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

Vanessa Brinkmann; Gerhard Fritz

doi:10.1016/j.neuro.2022.04.009

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

Neurotoxicology. 2022 Jul:91:1-10. doi: 10.1016/j.neuro.2022.04.009. Epub 2022 Apr 26.

Authors

Vanessa Brinkmann¹, Gerhard Fritz²

Affiliations

¹ Institute of Toxicology, Medical Faculty, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany. Electronic address: vanessa.brinkmann@uni-duesseldorf.de.
² Institute of Toxicology, Medical Faculty, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany. Electronic address: fritz@hhu.de.

PMID: 35487345
DOI: 10.1016/j.neuro.2022.04.009

Abstract

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.

Keywords: Anticancer drugs; CIPN; DNA damage; DNA damage response; Neurotoxicity.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Antineoplastic Agents* / adverse effects
DNA Damage
Humans
Neoplasms* / drug therapy
Peripheral Nervous System Diseases* / chemically induced
Peripheral Nervous System Diseases* / drug therapy
Peripheral Nervous System Diseases* / prevention & control
Quality of Life

Substances

Antineoplastic Agents