Abstract
Background: Paclitaxel-induced peripheral neuropathy is a common and limiting side effect of an approved and effective chemotherapeutic agent. The cause of this nociception is still unknown. Methods: To uncover the mechanism involved in paclitaxel-induced pain, we developed a Drosophila thermal nociceptive model to show the effects of paclitaxel exposure on third instar larvae. Results: We found that paclitaxel increases pain perception in a dose-dependent manner, without overt morphological changes. Conclusions: Our simple, high throughput model can be combined with genomics approaches to identify regulators of chemotherapy-induced pain to eliminate its adverse side effects.
Highlights
Chemotherapy-induced peripheral neuropathy (CIPN) is a doselimiting side effect of many effective cancer treatments (Burton et al, 2007), and can have a lasting impact on the quality of life of cancer survivors (Hausheer et al, 2006 and Shimozuma et al, 2012)
A meta-analysis of 31 studies from over 4000 chemotherapytreated patients revealed that CIPN was prevalent in 68.1% of patients in the first month following chemotherapy, in 60% of patients at 3 months, and in 30% at 6 months or more (Seretny et al, 2014)
Our goal here was to develop a reproducible paradigm to investigate the effects of paclitaxel on nociception in the fly larvae
Summary
Chemotherapy-induced peripheral neuropathy (CIPN) is a doselimiting side effect of many effective cancer treatments (Burton et al, 2007), and can have a lasting impact on the quality of life of cancer survivors (Hausheer et al, 2006 and Shimozuma et al, 2012). Patients treated with paclitaxel experience side effects as early as one to three days following treatment (Lipton et al, 1989; Reyes-Gibby et al, 2009). Paclitaxel-induced peripheral neuropathy is a common and limiting side effect of an approved and effective chemotherapeutic agent. The cause of this nociception is still unknown. Conclusions: Our simple, high throughput model can be combined with genomics approaches to identify regulators of chemotherapy-induced pain to eliminate its adverse side effects.
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