Abstract
Chronic stress has been increasingly investigated as a factor influencing cancer development and progression. This review examines the biological and psychosocial mechanisms linking chronic stress to oncogenesis, including prolonged activation of the hypothalamic-pituitary-adrenal (HPA) axis, inflammation, immune dysregulation, and β-adrenergic signaling. Evidence from mechanistic studies demonstrates that chronic stress promotes tumor-supportive environments by impairing immune surveillance, increasing inflammatory cytokine production, and altering cellular signaling pathways. Epidemiologic findings remain heterogeneous, with some studies showing modest associations between stress and cancer incidence, while others report no consistent relationship. Additionally, metabolic comorbidities and psychosocial factors, such as social support, can further influence these effects. Overall, while causality is not definitively established, chronic stress appears to contribute to biological conditions that may facilitate cancer development and progression. Future research integrating objective stress biomarkers and longitudinal designs is needed to clarify these relationships.