Journal: British journal of pharmacology
This publication is a narrative review of contemporary understanding and management of cancer pain, emphasizing the transition from empiric to mechanism-based, personalized approaches.
Key points:
- Pathophysiology of cancer pain
- Cancer pain is typically mixed, incorporating nociceptive, neuropathic, and neuroinflammatory components.
- Pain mechanisms differ by tumour type and disease stage.
- Cancer pain is framed as a disorder of aberrant crosstalk among:
- The tumour itself
- Sensory nerves that are recruited or remodeled by the tumour
- Immune cells attracted by these nerves
- This triad generates maladaptive signalling in the tumour microenvironment, driving persistent pain.
- Current management
- Despite substantial research, clinical practice still relies mainly on:
- NSAIDs and other non-opioid analgesics
- Opioids as the primary systemic therapy
- Existing treatments are often nonspecific and do not directly target the underlying neurobiological mechanisms.
- Despite substantial research, clinical practice still relies mainly on:
- Advances in cancer neuroscience
- Recent work has identified molecular mediators and signalling pathways involved in tumour–nerve–immune interactions.
- These findings are beginning to clarify why pain phenotypes differ across cancers and patients, and suggest new targets beyond traditional analgesics.
- Future directions
- The authors propose a shift toward precision, mechanism-driven pain therapy, where treatment strategies are tailored to the dominant biological drivers of pain in a given patient or tumour type.
- They highlight the potential for targeted interventions that disrupt specific components of the tumour–nerve–immune signalling cascade.
Overall, the article bridges basic cancer neuroscience with clinical pain management, advocating for individualized, mechanism-based strategies rather than a one-size-fits-all reliance on NSAIDs and opioids.