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.
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Chen, CS., Hertz, D.L. (2022). Chemotherapy-Induced Peripheral Neuropathy. In: Ghini, V., Stringer, K.A., Luchinat, C. (eds) Metabolomics and Its Impact on Health and Diseases. Handbook of Experimental Pharmacology, vol 277. Springer, Cham. https://doi.org/10.1007/164_2022_609
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