Beta-blocker drug therapy reduces secondary XXXX formation in @entity0 and improves @entity5 specific survival.

@entity1169 @entity1 @entity0 @entity101 @entity5 @entity3 @entity3918 @entity1063
Laboratory models show that the beta-blocker, @entity1169 , can inhibit @entity1063 -induced @entity0 cell migration. We hypothesised that @entity0 @entity1 receiving beta-blockers for @entity101 would show reduced @entity3 and improved clinical outcome. Three @entity1 subgroups were identified from the medical records of 466 consecutive female @entity1 (median age 57, range 28-71) with operable @entity0 and follow-up (>10 years). Two subgroups comprised 43 and 49 @entity101 @entity1 treated with beta-blockers or other antihypertensives respectively, prior to @entity5 diagnosis. 374 @entity1 formed a non- @entity101 control group. @entity3 development, @entity5 recurrence and hazards risk were statistically compared between groups. Kaplan-Meier plots were used to model survival and @entity3918 . Beta-blocker treated @entity1 showed a significant reduction in @entity3 development (p=0.026), @entity5 recurrence (p=0.001), and longer disease free interval (p=0.01). In addition, there was a 57% reduced risk of @entity3 (Hazards ratio=0.430; 95% CI=0.200-0.926, p=0.031), and a 71% reduction in @entity0 mortality after 10 years (Hazards ratio=0.291; 95% CI=0.119-0.715, p=0.007). This proof-of-principle study showed beta-blocker therapy significantly reduces distant @entity3 , @entity5 recurrence, and @entity5 -specific mortality in @entity0 @entity1 suggesting a novel role for beta-blocker therapy. A larger epidemiological study leading to randomised clinical trials is needed for breast and other @entity5 types including colon, prostate and ovary.
