Assessing the effects of beta-blockers on pancreatic cancer risk: A nested case-control study.
beta-blockers
pancreas
pancreatic cancer
pancreatic cancer risk
pharmacoepidemiology
Journal
Pharmacoepidemiology and drug safety
ISSN: 1099-1557
Titre abrégé: Pharmacoepidemiol Drug Saf
Pays: England
ID NLM: 9208369
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
24
04
2019
revised:
19
02
2020
accepted:
04
03
2020
pubmed:
21
3
2020
medline:
10
4
2021
entrez:
21
3
2020
Statut:
ppublish
Résumé
Both β1- and β2-adrenoceptor proteins were detected on the cell surface of pancreatic ductal adenocarcinoma. The current study evaluated the association between beta-blocker use and pancreatic cancer risk. We conducted a nested case-control study in a large population representative database. Each pancreatic cancer case was matched with four controls based on age, sex, practice site, and duration of follow-up using incidence density sampling. Beta-blocker use was defined as any prescription prior to index date and was stratified into non-selective and selective β The study included 4113 patients with pancreatic cancer and 16 072 matched controls. When compared to never users, there was no association between any beta-blocker use and pancreatic cancer risk (adjusted OR 1.06, 95% CI 0.97-1.16, P = .16). Analysis by receptor selectivity showed use of non-selective beta-blockers for more than 2 years was associated with a reduced pancreatic cancer risk (OR 0.75, 95% CI 0.57-1.00, P = .05). When compared to former users both users of selective β1-blockers and non-selective beta-blockers had a reduced pancreatic cancer risk (OR 0.78, 95% CI 0.67-0.90, P = .001) and (OR 0.67, 95% CI 0.49-0.92, P = .01), respectively. Beta-blocker use was not associated with increased pancreatic cancer risk. However, long-term use of beta-blockers may be associated with decreased pancreatic cancer risk.
Substances chimiques
Adrenergic beta-Antagonists
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
599-604Informations de copyright
© 2020 John Wiley & Sons Ltd.
Références
Siegel RL, Miller KD, Jemal A. Cancer statistics, 2015. CA Cancer J Clin. 2015;65(1):5-29. Accessed February 15, 2020.
Cancer Resarch UK. https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/pancreatic-cancer#heading-Zero. Accessed February 15, 2020.
National Cancer Institute. Surveillance, epidemiology, and end results. http://seer.cancer.gov/statfacts/html/pancreas.html. Accessed February 15, 2020.
Boursi B, Finkelman B, Giantonio BJ, et al. A clinical prediction model to assess risk for pancreatic cancer among patients with new-onset diabetes. Gastroenterology. 2017;152(4):840-850.e843.
Wiysonge CS, Bradley HA, Volmink J, Mayosi BM, Opie LH. Beta-blockers for hypertension. Cochrane Database Syst Rev. 2017;1(1):CD002003.
Schuller HM. Neurotransmission and cancer: implications for prevention and therapy. Anticancer Drugs. 2008;19(7):655-671.
McGraw DW, Liggett SB. Molecular mechanisms of beta2-adrenergic receptor function and regulation. Proc Am Thorac Soc. 2005;2(4):292-296; discussion 311-292.
Boudonas GE. β-Blockers in coronary artery disease management. Hippokratia. 2010;14(4):231-235.
Wang HM, Liao ZX, Komaki R, et al. Improved survival outcomes with the incidental use of beta-blockers among patients with non-small-cell lung cancer treated with definitive radiation therapy. Ann Oncol. 2013;24(5):1312-1319.
Melhem-Bertrandt A, Chavez-Macgregor M, Lei X, et al. Beta-blocker use is associated with improved relapse-free survival in patients with triple-negative breast cancer. J Clin Oncol. 2011;29(19):2645-2652.
Powe DG, Voss MJ, Zänker KS, et al. Beta-blocker drug therapy reduces secondary cancer formation in breast cancer and improves cancer specific survival. Oncotarget. 2010;1(7):628-638.
Udumyan R, Montgomery S, Fang F, et al. Beta-blocker drug use and survival among patients with pancreatic adenocarcinoma. Cancer Res. 2017;77(13):3700-3707.
Shah SM, Carey IM, Owen CG, Harris T, Dewilde S, Cook DG. Does beta-adrenoceptor blocker therapy improve cancer survival? Findings from a population-based retrospective cohort study. Br J Clin Pharmacol. 2011;72(1):157-161.
Beg MS, Gupta A, Sher D, et al. Impact of concurrent medication use on pancreatic cancer survival-SEER-Medicare analysis. Am J Clin Oncol. 2018;41(8):766-771.
Johnson M. Molecular mechanisms of beta(2)-adrenergic receptor function, response, and regulation. J Allergy Clin Immunol. 2006;117(1):18-24; quiz 25.
Majidi M, Al-Wadei HA, Takahashi T, Schuller HM. Nongenomic beta estrogen receptors enhance beta1 adrenergic signaling induced by the nicotine-derived carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in human small airway epithelial cells. Cancer Res. 2007;67(14):6863-6871.
Vargiu P, De Abajo R, Garcia-Ranea JA, et al. The small GTP-binding protein, Rhes, regulates signal transduction from G protein-coupled receptors. Oncogene. 2004;23(2):559-568.
Luttrell LM, Ferguson SS, Daaka Y, et al. Beta-arrestin-dependent formation of beta2 adrenergic receptor-Src protein kinase complexes. Science. 1999;283(5402):655-661.
Zhang D, Ma Q, Wang Z, et al. Beta2-adrenoceptor blockage induces G1/S phase arrest and apoptosis in pancreatic cancer cells via Ras/Akt/NFkappaB pathway. Mol Cancer. 2011;10:146.
Zhang D, Ma Q, Shen S, Hu H. Inhibition of pancreatic cancer cell proliferation by propranolol occurs through apoptosis induction: the study of beta-adrenoceptor antagonist's anticancer effect in pancreatic cancer cell. Pancreas. 2009;38(1):94-100.
Zhang D, Ma QY, Hu HT, Zhang M. Beta2-adrenergic antagonists suppress pancreatic cancer cell invasion by inhibiting CREB, NFkappaB and AP-1. Cancer Biol Therapy. 2010;10(1):19-29.
Blak BT, Thompson M, Dattani H, Bourke A. Generalisability of The Health Improvement Network (THIN) database: demographics, chronic disease prevalence and mortality rates. Inform Prim Care. 2011;19(4):251-255.
Lewis JD, Schinnar R, Bilker WB, Wang X, Strom BL. Validation studies of The Health Improvement Network (THIN) database for pharmacoepidemiology research. Pharmacoepidemiol Drug Safety. 2007;16(4):393-401.
Bourke A, Dattani H, Robinson M. Feasibility study and methodology to create a quality-evaluated database of primary care data. Inform Prim Care. 2004;12(3):171-177.
Haynes K, Forde KA, Schinnar R, Wong P, Strom BL, Lewis JD. Cancer incidence in The Health Improvement Network. Pharmacoepidemiol Drug Safety. 2009;18(8):730-736.
Lubin JH, Gail MH. Biased selection of controls for case-control analyses of cohort studies. Biometrics. 1984;40(1):63-75.
Lewis JD, Bilker WB, Weinstein RB, Strom BL. The relationship between time since registration and measured incidence rates in the general practice research database. Pharmacoepidemiol Drug Safety. 2005;14(7):443-451.
Wang Z, White DL, Hoogeveen R, et al. Anti-hypertensive medication use, soluble receptor for glycation end products and risk of pancreatic cancer in the Women's Health Initiative Study. J Clin Med. 2018;7(8):197.
Lu Y, Garcia Rodriguez LA, Malgerud L, et al. New-onset type 2 diabetes, elevated HbA1c, anti-diabetic medications, and risk of pancreatic cancer. Br J Cancer. 2015;113(11):1607-1614.