Neurobiology of Cancer Pain: A Narrative Review
Abstract
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, and endothelin-1 drive nociceptor sensitization via G-protein–coupled and tyrosine kinase pathways. In bone metastases, osteoclast-mediated resorption generates an acidic microenvironment that activates acid-sensing ion channels and transient receptor potential (TRP) channels, linking skeletal destruction with movement-evoked pain. Pathological nerve remodeling and perineural invasion further contribute to neuropathic components and adverse oncological outcomes. Treatment-induced syndromes, notably chemotherapy-induced peripheral neuropathy, result from axonal injury, mitochondrial dysfunction, and neuroinflammation. At the central level, persistent afferent input induces glial activation and chemokine signaling, amplifying synaptic transmission and…
Read the paper
Related studies
- Noninvasive and Point-of-Care Surface-Enhanced Raman Scattering (SERS)-Based Breathalyzer for Mass Screening of Coronavirus Disease 2019 (COVID-19) under 5 min
- De Novo Transcriptome Analysis and Detection of Antimicrobial Peptides of the American Cockroach Periplaneta americana (Linnaeus)
- Molecular Characterization and Expression Profiling of Tomato GRF Transcription Factor Family Genes in Response to Abiotic Stresses and Phytohormones
- Assembly of Tight Junction Strands: Claudin-10b and Claudin-3 Form Homo Tetrameric Building Blocks that Polymerise in a Channel-Independent Manner
- Update of the Pompe variant database for the prediction of clinical phenotypes: Novel disease‐associated variants, common sequence variants, and results from newborn screening
- Machine Learning-Based SERS Chemical Space for Two-Way Prediction of Structures and Spectra of Untrained Molecules
Go deeper in Evidence Hub
Evidence Hub adds a study data sheet (design, sample size, evidence level, key numbers), an AI summary and a chat grounded in the paper's text.