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Stress and cancer: mechanisms, significance and future directions
Nature Reviews Cancer ( IF 72.5 ) Pub Date : 2021-09-10 , DOI: 10.1038/s41568-021-00395-5
Anabel Eckerling 1 , Itay Ricon-Becker 1 , Liat Sorski 1 , Elad Sandbank 1 , Shamgar Ben-Eliyahu 1
Affiliation  

The notion that stress and cancer are interlinked has dominated lay discourse for decades. More recent animal studies indicate that stress can substantially facilitate cancer progression through modulating most hallmarks of cancer, and molecular and systemic mechanisms mediating these effects have been elucidated. However, available clinical evidence for such deleterious effects is inconsistent, as epidemiological and stress-reducing clinical interventions have yielded mixed effects on cancer mortality. In this Review, we describe and discuss specific mediating mechanisms identified by preclinical research, and parallel clinical findings. We explain the discrepancy between preclinical and clinical outcomes, through pointing to experimental strengths leveraged by animal studies and through discussing methodological and conceptual obstacles that prevent clinical studies from reflecting the impacts of stress. We suggest approaches to circumvent such obstacles, based on targeting critical phases of cancer progression that are more likely to be stress-sensitive; pharmacologically limiting adrenergic–inflammatory responses triggered by medical procedures; and focusing on more vulnerable populations, employing personalized pharmacological and psychosocial approaches. Recent clinical trials support our hypothesis that psychological and/or pharmacological inhibition of excess adrenergic and/or inflammatory stress signalling, especially alongside cancer treatments, could save lives.



中文翻译:

压力与癌症:机制、意义和未来方向

几十年来,压力和癌症相互关联的观念一直主导着外行话语。最近的动物研究表明,压力可以通过调节大多数癌症标志显着促进癌症进展,并且已经阐明了介导这些影响的分子和系统机制。然而,由于流行病学和减轻压力的临床干预对癌症死亡率产生了不同的影响,因此此类有害影响的现有临床证据并不一致。在这篇综述中,我们描述并讨论了通过临床前研究和平行临床发现确定的特定中介机制。我们解释了临床前和临床结果之间的差异,通过指出动物研究所利用的实验优势,并通过讨论阻止临床研究反映压力影响的方法和概念障碍。我们建议基于更可能对压力敏感的癌症进展的关键阶段来规避这些障碍的方法;药理学限制由医疗程序引发的肾上腺素能-炎症反应;并关注更脆弱的人群,采用个性化的药理学和社会心理方法。最近的临床试验支持我们的假设,即对过量肾上腺素能和/或炎症应激信号进行心理和/或药理学抑制,尤其是在癌症治疗的同时,可以挽救生命。我们建议基于更可能对压力敏感的癌症进展的关键阶段来规避这些障碍的方法;药理学限制由医疗程序引发的肾上腺素能-炎症反应;并关注更脆弱的人群,采用个性化的药理学和社会心理方法。最近的临床试验支持我们的假设,即对过量肾上腺素能和/或炎症应激信号进行心理和/或药理学抑制,尤其是在癌症治疗的同时,可以挽救生命。我们建议基于更可能对压力敏感的癌症进展的关键阶段来规避这些障碍的方法;药理学限制由医疗程序引发的肾上腺素能-炎症反应;并关注更脆弱的人群,采用个性化的药理学和社会心理方法。最近的临床试验支持我们的假设,即对过量肾上腺素能和/或炎症应激信号进行心理和/或药理学抑制,尤其是在癌症治疗的同时,可以挽救生命。采用个性化的药理学和社会心理方法。最近的临床试验支持我们的假设,即对过量肾上腺素能和/或炎症应激信号进行心理和/或药理学抑制,尤其是在癌症治疗的同时,可以挽救生命。采用个性化的药理学和社会心理方法。最近的临床试验支持我们的假设,即对过量肾上腺素能和/或炎症应激信号进行心理和/或药理学抑制,尤其是在癌症治疗的同时,可以挽救生命。

更新日期:2021-09-12
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