO1 myeloma bearing mice. NSG mice (n = 6–12 per group) were inoculated intravenously with luciferase-expressing AMO1 cells. Mice underwent baseline imaging on day 10 using IVIS and were randomized into 4 groups. The treatment schedule and doses are summarized on the left. The whole-body tumor burden (detected by IVIS in vivo imaging system) was determined on day 27, as was infiltration of tumor cells (human CD38+ve) in the bone morrow (BM) or peripheral blood (PB); the statistical significance between the different treatment groups was calculated using unpaired Student’s t test.

Back to article page