Animal models are compelling that activating the beta-adrenergic pathway (via stress) results in tumor growth and metastasis. Beta-blockers blunt this effect in animals. All of Us could design a randomized intervention trial to test this potential benefit in humans. An observational approach could also be taken with careful attention to pharmacoepi principles and biases such as confounding by indication.
The built environment is only one contextual exposure of interest to investigators who study these factors in relation to disease (and even these function variably across rural and urban areas). New technology could assist in better clarifying a fuller scope of residential exposures, including what elements/exposures the All of Us participants actually come into contact with.
Prostate cancer has long been suspected to include an infectious etiology, although no agent has been identified. It is possible that one specific virus or bacterium is not significant, but rather the characteristics of the entire microbiota to which the prostate is exposed (e.g., the abundance and diversity of all microorganisms). This may be capturable by examining the seminal fluid microbiome.
Existing evidence does not adequately evaluate the effects with consideration of the patients’ past history of tobacco use and the tobacco use during and after cancer treatment. The toxicity and expense of many cancer therapies warrant a better understanding of how concurrent tobacco use undermines efficacy or increases morbidity.
In animal models, stress is a trigger for tumor growth and metastasis, yet we have not adequately addressed this question in human cancer patients or survivors.
All of Us could longitudinally assess the biological experience of psychosocial stress (via biomarker or wearable technology) at specified times in the cancer survivorship period, and conduct an analysis of time to recurrence or time to death.
Randomized trials could be set within All of Us to test these interventions at specific research sites.
Chronic stress has significant suppressive impact on the immune system and would influence the risk of infection-associated cancers if high risk infections are allowed to persist. In general populations and healthy adult populations, this question has not been addressed. It would involve serial measurement of oral or anogenital human papillomavirus, or even helicobacter pylori.