Painful peripheral neuropathies resulting from cancer chemotherapy treatment is frequently dose-dependent and may diminish following dose reduction or termination of chemotherapy. However, dose reduction or treatment termination could lead to reemergence of the cancer. In addition, chemotherapy-induced peripheral neuropathy (CIPN) may persist long after termination of chemotherapy. Thus, there is a need for treatments to ameliorate pain during the course of an effective cancer treatment regimen. Because the mechanism underlying CIPN has yet to be fully characterized, there is a current lack of effective treatments for CIPN. Preclinical studies in CIPN rodent models have suggested a number of potential neuropathological mechanisms, which could serve as platforms for the development of novel therapeutics. Although a number of potential analgesic therapies have demonstrated robust efficacy in preclinical studies, rigorous clinical testing has yet to fully validate the preclinical findings. The lack of congruence between preclinical and clinical findings could be in part due to the phylogenetic distance between the main model species and humans. Thus, a CIPN model in nonhuman primates could serve to bridge the translational gap between laboratory findings in small animals and clinical utility. The current review points out the short comings of current CIPN rodent models and suggests the use of large animals, such as the nonhuman primate, to narrow the translational gap between preclinical and clinical findings and the discovery of novel therapeutics.
Keywords: Neuropathic pain, preclinical animal disease models, translational science, allodynia, clinical relevance.
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