Cure Alveolar Soft Part Sarcoma International (iCureASPS)

Breelyn Wilky tweeted of the possible use of propranolol use in immune therapy to aid in metastatic cancer treatments and as not all of us have access to Medscape ,this was the closest I could come to information.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5102691/

It's my limited understanding that propranolol is being seen as working on different anti cancer levels along side chemo to aid in delivery and effects .
And the best part is it costs only pennies on the dollar .

https://www.ncbi.nlm.nih.gov/pubmed/27211551

Medscape link

http://www.medscape.com/viewarticle/875136

Beta blockers being used against positive beta receptor tumors ie hemgionmas ( benign tumors) was seen as successful so it made sense to try them as a co drug, if you will ,along some chemo treatments.

Beta-blockers are drugs that are usually prescribed for high blood pressure (hypertension), irregularities in heart beat (arrhythmias), and to prevent heart attacks after a first heart attack has already occurred. Beta-blockers work by stopping adrenaline and noradrenaline from triggering the body’s “fight or flight” response to stress or danger. Beta blockers help the body feel more relaxed, lowering blood pressure and increasing blood flow.

Beta-blockers are taken by so many Americans that they are the fifth most widely prescribed class of drugs.[1] Since they are safe and inexpensive, wouldn’t it be great if they were effective for treating cancer, too?

Doctors and researchers noticed that when cancer patients took beta-blockers because of their heart disease, they tended to live longer than other cancer patients. They decided to study whether beta-blockers significantly improve survival for several different types of cancer.

Abstract

Acute mental stress elicits increases in plasma cytokine concentrations in humans, but the underlying mechanisms remain poorly understood. We assessed the impact of beta-adrenergic blockade on plasma interleukin 6 (IL-6) and IL-1 receptor antagonist (IL-1Ra) responses in a parallel group, double-blind randomised placebo-controlled trial involving 64 healthy young adult volunteers. Participants were administered 80 mg slow-release propranolol or placebo daily for 7 days before the stress testing session in which responses to 3 behavioural challenges (public speaking, mirror tracing, mental arithmetic) were evaluated. Propranolol administration was associated with reduced baseline levels of heart rate and IL-1Ra, and systolic blood pressure (BP) in men. Tasks stimulated increased plasma IL-6 concentrations sampled 45 min and 75 min after challenge, but these responses were blocked by propranolol in men (p < 0.001). Propranolol did not influence IL-6 responses in women, or IL-1Ra in either sex. Blood pressure and heart rate increased markedly during the tasks, but there was no differential stress reactivity in propranolol and placebo conditions. The results of the study support a role of sympathetic nervous system activation in stimulating acute IL-6 responses to stress, but only in men. The reasons for the differences between men and women remain to be resolved.

Keywords: Inflammation, Stress, Sympathetic nervous system, Sex differences, Blood pressure, Pharmacological blockade

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5965252/

1. Introduction

Inflammation is involved in a range of serious health problems including coronary heart disease (CHD), some cancers, chronic pain, and depression (Elinav et al., 2013, Hansson and Hermansson, 2011, Louati and Berenbaum, 2015, Miller and Raison, 2016). Psychosocial factors such as early life trauma, low socioeconomic status (SES), caregiver strain and other adult stressors have also been associated with low-grade systemic inflammation (Danese and Lewis, 2017, Kiecolt-Glaser et al., 2015, Rohleder, 2014, Stringhini et al., 2013). This has led to the conjecture that inflammation mediates in part the association between psychosocial adversity and health outcomes. This link is supported by experimental studies demonstrating that acute psychological stress stimulates increased concentration of circulating inflammatory markers, notably interleukin 6 (IL-6) but also IL-1β and tumor necrosis factor alpha (TNFα) (Marsland et al., 2017, Steptoe et al., 2007). Additionally, individual differences in psychosocial factors such as loneliness and hostility appear to modulate the magnitude of inflammatory responses to acute psychological stress (Hackett et al., 2012, Hackett et al., 2015).

The biological mechanisms underlying inflammatory responses to acute stress are only partly understood. Psychological stress elicits rapid increases in expression of nuclear factor κB (NF- κB), a transcription factor promoting the production of IL-6 and IL-1β (Bierhaus et al., 2003, Kuebler et al., 2015). Increases in IL-1β and IL-6 mRNA expression from leukocytes have also been described (Brydon et al., 2005, Kuebler et al., 2015, McInnis et al., 2015). Other factors that may be relevant include redistribution of circulating white blood cell subpopulations that expression proinflammatory cytokines, and release of lymphocytes from marginal pools (Steptoe et al., 2007). Research in animal models strongly implicates sympathetic nervous system activation in these responses (Bierhaus et al., 2003, Sanders and Kavelaars, 2007). In humans, positive correlations between plasma IL-6 responses to acute stress and cardiovascular activity have also been observed, again suggestive of sympathetic nervous system involvement (Brydon et al., 2005, Kop et al., 2008).

Another approach to investigating the pathways underlying acute inflammatory responses involves pharmacological blockade (Van Hedger et al., 2017). Rodent studies indicate that beta-adrenergic blockade inhibits stress-induced increases in inflammation (Hanke et al., 2012, Powell et al., 2013), but evidence from humans is inconclusive. The most detailed study was a double-blind analysis of 64 healthy middle-aged men and women randomised to daily 80 mg propranolol, 100 mg aspirin or placebo for 5 days (von Kanel et al., 2008). There was no effect of propranolol on plasma IL-6 responses up to 105 min after the Trier Social Stress Test (TSST), while aspirin attenuated stress-induced increases. The explanation for the lack of effect of propranolol is not clear. Rohleder (2008) suggested that the timing of stress testing might have been relevant, but it is difficult to know what would have been more appropriate. In an attempt to understand these processes better, we therefore carried out a parallel group double-blind trial evaluating the effect of propranolol vs placebo on IL-6 and cardiovascular responses to acute psychological stress in healthy young adults. We did not use the TSST but a similar battery of behavioural challenges, and measured IL-1Ra as an additional inflammatory biomarker. We hypothesised that 7 days of 80 mg propranolol would block stress-induced increases in inflammation and reduce systolic blood pressure (BP) and heart rate stress reactivity.