Propranolol Reduces Cancer Risk

Chang, Ping‐Ying; Huang, Wen‐Yen; Lin, Cheng‐Li; Huang, Tseng; Wu, Yi-Ying; Chen, Jiahong; Kao, Chia‐Hung

doi:10.1097/md.0000000000001097

Cited by 110 publications

(68 citation statements)

References 36 publications

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“…Propranolol, a non-selective antagonist of beta-adrenoceptors, is suggested to reduce disease progression in different cancer types [6, 7, 39–43]. Because of its dramatic efficacy in the involution of infantile hemangioma [44], it has been proposed that propranolol affects tumor angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

Propranolol induces a favourable shift of anti-tumor immunity in a murine spontaneous model of melanoma

et al. 2016

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In a previous study on a xenograft model of melanoma, we showed that the beta-adrenergic receptor antagonist propranolol inhibits melanoma development by modulating angiogenesis, proliferation and cell survival. Stress hormones can influence tumor development in different ways and norepinephrine was shown to downregulate antitumor immune responses by favoring the accumulation of immunosuppressive cells, impairing the function of lymphocytes. We assessed the effect of propranolol on antitumor immune response in the MT/Ret mouse model of melanoma. Propranolol treatment delayed primary tumor growth and metastases development in MT/Ret mice. Consistent with our previous observations in human melanoma xenografts, propranolol induces a decrease in cell proliferation and vessel density in the primary tumors and in metastases. In this immunocompetent model, propranolol significantly reduced the infiltration of myeloid cells, particularly neutrophils, in the primary tumor. Inversely, cytotoxic tumor infiltrating lymphocytes were more frequent in the tumor stroma of treated mice. In a consistent manner, we observed the same shift in the proportions of infiltrating leukocytes in the metastases of treated mice. Our results suggest that propranolol, by decreasing the infiltration of immunosuppressive myeloid cells in the tumor microenvironment, restores a better control of the tumor by cytotoxic cells.

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Section: Discussionmentioning

confidence: 99%

Propranolol induces a favourable shift of anti-tumor immunity in a murine spontaneous model of melanoma

et al. 2016

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“…In patients with hepatitis C associated cirrhosis Nkontchou et al reported that PRO use was associated with a decreased risk hepatocellular carcinoma (HCC), with a hazard ratio (HR) = 0.25; (95% CI = 0.09 – 0.65; P < 0.004) [75]. Chang et al published a large cohort study of over 24 238 patients, with a PRO group (> 6 months use, n = 12 119) compared to a non-PRO use group (n = 12 119) over a 12 year period [76]. Overall the risk of cancer was lower in the PRO group (HR = 0.75; 95% CI = 0.67–0.85; P < 0.001), and site specific analysis showed a decreased risk in head and neck cancers (HR = 0.58; 95% CI = 0.35–0.95), oesophagus (HR = 0.35; 95% CI = 0.13 – 0.96), stomach (HR = 0.54; 95% CI = 0.30 – 0.98), colon (HR = 0.68; 95% CI = 0.49 – 0.93), and prostate cancers (HR = 0.52; 95% CI = 0.33 – 0.83).…”

Section: Human Datamentioning

confidence: 99%

Repurposing Drugs in Oncology (ReDO)—Propranolol as an anti-cancer agent

Pantziarka

Bouche

Sukhatme³

et al. 2016

ecancer

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Propranolol (PRO) is a well-known and widely used non-selective beta-adrenergic receptor antagonist (beta-blocker), with a range of actions which are of interest in an oncological context. PRO displays effects on cellular proliferation and invasion, on the immune system, on the angiogenic cascade, and on tumour cell sensitivity to existing treatments. Both pre-clinical and clinical evidence of these effects, in multiple cancer types, is assessed and summarised and relevant mechanisms of action outlined. In particular there is evidence that PRO is effective at multiple points in the metastatic cascade, particularly in the context of the post-surgical wound response. Based on this evidence the case is made for further clinical investigation of the anticancer effects of PRO, particularly in combination with other agents. A number of trials are on-going, in different treatment settings for various cancers.

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“…Some studies reported that NSBB was not associated with increased mortality among decompensated cirrhotic patients with ascites [6][7][8][9], whereas Kalambokis GN, et al [10] found that an increased mortality was observed in Child-Pugh C cirrhotic patients with ascites if using NSBB for more than six months. Moreover, NSBB could reduce cancer risk [11,12], including hepatocellular carcinoma (HCC) [13,14]. The issue about the use of NSBB on the prognosis in compensated cirrhotic patients without major complications has seldom been reported.…”

Section: Introductionmentioning

confidence: 99%

The Role of Non-Selective β-Blockers in Compensated Cirrhotic Patients without Major Complications

et al. 2019

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Background and Objectives: Non-selective β-blockers (NSBB) could prevent decompensation and hepatocellular carcinoma (HCC) in cirrhotic patients with clinically significant portal hypertension (CSPH), but remained uncertain for compensated cirrhotic patients without major complications. We aimed to compare the clinical outcomes between propranolol users and non-users of a CC group without major complications. Material and Methods: We conducted this population-based cohort study by using the Taiwanese Longitudinal Health Insurance Database 2000. Propranolol users (classified as cumulative defined daily dose (cDDD)) and non-PPL users were matched with a 1:1 propensity score in both cohorts. Results: This study comprised 6896 propranolol users and 6896 non-propranolol users. There was no significant impact on the development of spontaneous bacterial peritonitis between the two groups (aHR: 1.24, 95% confidence interval (CI): 0.88~1.75; p = 0.2111). Male gender, aged condition, and non-liver related diseases (peripheral vascular disease, cerebrovascular disease, dementia, pulmonary disease, and renal disease) were the independent risk factors of mortality. PPL users had significantly lower incidence of HCC development than non-users (aHR: 0.81, p = 0.0580; aHR: 0.80, p = 0.1588; and aHR: 0.49, p < 0.0001 in the groups of 1–28, 29–90, and >90 cDDD, respectively). Conclusion: The current study suggested that high cumulative doses of propranolol could decrease the risk of hepatocellular carcinoma among compensated cirrhotic patients without major complications. Further large-scale prospective studies are still required to confirm the findings in this study. Results: It remained uncertain whether non-selective β-blockers (NSBB) could prevent decompensation and hepatocellular carcinoma (HCC) in compensatory cirrhotic patients without major complications. This study aimed to compare the clinical outcomes between propranolol users and non-users of the CC group without major complications.

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Propranolol Reduces Cancer Risk

Cited by 110 publications

References 36 publications

Propranolol induces a favourable shift of anti-tumor immunity in a murine spontaneous model of melanoma

Propranolol induces a favourable shift of anti-tumor immunity in a murine spontaneous model of melanoma

Repurposing Drugs in Oncology (ReDO)—Propranolol as an anti-cancer agent

The Role of Non-Selective β-Blockers in Compensated Cirrhotic Patients without Major Complications

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