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Войти в исследования Current opinion in supportive and palliative care · 2026
Peripheral neuron circuitry mediating pain in head and neck cancer.
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Sharma Gaurav, Ruparel Shivani
Аннотация
PURPOSE OF REVIEW: Pain is a major source of morbidity in head and neck cancer (HNC), yet its neural mechanisms remain incompletely defined. This review examines how malignant cells, the tumor microenvironment, and cancer treatment remodel peripheral sensory and autonomic circuits, and how neural activity reciprocally influences tumor biology, with particular attention to findings published since 2023.
RECENT FINDINGS: Recent studies show that HNC selectively reorganizes tumor-associated nerves rather than merely injuring a pre-existing neural scaffold. Sensory-neuron transcriptional responses differ by sex, perineural invasion redistributes mechanosensory and nociceptive activity, and cancer-induced injury establishes sympathetic-sensory crosstalk. Tumor-derived extracellular vesicles can program persistent nociceptor hypersensitivity, while adenosine-A2A, protease-PAR2, NGF-neuropilin-1, and EGFR pathways connect tumor metabolism and signaling to neuronal excitability and analgesic tolerance. Conversely, sensory and sympathetic signals promote tumor growth through direct effects on malignant cells, metabolic reprogramming, and local or systemic immune suppression. Surgery and radiotherapy add distinct patterns of denervation, sensitization, and reparative remodeling.
SUMMARY: HNC pain arises from reciprocal remodeling across tumor, immune, stromal, glial, and neural compartments. Defining how these circuits generate clinical pain phenotypes may support mechanism-based analgesia while avoiding unintended effects on antitumor immunity, tumor progression, or treatment response.
RECENT FINDINGS: Recent studies show that HNC selectively reorganizes tumor-associated nerves rather than merely injuring a pre-existing neural scaffold. Sensory-neuron transcriptional responses differ by sex, perineural invasion redistributes mechanosensory and nociceptive activity, and cancer-induced injury establishes sympathetic-sensory crosstalk. Tumor-derived extracellular vesicles can program persistent nociceptor hypersensitivity, while adenosine-A2A, protease-PAR2, NGF-neuropilin-1, and EGFR pathways connect tumor metabolism and signaling to neuronal excitability and analgesic tolerance. Conversely, sensory and sympathetic signals promote tumor growth through direct effects on malignant cells, metabolic reprogramming, and local or systemic immune suppression. Surgery and radiotherapy add distinct patterns of denervation, sensitization, and reparative remodeling.
SUMMARY: HNC pain arises from reciprocal remodeling across tumor, immune, stromal, glial, and neural compartments. Defining how these circuits generate clinical pain phenotypes may support mechanism-based analgesia while avoiding unintended effects on antitumor immunity, tumor progression, or treatment response.