PROPRANOLOL

A well known so called beta blocker that reduces the action of stress inducing hormones and has a variety of potential anti-cancer actions, including those that may suppress metastatic progression especially after surgery.

At least for colorectal and breast cancer, the combination of propranolol, with anti-inflammatory drug etodolac has shown significantly reduced cancer specific and all cause mortality subsequent to surgery (see also etodolac). And recently combined with statins and lung cancer radiotherapy. Notably, there is evidence that propranolol is effective at multiple points in the metastatic cascade, particularly in the context of the post-surgical wound response, and this being the driver of such improved survival rates.

Another pilot study in colorectal cancer from 2023 showed radically improved disease free progression patients, post-surgery . The same team showed earlier that this drug combination resulted in significantly lowered biomarkers of metastatic activity in colorectal cancer surgery, and increased natural killer immune cell responses. Additional data was also produced in post surgery studies for early phase breast cancer in a phase II trial (Highlights 2,3), results independently confirmed in other studies (see References)

An earlier clinical study by a different research group in breast cancer found very strong suppression of cancer progression in propranolol users vs none users (Highlight 4). And a small pilot in melanoma showed postive tendencies but was underpowered to reach high levels of certainty. There are preliminary positive reports with immunotherapy for melanoma which need more evidence. Other positive findings for beta blocker cousin landiolol have been published for reducing progression of lung cancers.

Ongoing studies include the PROSPER pancreatic cancer clinical trial, where etodolac-proproanol is seen as a viable candiate protocol. The PRESERVE trial onging in ovarian cancer therapy is looking at etodolac for stress reduction. Meta-analysis of case controlled and population studies show several cancers have reduced incidence in user of propranolol, though others show no associations for instance in breast cancer case controlled studies.

Although patients with CVD were more often in older age, and they more often experienced cardiac and nephrological complications..there was a statistically nonsignificant trend for lower all-cause mortality in patients with CVD. The lowest all-cause mortality was observed in patients treated with beta-blockers and statins after two (HR = 0.31) [Hazard Ratio], three (HR = 0.33) and even four (HR = 0.45) years of follow-up. The benefit in OS remained significant in 101 patients with CVD treated with beta-blockers (HR = 0.65), and eventually statin,...

In this pilot randomized-controlled COMPIT trial [colorectal cancers], 20-day perioperative treatment with propranolol and etodolac significantly increased 5-year disease-free survival rate compared to a placebo control treatment. Among both protocol compliant and intent-to-treat patients, 0/11 and 2/16 (respectively) exhibited recurrence during the 5-year follow-up, compared to 8/17 and 9/18 control patients. Overall survival rates showed similar favorable trends for the treated groups,

Perioperative inhibition of COX-2 and β-adrenergic signaling provides a safe and effective strategy for inhibiting multiple cellular and molecular pathways related to metastasis and disease recurrence in early-stage breast cancer…Drug treatment also significantly abrogated presurgical increases in serum interleukin-6 (IL-6) and C-reactive protein levels, abrogated perioperative declines in stimulated interleukin-12 and interferon-gamma production, abrogated postoperative mobilization of CD16− “classical” monocytes, and enhanced expre...

Propranolol users were significantly less likely to present with a T4 (odds ratio [OR], 0.24) or N2/N3/M1 (OR, 0.20) tumor compared with matched nonusers. The cumulative probability of breast cancer–specific mortality was significantly lower for propranolol users compared with matched nonusers (hazard ratio, 0.19). There was no difference in T4 or N2/N3/M1 tumor incidence or breast cancer–specific mortality between atenolol users and matched nonusers

TABLE OF REFERENCES

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URL	Rating	Highlight	Highlight 2
https://www.mdpi.com/2072-6694/15/4/1277	4	Although patients with CVD were more often in older age, and they more often experienced cardiac and nephrological complications (p < 0.05 for all), there was a statistically nonsignificant trend for lower all-cause mortality in patients with CVD. The lowest all-cause mortality was observed in patients treated with beta-blockers and statins after two (HR = 0.31; 95%CI: 0.1–0.98; p = 0.047), three (HR = 0.33; 95%CI: 0.13–0.81; p = 0.015) and even four (HR = 0.45; 95%CI: 0.22–0.97; p = 0.027) years of follow-up. The benefit in OS remained significant in 101 patients with CVD treated with beta-blockers (HR = 0.65; 95%CI: 0.43–0.99; p = 0.045), and eventually statin, throughout the whole follow-up (log-rank p < 0.05). Further prospective studies are necessary to confirm the role of beta-blockers and statins in reduction of mortality in NSCLC patients undergoing radical CRT.	Among the 47 patients receiving beta-blockers, as many as 46 were diagnosed with CVD, 18 had diagnosis of chronic coronary syndrome, 20 had a history of ATE, 35 had arterial hypertension, and one had atrial fibrillation. Of the 16 patients receiving beta- blockers and statin, all had CVD, 12 had chronic coronary syndrome and a history of ATE, and only 7 had arterial hypertension. Analyzing the OS only in the subgroup of 101 patients with CVD, treatment with beta-blockers was still associated with a significantly better outcome (Figure 4). Thanks to beta-blocker therapy, all-cause mortality in CVD was reduced by 35% (HR = 0.65; 95%CI: 0.43–0.99; p = 0.045). Similarly, among patients with CVD, an improvement in OS was demonstrated for patients treated with a beta-blocker and statin
https://www.sciencedirect.com/science/article/abs/pii/S0748798322007053	4	Between May 2010 and March 2015, 34 patients newly diagnosed with colorectal cancer, without evidence of metastasis, undergoing surgery were randomised to receive oral propranolol and etodolac (n=16) or placebo (n=18). The 20-day treatment regimen was initiated five days before surgery and ended two weeks after surgery. Results of the intent-to-treat analysis at five years follow-up showed that 12.5% (2/16) patients in the propranolol and etodolac arm versus 50% (9/18) in the placebo arm experienced recurrence, and that 12.5% (2/16) patients died in the propranolol and etodolac arm versus 22% (4/18) in the placebo arm).	For patients who adhered to the protocol, 0% (0/11) patients in the treatment group versus 47% (8/17) in the placebo group exhibited recurrence (P=0.007), and 0% (0/11) in the treatment group versus 17.6% (3/17) in the placebo group died . Mean disease-free survival (DFS) was 53.3 months in the treatment arm versus 40.65 months in the control arm. Adverse events were equivalent between the two groups.
https://www.nature.com/articles/s41598-019-41520-7	4	The postoperative relapse-free survival rate at 2 years was 0.89 (95% CI, 0.78–1.01) in the landiolol group and 0.76 (95% CI, 0.60–0.91) in the control group (Chi-squared test; P = 0.1828). The relapse-free survival rate tended to be higher in the landiolol group than in the control. Hazard ratio for relapse-free survival in the landiolol group compared to the control was 0.41 (95% CI, 0.13–1.34), demonstrating that relapse free survival was prolonged in the landiolol group	Administering landiolol hydrochloride at low doses during cancer surgery for a short period of time tends to improve relapse-free survival rate as well as prolong relapse-free survival and overall survival. This study was a retrospective, exploratory clinical study in a small sample size; it would be beneficial if large-scale, prospective clinical studies are conducted in the future.
https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.32950	3.5	This clinical trial is the first to investigate the combined perioperative inhibition of β-adrenoceptors and COX2 in patients with CRC. The outcomes indicate a favorable impact on molecular biomarkers associated with tumor growth and metastatic disease. We recently observed similar favorable effects of a similar drug treatment regimen on biomarkers in patients with breast cancer,18, 27 which strengthens the relevance and generalizability of the current findings. Overall, our findings indicate that the perioperative propranolol/etodolac protocol is empirically safe, easy to administer, and inexpensive and has overall favorable molecular impacts on tumor tissues. These findings also provide a strong rationale for future clinical trials in larger samples to assess the impact of this protocol on clinical endpoints such as disease recurrence and survival.	This study was not designed or powered to assess drug effects on disease recurrence and survival, though we did collect data on 3-year recurrence rate to assess long-term safety. The results revealed a favorable trend toward reduced CRC recurrence in treated patients. Specifically, in protocol-compliant patients, metastases occurred in 0 of 11 patients who received drug treatment versus 5 of 17 patients who received placebo (P = .063). Kaplan-Meier survival analysis (log-rank test for recurrence at 3-year follow-up) showed a marginally significant (P = .054) reduction in recurrence (Fig. 4B). In intent-to-treat patients, the same analysis indicated a nonsignificant trend toward reduced recurrence in patients who received drug treatment (2/16) versus patients who received placebo
https://pmc.ncbi.nlm.nih.gov/articles/PMC5559335/	3.5	These data show that perioperative administration of the β-adrenergic antagonist propranolol and the COX-2 inhibitor etodolac induces multiple favorable impacts on (i) primary tumor gene expression profiles (bioinformatic indications of reduced EMT; reduced activity of GATA-1, GATA-2, EGR3, GRE, and STAT3 transcription factors; and reduced tumor-associated monocytes and increased tumor-associated B cells) and on (ii) circulating immune parameters (serum and ex vivo-induced cytokine levels, reduced classical monocyte influx, and increased NK cell activation markers). Each of these outcomes has previously been linked to reduced tumor progression	IL-6 and CRP are associated with tumor progression and poor prognosis in multiple solid tumor types, including breast, lung, and prostate, and hematopoietic malignancies (37,45). IL-6 activates the janus-kinase-STAT signaling pathway, which is well known to promote tumor cell proliferation, survival, and invasion, as well as immunosuppression and inflammation. STAT3 and STAT5 are strongly associated with cancer progression (37). Here, both plasma IL-6 levels and indicators of tumor STAT3 activity were reduced by the drug treatment. Drug treatment also effectively blocked a marked postoperative (T3) mobilization of “classical” pro-inflammatory CD14++CD16− monocytes
https://ascopubs.org/doi/10.1200/JCO.2010.33.5422	3.5	Propranolol users were significantly less likely to present with a T4 (odds ratio [OR], 0.24) or N2/N3/M1 (OR, 0.20) tumor compared with matched nonusers. The cumulative probability of breast cancer–specific mortality was significantly lower for propranolol users compared with matched nonusers (hazard ratio, 0.19). There was no difference in T4 or N2/N3/M1 tumor incidence or breast cancer–specific mortality between atenolol users and matched nonusers	The results of this study suggest that the use of propranolol, a nonselective β1/β2-adrenergic receptor antagonist, is associated with less advanced disease at diagnosis and lower breast cancer–specific mortality. Women taking propranolol in the year before breast cancer diagnosis were significantly less likely to present with a T4 tumor, node-positive (N2/N3), or metastatic disease when compared with those not taking a beta blocker. Furthermore, a longer duration of propranolol use was associated with fewer T4 tumors suggesting the possibility of a dose-response relationship. Propranolol use was also associated with low or intermediate tumor grade at diagnosis.
https://www.sciencedirect.com/science/article/abs/pii/S0889159118301879?via%3Dihub	3.5	Results based on a-priori hypotheses indicated that already before surgery (T2), serum levels of pro-inflammatory IL-6, CRP, and IFNγ, and anti-inflammatory, cortisol and IL-10, increased. At T2 and/or T3, drug treatment reduced serum levels of the above pro-inflammatory cytokines and of TRAIL, as well as activity of multiple inflammation-related transcription factors (including NFκB, STAT3, ISRE), but not serum levels of cortisol, IL-10, IL-18, IL-8, VEGF and TNFα.	Exploratory analyses of transcriptome modulation in PBMCs revealed treatment-induced improvement at T2/T3 in several transcription factors that in primary tumors indicate poor prognosis (CUX1, THRa, EVI1, RORa, PBX1, and T3R), angiogenesis (YY1), EMT (GATA1 and deltaEF1/ZEB1), proliferation (GATA2), and glucocorticoids response (GRE), while increasing the activity of the oncogenes c-MYB and N-MYC. Overall, the drug treatment may benefit breast cancer patients through reducing systemic inflammation and pro-metastatic/pro-growth biomarkers in the excised tumor and PBMCs.
https://aacrjournals.org/clincancerres/article/26/8/1803/83212	3.5	This trial is the first prospective, blinded, randomized clinical trial examining the effect of single-agent nonselective β-blockade with propranolol on cancer gene expression. Preoperative propranolol downregulated biomarkers of invasive potential and inflammation, and improved cellular immune response in breast cancer. Propranolol was well-tolerated by patients, appears safe, and achieved beneficial anxiolytic effects. Although trials powered for a primary endpoint of clinical outcome will be required before propranolol can be considered in breast cancer treatment,	Propranolol downregulated primary tumor expression of mesenchymal genes (P = 0.002) without affecting epithelial gene expression (P = 0.21). Bioinformatic analyses implicated downregulation of Snail/Slug (P = 0.03), NF-κB/Rel (P < 0.01), and AP-1 (P < 0.01) transcription factors in structuring the observed transcriptome alterations, and identified changes in intratumoral neutrophil, natural killer cell, and dendritic cell recruitment (all P < 0.01). Patients with clinical evidence of drug response (lowered heart rate and blood pressure) demonstrated elevated tumor infiltration of CD68+ macrophages and CD8+ T cells.
https://www.nature.com/articles/nrclinonc.2017.170	3	At 3 years, [melanoma] disease-free survival was 84.2% and 58.8% in the propranolol and control arms, respectively, equating to an 80% risk reduction from propranolol (HR 0.18; 95% CI 0.04–0.89; P = 0.03) after multivariate Cox modelling. The short follow-up duration limited the power to demonstrate a significant effect on mortality, although a trend towards improved overall survival was observed with propranolol (HR 0.64) [hazard ratio]. Importantly, no adverse effects of propranolol were reported	Of 53 patients with thick cutaneous melanoma (stage IB–IIIA) enrolled, 19 consented at the time of diagnosis to take off-label propranolol (80 mg daily) as an adjuvant therapy, and the 34 patients who were unwilling to receive propranolol formed the control group. Notably, ulcerated melanoma was more prevalent in the propranolol group (63% versus 35%; P = 0.05); the two treatment groups were otherwise well-balanced for baseline clinical characteristics and prognostic factors.
https://aacrjournals.org/clincancerres/article/17/11/3803/12036/Randomized-Double-Blind-Trial-of-Sulindac-and	3	Further, the relatively high proportion of polypectomized subjects compared with polyp-free subjects was probably because of their higher motivation to participate in the current trial. Nevertheless, the results of the 2-month treatment on ACF both in comparison analysis among groups (Table 2) and in the intragroup analysis (Supplementary Table S1) clearly indicated the effectiveness of sulindac in eradicating the lesions, particularly in polypectomized subjects. Thus, the primary endpoint of the present study was achieved. The failure of etodolac to eradicate ACF is probably explained by the fact that most ACF do not express COX-2 (20). Moreover, it is surmised that in short-term treatment etodolac, which could not eradicate ACF, was ineffective in suppressing polyp development whereas sulindac was able to inhibit incidence of polyp 1 year after the initiation of treatment by eradicating ACF with short-term treatment	Results showing in both analyses of the number and incidence of adenoma or total polyps either a significant or marked (marginal) reduction in the sulindac group strongly suggest not only the effectiveness of short-term treatment with sulindac in suppressing polyp occurrence but also the utility of ACF as precursor lesions for polyps although the possibility that the reduction in ACF was indirectly related to that of polyp occurrence cannot be completely denied. This notion was further supported by results of the analysis of responders versus nonresponders that showed significantly fewer polyps in the former than in the latter subjects in the sulindac group. Moreover, the average polyp size in the sulindac group was smaller than in the placebo group, although without statistical significance
https://breast-cancer-research.biomedcentral.com/articles/10.1186/s13058-016-0782-5	3	. Overall, there was no association between propranolol use after diagnosis of breast cancer and breast cancer-specific or all-cause mortality (fully adjusted HR = 0.94, 95% CI, 0.77, 1.16 and HR = 1.09, 95% CI, 0.93, 1.28, respectively). There was little evidence of a dose–response relationship. There was also no association between propranolol use before breast cancer diagnosis and breast cancer-specific or all-cause mortality (fully adjusted HR = 1.03 and HR = 1.02). Similar null associations were observed for non-selective beta-blockers.	Our pooled analysis supports the findings of two earlier epidemiological studies of the association between propranolol use after diagnosis and cancer outcomes [15, 16]. The first, an earlier analysis of Danish data [16], showed no association between propranolol use after diagnosis and recurrence (adjusted HR = 1.3, 95% CI, 0.92, 1.9); however, that study did not investigate mortality or the influence of propranolol use before diagnosis. The second study, an earlier analysis of English data [15], based upon a case–control design, showed no association between propranolol and cancer-specific mortality (adjusted HR = 0.98, 95% CI, 0.57, 1.71).
https://aacrjournals.org/clincancerres/article-abstract/27/1/87/83678/	3	Combination of propranolol with pembrolizumab in treatment-naïve metastatic melanoma is safe and shows very promising activity. Propranolol 30 mg twice a day was selected as RP2D in addition to pembrolizumab based on safety, tolerability, and preliminary antitumor activity.	Most common treatment-related adverse events (TRAEs) were rash, fatigue, and vitiligo, observed in 44% patients. One patient developed two grade ≥3 TRAEs. Objective response rate was 78%. While no significant changes in treatment-associated biomarkers were observed, an increase in IFNγ and a decrease in IL6 was noted in responders.
https://pmc.ncbi.nlm.nih.gov/articles/PMC4618628/	2	A major strength of our approach is its potential clinical relevance. By conducting this biomarker study in patients with breast cancer, we have, by definition, controlled for the tumor microenvironment, pharmacokinetics of study drug, and other unknown factors which can generate misleading results in model systems 25. To the best of our knowledge, this is the first clinical observation of a COX-2 increase in gene expression with etodolac treatment. Notably, feedback gene expression upregulation has been reported with other inhibitors such as a BRAF inhibitor which causes upregulation of EGFR gene expression in colon cancer, in this case leading to therapeutic resistance.	We also observed an increase in COX-2 pathway (COX-2 and possibly β-catenin) gene expression after etodolac exposure. Although etodolac is a well-known selective COX-2 enzymatic inhibitor 17, compensatory increased gene expression of COX-2 with NSAIDs has been reported in the past 21,22. Additional study, such as analysis of prostaglandin E2 levels, will be required to determine if the increased gene expression level of COX-2 after etodolac exposure is associated with preserved enzymatic activity. Our results for COX-2 demonstrate the need for optimized biomarkers to monitor the effect of agents that may be subject to compensatory responses. The compensatory effect seen in this study may partially explain why previous studies evaluating NSAIDs in breast cancer prevention have had conflicting results
https://journals.lww.com/md-journal/fulltext/2015/07020/propranolol_reduces_cancer_risk__a.35.aspx	2	The study sample comprised 24,238 patients. After a 12-year follow-up period, the cumulative incidence for developing cancer was low in the propranolol cohort (HR: 0.75; 95% CI: 0.67–0.85; P < 0.001). Patients with propranolol treatment exhibited significantly lower risks of cancers in head and neck (HR: 0.58; 95% CI: 0.35–0.95), esophagus (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). The protective effect of propranolol for head and neck, stomach, colon, and prostate cancers was most substantial when exposure duration exceeded 1000 days. This study supports the proposition that propranolol can reduce the risk of head and neck, esophagus, stomach, colon, and prostate cancers. Further prospective study is necessary to confirm these findings.	Patients using propranolol exhibited a 25% reduction in the risk of cancer compared with patients not using propranolol (95% CI: 0.67–0.85). We selected patients who were 20 years of age and older from the LHID2000 as a cohort representing the general population and calculated the cancer incidence. The incidence rates of cancer in the general population, propranolol, and nonpropranolol cohort were 3.85, 5.31, and 7.47 per 1000 person-years, respectively. Compared with the general population, the incidence rate ratios of the propranolol and nonpropranolol cohorts were 1.38 (95% CI: 1.32–1.44) and 1.94 (95% CI: 1.87–2.01).
https://aacrjournals.org/cancerpreventionresearch/article/5/8/1007/50037/Effect-of-Long-term-Propranolol-Treatment-on	2	In this large observational study, we assessed the impact of propranolol treatment on HCC occurrence in patients with compensated HCV cirrhosis and persistent infection prospectively and closely followed for a median period of 54 months and found that long-term use of propranolol reduced the incidence of HCC [liver cancer]. In our study, propranolol treatment was still associated with low HCC occurrence using propensity score	The 3- and 5-year HCC incidence was 4% and 4%, and 10% and 20% for patients treated and not treated by propranolol, respectively (Gray test, P = 0.03). In multivariate analysis, propranolol treatment was associated with a decrease risk of HCC occurrence [HR, 0.25]
https://www.tandfonline.com/doi/full/10.2217/fon-2017-0635	1	Given pre-clinical and clinical observations described above, we believe that cancer mortality could be reduced by a safe perioperative blockade of SIRs. It is now justified and crucial to conduct larger clinical trials, assessing disease-free survival (DFS) and overall survival (OS), as without these long-term outcomes such interventions will not become a clinical routine. However, recruiting funds for such large trials is an ongoing challenge, as drugs that can be used for this purpose (e.g., propranolol and etodolac) are not patented and are inexpensive, and thus such trials are unattractive for pharmaceutical companies. Unfortunately, propranolol and/or etodolac are contraindicated for approximately 50% of patients (mostly due to asthma, cardiovascular disease, diabetes or low blood pressure). Therefore, the development of alternative approaches to limit perioperative SIRs is required	Catecholamines (CAs) and prostaglandins (PGs; specifically PGE2), which are abundant perioperatively, were repeatedly shown to mediate numerous pro-metastatic effects of stress and surgery, through various mechanisms [Citation2,Citation7]. For example, these ligands were shown to regulate the secretion of pro- and anti-inflammatory soluble factors (e.g. IL-6, CRP, TNF-α and IL-10), locally and systemically, to suppress NK and T-cell cytotoxicity, thus promoting cancer metastasis [Citation2], and to directly impact tumor cells, promoting their growth, motility, resistance to cell death (apoptosis and anoikis), epithelial-to-mesenchymal transition [Citation8] and secretion of pro-angiogenic and pro-metastatic factors (e.g., VEGF, MMP2, MMP9) . Recently, neuroendocrine stress responses were also suggested to promote an escape from dormancy of cancer cells
https://www.mdpi.com/2077-0383/11/15/4539	1	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.	There is a significant volume of data from in vitro, animal and human studies to indicate that there are multiple clinically relevant anti-cancer effects associated with PRO. This data has been summarised and presented to make the case that PRO is a very strong candidate for repurposing as an anticancer agent. In particular the potential for synergistic interactions with other drugs has been outlined, including repurposed COX-2/PGE2 inhibitors and a range of chemotherapeutics at both metronomic and standard dosing. The anti-metastatic properties of PRO may be particularly valuable to exploit during surgical intervention, and a number of possible combinations with other agents is discussed in this setting.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10943275/	N/A	In this systematic review, between 2000 and 2023, most of the 67 randomized controlled trials evaluating the efficacy of cardiovascular and anti‐inflammatory drugs in treating or preventing recurrence of cancer did not demonstrate clinical benefit. In fact, three studies demonstrated worse progression‐free survival or overall survival. Only two small studies demonstrated an improvement in overall survival for advanced/metastatic non‐small‐cell lung cancer and advanced hepatocellular carcinoma. The patient population from the two small positive trials composed a small portion (0.7%, 210/28,266) of the total patient population among all randomized controlled trials. There was a relatively equal distribution of the type of cardiovascular drug used (NSAID versus statin versus metformin) used in these clinical trials	Despite promising pre‐clinical and observational data involving cardiovascular drugs and anti‐inflammatory drugs in treating cancer or preventing cancer recurrence, randomized controlled trial data have thus far not demonstrated the previously anticipated improvement in survival or risk reduction in recurrence. While the biological plausibility for anti‐cancer effect may be present as shown by pre‐clinical studies, it is possible that current anti‐cancer therapies such as chemotherapy and radiation are effective at disrupting specific pathways that are more influential in tumorigenesis than the pathways acted upon by cardiovascular drugs and anti‐inflammatory drugs. As such, the effect of cardiovascular and anti‐inflammatory drugs may be less significant and not translate to clinical benefit as demonstrated by this systematic review and meta‐analysis.

PROPRANOLOL

TABLE OF REFERENCES

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