作为伤害性刺激的主要传入通路，伤害性感觉神经元已被证实主动参与肿瘤进展。众多研究表明，感觉 神经元与肿瘤之间存在复杂的双向串扰：肿瘤通过释放神经营养因子与轴突引导分子促进肿瘤的神经支配；感 觉神经元通过释放神经肽重塑肿瘤微环境，调控肿瘤生长、血管生成、免疫逃逸与转移。然而，这一感觉神经— 肿瘤互作在不同器官来源的肿瘤中呈现显著异质性，其特异性机制尚未系统阐明。基于此，本文拟系统梳理伤 害性感觉神经元在多种实体瘤发生与进展中的器官特异性作用机制，评估靶向感觉神经—肿瘤信号轴的治疗 潜力，并为开发器官特异性的神经调控策略提供理论依据与研究方向。

As the principal afferent pathway for noxious stimuli, nociceptive sensory neurons have been shown to actively participate in tumor progression. Numerous studies indicate a complex bidirectional crosstalk between sensory neurons and tumors: tumors promote tumor innervation by releasing neurotrophic factors and axon guidance molecules, while sensory neurons remodel the tumor microenvironment by releasing neuropeptides, thereby modulating cancer proliferation, angiogenesis, immune evasion, and metastasis. However, this sensory neuro-tumor interaction exhibits marked heterogeneity across tumors of different organ origins, and its organ-specific mechanisms have yet to be systematically elucidated. Accordingly, this review aims to systematically delineate the organ-specific mechanisms by which nociceptive sensory neurons contribute to the initiation and progression of multiple solid tumors, evaluate the therapeutic potential of targeting the sensory neuron-tumor signaling axis, and provide a theoretical basis and research directions for developing organ-specific neuromodulatory strategies.