Biobehavioral influences on cancer progression

Abstract

This review focuses on the contributions of stress-related behavioral factors to cancer growth and metastasis and the biobehavioral mechanisms underlying these relationships. Behavioral factors that are important in modulation of the stress response and the pivotal role of neuroendocrine regulation in the downstream alteration of physiologic pathways relevant to cancer control, including the cellular immune response, inflammation, and tumor angiogenesis, invasion, and cell signaling pathways are described. Consequences for cancer progression and metastasis, as well as quality of life, are delineated. Behavioral and pharmacologic interventions with the potential to alter these biobehavioral pathways for patients with cancer are discussed.

Figure 1

In addition to known biomedical risk factors, this biobehavioral model of cancer control illustrates the contributions of behavioral risk and resilience factors to cancer outcomes. Stress-related behavioral factors can activate (or inhibit) the hypothalamic pituitary adrenocortical (HPA) axis and sympathetic nervous systems (SNS). The products of these pathways, including glucocorticoids, catecholamines, and other neuroendocrine factors, have downstream effects on physiological mechanisms in the tumor micorenvironment important for the control of malignancy. These include the modulation of cellular immune processes relevant to tumor surveillance and containment, inflammation, and other pathophysiological processes critical to cancer growth and progression, including angiogenesis, invasion, and tumor-promoting cell-signaling pathways. Alteration of these physiological processes can encourage or inhibit tumor progression and metastasis. The potential effects of tumor- and treatment-derived inflammatory processes on depression (dashed arrow) and quality of life are also illustrated.