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Chronic cancer pain results from the complex interaction of nociceptive, neuropathic, and neuroimmune mechanisms, which vary according to tumor type, location, stage, and treatment history. Recent advances in cancer neuroscience have reframed pain as a dynamic manifestation of reciprocal tumor–nerve–immune interactions, rather than a mere consequence of tissue damage. In this model, malignant, stromal, and immune cells remodel nociceptive circuits at peripheral and central levels. This narrative review, conducted in accordance with SANRA criteria, synthesizes current mechanistic insights into the neurobiology of cancer pain. At the peripheral level, tumor-derived mediators such as prostaglandins, cytokines, chemokines, glutamate
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