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This review systematizes mechanistic and translational evidence to propose a testable model: in selected contexts, cancer progression reflects maladaptive over-adaptation to sustained stress within a hierarchical neuro-endocrine-immune network. Stress signals converge in brainstem-hypothalamic control circuits and act through sympathetic, HPA-axis, and vagal pathways, influencing cellular programs, microenvironment remodeling, and systemic dissemination. It further discusses psychosocial support, exercise, mindfulness-based interventions, vagal modulation, and perioperative β-blocker/COX-2 strategies, noting strongest evidence for symptom and biomarker improvements while survival effects remain uncertain, and presenting a conceptual framework for future host–tumor research.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/chronic-stress-and-cancer-progression-through-neuro-endocrine-immune-networks-review/363393/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/chronic-stress-and-cancer-progression-through-neuro-endocrine-immune-networks-review/363393.png","ImageObject",300,407,{"name":92,"@type":93},"supergirl","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-24","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":34},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"How does chronic stress relate to cancer progression according to this review?","Question",{"text":112,"@type":113},"The review proposes that, in selected contexts, cancer progression can represent over-adaptation to sustained stress within a hierarchical neuro-endocrine-immune (NEI) network, rather than being determined only by tumor-intrinsic drivers.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"Which neuro-endocrine and immune pathways are emphasized as mediators?",{"text":117,"@type":113},"Stress-related signals are described as converging in brainstem-hypothalamic control circuits and engaging sympathetic, hypothalamic-pituitary-adrenal, and vagal effector pathways that can affect cellular programs, microenvironment remodeling, and dissemination.",{"name":119,"@type":110,"acceptedAnswer":120},"What evidence and outcomes are most supported for the discussed interventions?",{"text":121,"@type":113},"The review states that current strongest clinical evidence supports improvements in symptoms, patient-reported outcomes, and selected biomarkers, while durable effects on tumor control or survival remain uncertain.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},363393,1790348132,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":34,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},962088121634,"https://ap-avatar.wpscdn.com/davatar_9964176cb1d06d4a9deccf72a44ae3dc","ONCOLOGY REPORTS 56: 123, 2026  \nChronic stress and cancer progression through neuro‑endocrine‑immune networks (Review)  \nZHANGXIANG ZHU 1* , XIAOHU ZHANG2* , JING YAN2 , MINGQUAN WANG 1 , YANG LV2 , WUQIONG ZHANG2 , HUI GUO2 and AIMEI ZHENG2  \n1Department of Radiology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China; 2Department of Oncology, Dingyuan County General Hospital, Chuzhou, Anhui 233200, P.R. China  \nReceived November 25, 2025; Accepted April 17, 2026  \nDOI: 10. 3892/or.2026.9128  \nAbstract. 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‑pitu‑ itary‑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 under‑ standing 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.  \nCorrespondence to: Dr Xiaohu Zhang, Department of Oncology, Dingyuan County General Hospital, 1 Xingfu East Road, Chuzhou, Anhui 233200, P.R. China  \nE‑mail: [tiger63111@outlook.com](tiger63111@outlook.com)  \n*Contributed equally  \nKey words: chronic stress, neuro‑endocrine‑immune network,β‑adrenergic signaling, glucocorticoid receptor, tumor microenvironment, cancer progression, multimodal intervention  \nContents  \n1. Introduction  \n2. NEI network mechanisms  \n3. Three stages of stress‑driven cancer progression  \n4. Clinical interventions  \n5. Discussion  \n6. Conclusion  \n1. Introduction  \nIn the clinic, some patients can live for years despite carrying a measurable tumor burden, indicating that survival cannot be reliably inferred from lesion size alone (1) . This clinicopathological heterogeneity is partly explained by host variables already considered in clinical practice, including functional status, comorbidities, nutritional state and indices of systemic inflammation; these factors add prognostic value beyond anatomic staging (2,3) . Expanding on this, converging evidence has indicated that chronic stress engages neuro‑endocrine‑immune (NEI) circuits that influence vascular remodeling, immune set‑points and metabolic alloca‑ tion, thereby altering the conditions in which tumors persist or regress (4,5). These host‑regulatory processes neither replace nor contradict tumor‑intrinsic drivers; rather, they operate alongside them and can tip the same tumor burden toward divergent trajectories. Framing cancer within this combined tumor‑host context thus provides a rationale for measuring, and, where feasible, modulating, stress‑related NEI activity to reduce outcome variability.  \nStrengths and limitations of prevailing tumor‑centered models. The Hallmarks of Cancer remains a powerful scaf‑ fold for characterizing tumor phenotypes (6), and cell‑centric m","cbCaiu58mOQwbRB7","https://ap.wps.com/l/cbCaiu58mOQwbRB7","pdf",2767213,18,"English","# Introduction\n# NEI network mechanisms\n# Three stages of stress-driven cancer progression\n# Clinical interventions\n# Discussion\n# Conclusion","[{\"question\":\"How does chronic stress relate to cancer progression according to this review?\",\"answer\":\"The review proposes that, in selected contexts, cancer progression can represent over-adaptation to sustained stress within a hierarchical neuro-endocrine-immune (NEI) network, rather than being determined only by tumor-intrinsic drivers.\"},{\"question\":\"Which neuro-endocrine and immune pathways are emphasized as mediators?\",\"answer\":\"Stress-related signals are described as converging in brainstem-hypothalamic control circuits and engaging sympathetic, hypothalamic-pituitary-adrenal, and vagal effector pathways that can affect cellular programs, microenvironment remodeling, and dissemination.\"},{\"question\":\"What evidence and outcomes are most supported for the discussed interventions?\",\"answer\":\"The review states that current strongest clinical evidence supports improvements in symptoms, patient-reported outcomes, and selected biomarkers, while durable effects on tumor control or survival remain uncertain.\"}]","Chronic stress and cancer progression through neuro-endocrine-immune networks - Review | PDF",1790151042,45]