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.
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.
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.
The purpose of this study is to understand reasons for minimal participation of urban community residents in longitudinal research. The study will also explore expectations of urban community residents as a result of participating in longitudinal research. The study will use qualitative focus group approach of urban community residents in the Midwest.
Assess religiosity as it may relate to social support to buffer stress, which could affect pregnancy length (# weeks gestation) and preterm birth rates.