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摘要:
Current research has revealed some links between psychological stress and cellular mutation,neoplastic proliferation and metastasis in patients with cancer.In stressful situations,the stress-related neuroendocrine mediators(e.g.,catecholamines,and glucocorticoids(GSs))are being secreted,via stimulation of the sympathetic nervous system(SNS),and the hypothalamic-pituitaryadrenocortical(HPA)axis.Catecholamine may affect the malignant progression,since they can regulate various cellular signaling pathways,via adrenergic receptors(ARs)that are expressed by different types of neoplastic cells.The ARs increase the proliferation and invasive potential of such cells,and change their“behavior”in the tumor microenvironment.Similarly,cortisol and its glucocorticoid receptors(GRs)can promote stress-induced malignant growth and metastasis.Maladaptation to stressful situations,often relevant to the cancer diagnosis and treatment,may accelerate tumor growth and spread(e.g.,via inflammation,angiogenesis,and migration).Studies have shown that psychological interventions can be helpful for adaptation to adverse circumstances during the therapeutic process in patients with cancer.This mini-review will address some interrelations between psychological stress and cancer.It will discuss how the receptor-mediated signaling pathways may lead to cancer initiation,propagation,and spread.In addition,it will describe a supportive role of the stress reduction strategies,for example,in patients with breast cancer(BC).
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篇名 Interrelations Between Psychological Stress and Cancer-Deciphering Molecular Signals in the Tumor Microenvironment
来源期刊 现代肿瘤学研究进展(英文) 学科 医学
关键词 PSYCHOLOGICAL STRESS CANCER tumor MICROENVIRONMENT CYTOKINES inflammation IMMUNE system cell signaling STRESS reduction
年,卷(期) xdzlxyjjzyw_2018,(5) 所属期刊栏目
研究方向 页码范围 18-29
页数 12页 分类号 R73
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节点文献
PSYCHOLOGICAL
STRESS
CANCER
tumor
MICROENVIRONMENT
CYTOKINES
inflammation
IMMUNE
system
cell
signaling
STRESS
reduction
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研究去脉
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期刊影响力
现代肿瘤学研究进展(英文)
双月刊
2424-7855
12 Eu Tong Sen Stree
出版文献量(篇)
49
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0
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