"Modulation of Pain in a model of Cancer induced bone pain"
Prof AH Dickenson
Wellcome Fellowship to Prof Dickenson
Description of Project:
Metastases to bone are common and this has been shown to be the most common cause of pain in cancer patients, It is therefore quite obvious that a means of controlling this form of pain would be of great use in the clinical environment, and in increasing a patient's quality of life. However, to truly tackle the problem of cancer-induced bone pain it is necessary to comprehend the mechanisms through which cancer-induced bone pain acts. The development of cancer-induced bone pain is complex sharing many modalities of other chronic pain states, however it is now well recognised that cancer-induced bone pain is unique from other forms of pain. Glia have long been a subject of interest in the field of pain research since early studies noticed that the marker for astrocytes was increased in the dorsal horn in a model of neuropathic pain. Inhibiting both micoglia and astrocytes in neuropathic pain models have shown to be able to attenuate behavioural markers of neuropathic pain. Recently immuniohistochemical studies in both murine and rat models of cancer-induced bone pain have shown in both a astocyte and microglial hypertrophy after cancer injection at time of peak behavioural changes. it is therefore that it woudl be interesting to unravel the involvment of glia, both astrocytes and microglia, in the development of pain behaviour in this model of CIBP.