Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect of many common anti-cancer agents that can lead to dose reduction or treatment discontinuation, which decrease chemotherapy efficacy. Long-term CIPN can interfere with activities of daily living and diminish the quality of life. The mechanism of CIPN is not yet fully understood, and biomarkers are needed to identify patients at high risk and potential treatment targets. Metabolomics can capture the complex behavioral and pathophysiological processes involved in CIPN. This chapter is to review the CIPN metabolomics studies to find metabolic pathways potentially involved in CIPN. These potential CIPN metabolites are then investigated to determine whether there is evidence from studies of other neuropathy etiologies such as diabetic neuropathy and Leber hereditary optic neuropathy to support the importance of these pathways in peripheral neuropathy. Six potential biomarkers and their putative mechanisms in peripheral neuropathy were reviewed. Among these biomarkers, histidine and phenylalanine have clear roles in neurotransmission or neuroinflammation in peripheral neuropathy. Further research is needed to discover and validate CIPN metabolomics biomarkers in large clinical studies.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
