A major problem associated with clinical management of
cancer is controlling the accompanying
pain, and various
analgesics are in common use for this purpose. Recent evidence suggests that some of the targets of
analgesics, such as
ion channels and receptors, may also be involved in the
cancer process, thereby raising the possibility that such use of some
analgesics may impact upon
cancer itself. The main aim of this study was to determine whether
gabapentin, a common adjuvant
analgesic in current use against
cancer-associated
neuropathic pain, would affect tumour development and progression in vivo. The Dunning rat model of
prostate cancer was used. Strongly metastatic Mat-LyLu cells were implanted subcutaneously into syngeneic Copenhagen rats which were then treated every other day with 4.6-16.8 μg/kg
gabapentin by gavage. Primary tumourigenesis was monitored daily. Lung
metastases were counted and measured after killing the rats 21 days later.
Gabapentin had no effect on primary tumourigenesis but produced dose-dependent effects on lung
metastasis. Whilst 4.6 μg/kg had no effect, 9.1 μg/kg
gabapentin decreased the number of lung
metastases significantly by 64%. In contrast, 16.8 μg/kg
gabapentin promoted
metastasis significantly by 112% and showed a strong tendency to shorten mean survival time. It is concluded that
gabapentin prescribed to
cancer patients against
pain could impact upon the
cancer process itself.