Impact of beta-blockers on prostate cancer mortality: a meta-analysis of 16,825 patients

Abstract

IntroductionIncreasing evidence suggests that beta-blocker use might be associated with reduced mortality in prostate cancer patients. To provide a quantitative assessment of this association, we pooled data available to examine the association between beta-blocker use and mortality of prostate cancer.MethodsWe identified studies by a literature search of MEDLINE (from 1 January 1966) and EMBASE (from 1 January 1974), through 10 September 2014, and by searching the reference lists of pertinent articles. Two authors independently screened and reviewed the eligibility of each study. The primary outcomes were prostate cancer-specific mortality and all-cause mortality.ResultsA total of four studies including 16,825 patients were included in this meta-analysis. Analysis of all studies showed that beta-blocker use was associated with reduced prostate cancer-specific mortality (hazard ratio =0.85, 95% confidence interval =0.77–0.94), without any heterogeneity between studies (Q=3.59, I 2=16.5%, P=0.309). However, we observed no association with all-cause mortality (hazard ratio =0.97, 95% confidence interval =0.90–1.04). There was also no evidence of the presence of significant heterogeneity between the four studies (Q=2.48, I 2=0.0%, P=0.480).ConclusionThese findings indicate that beta-blocker use was associated with reduced cancer-specific mortality among prostate cancer patients taking beta-blockers.

The impact of preoperative use of calcium channel blockers on outcomes of patients undergoing esophagectomy: a propensity score-matched cohort study

“…Another large population-based cohort study of patients with colorectal cancer in Germany indicated that beta-blocker use was associated with prolonged overall survival and colorectal cancer-specific survival in stage IV patients (10). Overall, these findings are in accordance with ours (7,10,29). Our study showed that a history of chronic lung disease was associated with poor recurrence-free survival, which could be because patients with a history of chronic lung disease were more likely to be complicated with other diseases and poor physical conditions (30).…”

“…Moreover, the association between antihypertensive medications and the risk of cancer, such as breast cancer (3), renal cell carcinoma (4), and prostate cancer (5), has been a concern for nearly 50 years (6). Recently, the potential of antihypertensive medications to affect cancer progression has received increasing interest (7). Some epidemiological studies have shown that beta-blockers might be associated with longer survival and reduced mortality in patients with non-small-cell lung cancer, colorectal cancer, and prostate cancer (8)(9)(10).…”

Sympathetic nervous system regulation of the tumour microenvironment

“…Consistent with that concept, several observational epidemiologic studies have documented associations between β-blocker exposure and reduced progression of prostate 47,48,104 , breast 39–41,45 , lung 44,105 , and ovarian cancer 106,107 , as well as malignant melanoma 42,43,46 . However, the epidemiological literature is also inconsistent, and some studies fail to find any evidence of a protective effect (likely due to methodological variations considered below).…”

Triiodothyronine Attenuates Prostate Cancer Progression Mediated by β-Adrenergic Stimulation

“…NE prostate tumors exhibit neurite-like (NE-like) projections; they synthesize and secrete amines and peptides, are androgenreceptor negative and apoptosis resistant (8,9,13,14). In humans, β2-adrenergic receptors (ADR-β 2) are highly expressed in androgen-refractory metastatic tumors and are strongly associated with for 3-5 years with adrenergic antagonists (2)(3)(4)(5)(6)(7). Studies in human prostate cancer cells show that β-adrenergic/protein kinase A (PKA) activation promotes prostate cancer progression: it reduces cell proliferation (by decreasing p42-mitogen activated protein kinase [MAPK] and β-arrestin2/proto-oncogene tyrosine-protein kinase [c-Src]), and it activates survival pathways (induces phosphorylation of Bcl-2-associated death promoter [Bad] and inhibits caspases)…”