Psychological stress, immune and endocrine function, and cancer risk

PL02-01

There is extensive evidence linking psychological stress and depression with immune and endocrine dysregulation. This presentation will primarily focus on stress-related changes in inflammation, a noteworthy component in tumor progression. Production of proinflammatory cytokines can be substantially enhanced by stress and depression. Furthermore, stress and depression also contribute to greater risk for infection, prolonged infectious episodes, and delayed wound healing, all processes that indirectly fuel sustained proinflammatory cytokine production. Compounding the risks, health behaviors including poor sleep are commonplace consequences of stress and depression; poor sleep enhances proinflammatory cytokine production. In addition to these pathways, evidence from animal and human studies suggest that stress and depression can permanently alter the responsiveness of the immune system; stressors can effectively prime the inflammatory response, promoting larger proinflammatory cytokine increases in response to subsequent stressors and/or minor infectious challenges. Furthermore, stress and depression have also been associated with two important processes for carcinogenesis, poorer repair of damaged DNA, and alterations in apoptosis. Stress hormones can modulate many different aspects of the tumor microenvironment, including local growth factors. These data have provided mechanistic explanations for some of the epidemiological evidence linking stress and depression with cancer incidence and progression. These studies and others suggest that psychological or behavioral factors may influence the incidence and progression of cancer through psychosocial influences on immune and endocrine function and other physiological pathways.