Prevention of anticancer therapy-induced neurotoxicity: Putting DNA damage in perspective

Chemotherapy-induced peripheral neuropathy (CIPN) is a severe side effect of conventional anticancer therapeutics (cAT) that significantly impacts the quality of life of tumor patients. The molecular mechanisms of CIPN are incompletely understood and there are no effective preventive or therapeutic measures available to date. Here, we present a brief overview of the current knowledge about mechanisms underlying CIPN and discuss DNA damage-related stress responses as feasible targets for the prevention of CIPN. In addition, we discuss that the nematode Caenorhabditis elegans is a useful 3R-conform model organism to further elucidate molecular mechanisms of CIPN and to identify novel lead compounds protecting from cAT-triggered neuropathy.

Automated summary

This article provides an overview of the mechanisms underlying chemotherapy-induced peripheral neuropathy (CIPN) and suggests that DNA damage-related stress responses could be potential targets for prevention. Additionally, the use of the nematode Caenorhabditis elegans as a model organism is discussed for further investigation of CIPN mechanisms and identification of protective compounds.