ArticleScience translational medicine2026
Cancer-induced nerve injury unveils a sympathetic-to-sensory nerve axis in a mouse model of head and neck squamous cell carcinoma.
Article in Science translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
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9 authors.
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Abstract
Oral squamous cell carcinoma (OSCC) is one of the most painful cancers, with patients frequently reporting spontaneous, neuropathic-like pain. Sympathetic and sensory nerves have been individually implicated in cancer progression, but whether and how these systems interact to drive pain and tumor growth have remained unclear. Here, we integrated prospective human data with reverse-translational mouse models to reveal that cancer-induced nerve injury unveils cross-talk between sympathetic postganglionic neurons and trigeminal sensory afferents in the tumor microenvironment. In patients, circulating norepinephrine (NE) correlated with spontaneous pain and perineural invasion, identifying a potential sympathetic contribution to disease burden. In mice, aggressive nonimmunogenic OSCC tumors evoked spontaneous nociceptive behaviors, elevated tumoral NE, and sensory nerve injury marked by ATF3 expression and hyperexcitability. Tumor-associated sensory neurons acquired adrenergic sensitivity through α1-adrenergic receptor plasticity, whereas sympathetic neurons exhibited plasticity characterized by sprouting, altered gene expression, and heightened excitability, creating a maladaptive feed-forward loop that amplified nociceptive signaling. Disrupting this sympathetic-sensory communication by sympathectomy or selective ablation of TRPV1
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