Stress is an inevitable part of life. Chronic stress on account of reasons like adversity, depression, anxiety, or loneliness/social isolation can endanger human health. Recent studies have shown that chronic stress can induce tumorigenesis and promote cancer development. This review describes the latest progress of research on the molecular mechanisms by which chronic stress promotes cancer development. Primarily, chronic stress activates the classic neuroendocrine system [the hypothalamic-pituitary-adrenal (HPA) axis] and the sympathetic nervous system (SNS) and leads to a decline and dysfunction of the prefrontal cortex and the hippocampus under stress. Stress hormones produced during the activation of both the HPA axis and the SNS can promote tumorigenesis and cancer development through a variety of mechanisms. Chronic stress can also cause corresponding changes in the body's immune function and inflammatory response, which is significant because a long-term inflammatory response and the decline of the body's immune surveillance capabilities are implicated in tumorigenesis. Stress management is essential for both healthy people and cancer patients. Whether drugs that limit the signaling pathways downstream of the HPA axis or the SNS can suppress chronic stress-induced cancers or prolong patient survival deserves further study.

压力是生活中不可避免的一部分。由于诸如逆境，沮丧，焦虑或孤独/社交孤立等原因而造成的长期压力会危害人类健康。最近的研究表明，慢性应激可以诱导肿瘤发生并促进癌症的发展。这篇综述描述了慢性应激促进癌症发展的分子机制研究的最新进展。首先，慢性应激会激活经典的神经内分泌系统[下丘脑-垂体-肾上腺（HPA）轴]和交感神经系统（SNS），并导致在压力下前额叶皮层和海马体功能下降和功能障碍。HPA轴和SNS激活过程中产生的应激激素可以通过多种机制促进肿瘤发生和癌症发展。慢性应激还可引起机体免疫功能和炎症反应的相应变化，这是很重要的，因为长期的炎症反应和机体免疫监视能力的下降与肿瘤的发生有关。压力管理对健康人和癌症患者都至关重要。限制HPA轴或SNS下游信号通路的药物是否可以抑制慢性应激诱发的癌症或延长患者生存期，值得进一步研究。