Feed

Chronic stress may influence cancer trajectories; however, the majority of current frameworks do not clearly define how organism‑level regulation interacts with tumor behavior. The present review summarizes mechanistic and translational evidence to propose a testable model in which cancer progression can, in selected contexts, be understood as over‑adaptation to sustained stress within a hierarchical neuro‑endocrine‑immune network. Within this framework, stress‑related signals converge in brainstem‑hypothalamic control circuits, and engage sympathetic, hypothalamic‑pituitary‑adrenal and vagal effector pathways, which may influence cellular programs, microenvironmental remodeling and systemic dissemination. The evidence is organized into three sections: Cellular adaptation, microenvironmental remodeling and systemic progression. This multiscale perspective provides a host‑context framework for understanding how chronic stress‑related physiology may interact with tumor‑intrinsic processes. Therapeutic implications are also discussed, including psychosocial support, exercise, mindfulness‑based interventions, vagal modulation and perioperative β‑blocker/COX‑2 strategies. At present, the strongest clinical evidence for these approaches supports improvements in symptoms, patient‑reported outcomes and selected biomarkers, whereas durable effects on tumor control or survival remain uncertain. Overall, this framework is presented as a conceptual and testable model intended to guide future research on host‑tumor interactions in cancer.