Chronic stress can promote tumor growth and progression through immunosuppressive effects and bi-directional interactions between tumor cells and their microenvironment. β-adrenergic receptor signaling plays a critical role in mediating stress-related effects on tumor progression. Stress-related mechanisms that modulate the dissemination of tumor cells to the brain have received scant attention. Brain metastases are highly resistant to chemotherapy and contribute considerably to morbidity and mortality in various cancers, occurring in up to 20% of patients in some cancer types. Understanding the mechanisms promoting brain metastasis could help to identify interventions that improve disease outcomes. In this review, we discuss biobehavioral, sympathetic, neuroendocrine, and immunological mechanisms by which chronic stress can impact tumor progression and metastatic dissemination to the brain. The critical role of the inflammatory tumor microenvironment in tumor progression and metastatic dissemination to the brain, and its association with stress pathways are delineated. We also discuss translational implications for biobehavioral and pharmacological interventions.

中文翻译：

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压力能促进脑转移的病理生理学吗？生物行为机制的批判性审查

慢性应激可以通过免疫抑制作用和肿瘤细胞与其微环境之间的双向相互作用促进肿瘤的生长和进展。β-肾上腺素能受体信号传导在介导与压力相关的肿瘤进展影响中起着关键作用。调节肿瘤细胞向大脑传播的压力相关机制很少受到关注。脑转移对化学疗法具有高度抵抗力，并且对各种癌症的发病率和死亡率有很大影响，在某些癌症类型中，高达 20% 的患者会发生这种情况。了解促进脑转移的机制可能有助于确定改善疾病结果的干预措施。在这篇综述中，我们讨论了生物行为、交感神经、神经内分泌、和免疫机制，慢性压力可以通过这些机制影响肿瘤进展和向大脑的转移性传播。描述了炎症性肿瘤微环境在肿瘤进展和转移到大脑中的关键作用，及其与应激途径的关联。我们还讨论了对生物行为和药理学干预的转化影响。