Presentation Authors: Ali Zahalka*, Ethan Fram, Wilson Lin, Larkin Mohn, Paul Frenette, Ilir Agalliu, Kara Watts, Bronx, NY
Introduction: Recent evidence from pre-clinical models of prostate cancer (PCa) suggests that disruption of adrenergic signaling by beta-adrenergic receptor blockade inhibits PCa progression to more aggressive pathology. We examined the in vivo association between use of oral beta-blockers and incident PCa on initial prostate biopsy in a diverse, urban academic center.
Methods: A retrospective review of men who underwent initial prostate biopsy for any clinical indication between 2006-2016 at a large urban academic center was performed. The oral use of a Beta-blocker - Atenolol, Metoprolol, or Carvedilol - was assessed by reviewing patientsâ€™ active prescriptions (determined by prescription refill history) within one year preceding their corresponding biopsy. Patient demographics, pre-biopsy prostate specific antigen (PSA), biopsy pathology, and clinical stage were collected. Multinomial logistic regression analysis was used to evaluate the association of Beta-blocker use with subsequent incident PCa risk group (controls were used as reference category).
Results: 4,182 men underwent initial prostate biopsy during the study period and were included in the study. 64% self-identified as Black or Hispanic. 669 (16%) men were included in the B-blocker cohort based on preceding prescription refill history, of which 350 (17.7%) had benign pathology and 319 (14.5%) with PCa. Of all men with PCa on biopsy, risk groups (NCCN criteria) were as follows: 337 (8.1%) high risk, 1,029 (25.0%) intermediate risk, 169 (4%) low risk, and 671 (16.0%) very low risk PCa. On multivariate analysis, the beta-blocker, Atenolol, displayed a significant protective effect on both incident low risk and intermediate risk PCa (OR 0.55, P=0.02; OR 0.11, P=0.03, respectively) after adjusting for age, PSA, BMI, socioeconomic status (SES), cardiovascular disease, and race (presented in the Table).
Conclusions: The oral beta-blocker, Atenolol, showed an approximately 50% reduction in incident intermediate risk PCa compared to men not taking a beta-blocker, as well as a dramatic reduction in incident low risk disease on prostate biopsy. Our results, combined with recent results from pre-clinical models of PCa, provide preliminary support for further research into the use of Atenolol as a potential protective pharmacologic agent against de novo PCa or PCa disease progression.
Source of Funding: NIH National Cancer Institute F30CA203446 and T32 NS007098