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Related Experiment Video

Updated: May 2, 2026

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

Lipidomic Predictors of Paclitaxel-Induced Peripheral Neuropathy.

Yaping Liu¹, Ciao-Sin Chen¹, Nam Nguyen-Hoang¹

¹Department of Clinical Pharmacy, University of Michigan College of Pharmacy, Ann Arbor, MI.

JCO Precision Oncology

|April 30, 2026

Summary

This study identified plasma lipid biomarkers associated with taxane-induced peripheral neuropathy (TIPN) severity and paclitaxel pharmacokinetics. These findings may help personalize cancer treatments to reduce nerve damage.

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Last Updated: May 2, 2026

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Carotid Artery Infusions for Pharmacokinetic and Pharmacodynamic Analysis of Taxanes in Mice

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Published on: October 27, 2014

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

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Area of Science:

Oncology
Pharmacology
Biochemistry

Background:

Taxane-induced peripheral neuropathy (TIPN) is a significant challenge in cancer therapy, often leading to dose reduction or treatment cessation.
Identifying reliable biomarkers for TIPN is crucial for managing treatment toxicity and improving patient outcomes.
Paclitaxel pharmacokinetics (PK) influence drug efficacy and toxicity, necessitating further investigation into predictive markers.

Purpose of the Study:

To identify and validate plasma lipidomic biomarkers associated with the severity of taxane-induced peripheral neuropathy (TIPN).
To explore the relationship between plasma lipid profiles and paclitaxel pharmacokinetics (PK).
To discover potential biomarkers for personalized cancer treatment strategies aimed at mitigating TIPN.

Main Methods:

Retrospective analysis of a prospective cohort of early-stage breast cancer patients receiving weekly paclitaxel.
Assessment of TIPN using the European Organization for Research and Treatment of Cancer QLQ-CIPN20 sensory subscale (CIPN8).
Quantification of plasma lipidomics and estimation of paclitaxel PK parameters (Cmax, Tc>0.05) using linear regression models.

Main Results:

Specific lipid profiles, including lower sphingomyelin (SM 40:1;3O) and lysophosphatidylethanolamine (LPE O-22:1), and higher ceramide (Cer 36:0;2O) and phosphatidylinositol (PI 34:2), were associated with greater sensory TIPN.
Reduced levels of certain (lyso)phosphatidylethanolamine and (lyso)phosphatidylcholine species correlated with higher paclitaxel Cmax.
Previously reported associations with other lipid classes were not replicated in this cohort.

Conclusions:

End-of-infusion plasma lipidomic profiles show promise as candidate biomarkers for TIPN severity and paclitaxel Cmax.
These findings support the potential for lipid-guided personalized treatment strategies to mitigate TIPN.
Larger prospective studies are required to validate these biomarkers and refine treatment approaches.