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Using an integrated omics approach to uncover the mechanisms underlying chemotherapy-induced peripheral neuropathy
Isabella Piga1,2, Roberta Bonomo3, Clizia Chinello4
1Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
Abstract:
Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect with limited treatment options. The primary challenge in developing therapies is the lack of identified neurotoxic mechanisms. To address this, an integrated omics approach, combining transcriptomics, proteomics, and metabolomics, is essential to map the biological changes underlying the condition. Here, we show how data from these complementary approaches converge on key mechanisms involved in CIPN through a critical summary of animal and human studies. Current research highlights several key drivers of CIPN, such as inflammatory signaling and oxidative stress, mitochondrial dysfunction, and disrupted lipid metabolism. Although most data currently stem from preclinical models, the pathways identified offer promising targets for biomarker discovery and treatment. To translate these findings into clinical applications, integrated omics studies in human samples are urgently needed, focusing on a personalized approach. Future breakthroughs depend on large-scale human studies to tailor antineoplastic choices and neuroprotective treatments to individual patient needs.
Insights
Chemotherapy-induced peripheral neuropathy (CIPN) is a severe side effect with few treatments. Integrated omics approaches are crucial for understanding CIPN mechanisms and developing targeted therapies.
Area of Science:
- Neuroscience
- Oncology
- Genomics
Background:
- Chemotherapy-induced peripheral neuropathy (CIPN) presents a significant clinical challenge due to limited therapeutic options.
- Understanding the underlying neurotoxic mechanisms is critical for developing effective treatments for CIPN.
Purpose of the Study:
- To critically review and integrate findings from transcriptomics, proteomics, and metabolomics studies.
- To identify key biological mechanisms driving CIPN in both preclinical models and human studies.
- To highlight the potential of integrated omics for biomarker discovery and personalized treatment strategies.
Main Methods:
- Comprehensive literature review of animal and human studies utilizing omics approaches (transcriptomics, proteomics, metabolomics).
- Data synthesis to identify converging biological pathways and mechanisms implicated in CIPN.
- Analysis of identified pathways for potential therapeutic targets and biomarkers.
Main Results:
- Integrated omics data implicate inflammatory signaling, oxidative stress, mitochondrial dysfunction, and disrupted lipid metabolism as key drivers of CIPN.
- Preclinical models provide valuable insights, but human studies are essential for clinical translation.
- Converging evidence from multiple omics layers strengthens the biological plausibility of identified mechanisms.
Conclusions:
- Integrated omics approaches are vital for elucidating complex CIPN pathogenesis.
- Identified mechanisms offer promising targets for novel neuroprotective agents and biomarkers.
- Large-scale, personalized human omics studies are necessary to advance CIPN treatment and prevention strategies.
