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Cytokine. 2012 Jul;59(1):3-9. doi: 10.1016/j.cyto.2012.03.027. Epub 2012 Apr 24.

Discovering cytokines as targets for chemotherapy-induced painful peripheral neuropathy.

Author information

1
National Institute of Nursing Research, National Institutes of Health, Bethesda, MD, USA. xmwang@mail.nih.gov

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN), a dose-limiting neurotoxic effect of chemotherapy, is the most common reason for early cessation of cancer treatment. This can result in an increased risk of recurrence and decreased survival rate. Inflammatory cascade activation, proinflammatory cytokine upregulation, and neuro-immune communication pathways play essential roles in the initiation and progression of CIPN. Most notably, TNF-α, IL-1β, IL-6, and CCL2 are involved in neuropathic pain. Further elucidation of the role of these cytokines could lead to their development and use as biomarkers for predicting the onset of painful peripheral neuropathy and early axonal damage. In this review, we provide evidence for the involvement of cytokines in CIPN, the possible underlying mechanisms, and their use as potential therapeutic targets and biomarkers to prevent and improve the painful peripheral neuropathy related to chemotherapeutic agents.

PMID:
22537849
PMCID:
PMC3512191
DOI:
10.1016/j.cyto.2012.03.027
[Indexed for MEDLINE]
Free PMC Article

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