Figure 5.
Kaplan-Meier survival curves for disseminated models. Mice bearing disseminated MM xenografts were treated on day 0 with 211At-CD38 or 211At-Ab−; n = 9 to 10 mice per group. Disease progression was monitored via weekly BLI and thrice weekly observations of mouse weight, condition, and mobility. Mice were euthanized when they experienced hind-limb paralysis or met IACUC weight loss or condition requirements. Statistics report Kaplan-Meier proportional hazards tests. (A) MOLP-8Luc model, treated at 12, 20, and 28 µCi. Across treatment levels, 211At-CD38 therapy strongly benefitted survival relative to untreated controls (P < .00001) and to 211At-Ab− groups (P < .00001) in a dose-dependent manner (P < .00001). (B) OPM-2Luc model, treated at 15, 30, and 45 µCi. 211At-CD38 therapy strongly improved survival across groups, relative to untreated controls (P < .00001) and to 211At-Ab− treatments (P = .00002) in a dose-dependent manner (P < .00001). Additional statistics in “Results.” (C) NCI-H929Luc model, treated at 8, 18, or 24 µCi. Mice treated with 211At-CD38 survived significantly longer than untreated control (P < .0001) and 211At-Ab− treated mice (P < .0006). Treatment benefits were dose-dependent with higher 211At dosing improving survival (P < .002).

Kaplan-Meier survival curves for disseminated models. Mice bearing disseminated MM xenografts were treated on day 0 with 211At-CD38 or 211At-Ab; n = 9 to 10 mice per group. Disease progression was monitored via weekly BLI and thrice weekly observations of mouse weight, condition, and mobility. Mice were euthanized when they experienced hind-limb paralysis or met IACUC weight loss or condition requirements. Statistics report Kaplan-Meier proportional hazards tests. (A) MOLP-8Luc model, treated at 12, 20, and 28 µCi. Across treatment levels, 211At-CD38 therapy strongly benefitted survival relative to untreated controls (P < .00001) and to 211At-Ab groups (P < .00001) in a dose-dependent manner (P < .00001). (B) OPM-2Luc model, treated at 15, 30, and 45 µCi. 211At-CD38 therapy strongly improved survival across groups, relative to untreated controls (P < .00001) and to 211At-Ab treatments (P = .00002) in a dose-dependent manner (P < .00001). Additional statistics in “Results.” (C) NCI-H929Luc model, treated at 8, 18, or 24 µCi. Mice treated with 211At-CD38 survived significantly longer than untreated control (P < .0001) and 211At-Ab treated mice (P < .0006). Treatment benefits were dose-dependent with higher 211At dosing improving survival (P < .002).

Close Modal

or Create an Account

Close Modal
Close Modal