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. 2016 Oct;30(3):521-9.
doi: 10.1007/s12640-016-9637-1. Epub 2016 Jun 7.

Chemotherapy-Induced Neurotoxicity: Evidence of a Protective Role of CC Homozygosis in the Interleukin-1β Gene-511 C>T Polymorphism

E Peila  1 , F D'Agata  2 , P Caroppo  1   3 , L Orsi  1 , P Mortara  1 , S Cauda  4 , M Manfredi  4 , M M Caglio  1 , P Fenoglio  1 , B Baudino  4 , G Castellano  4 , G Bisi  4 , L Pinessi  1 , S Gallone  1
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Free article

Chemotherapy-Induced Neurotoxicity: Evidence of a Protective Role of CC Homozygosis in the Interleukin-1β Gene-511 C>T Polymorphism

E Peila et al. Neurotox Res. 2016 Oct.
Free article

Abstract

We hypothesized that the IL-1β-511 C>T polymorphism could be associated with the development of neurotoxicity and that it could be a possible biomarker to rate the risk of occurrence of neurotoxicity in cancer patients. Genomic DNA was extracted from 85 cancer patients: 49 received systemic chemotherapeutic treatment (CHT) and 36 patients did not receive it (No-CHT). All subjects were genotyped for the functionally active polymorphisms of IL-1β-511 C>T. We estimated neurotoxicity with the evaluation of neurological deficits. CHT patients showed erythrocytopenia, neurological deficit and a slight lowering of cognitive performance. The subgroup of patients carrying the CC genotype of the IL-1β-511 C>T gene showed lesser neurological deficits. In the context of cancer treatment, we suggested the potential value of IL-1β-511 C>T as genetic biomarkers to identify patients with higher risk to develop neurological deficits.

Keywords: Cancer; Chemotherapy; Cytokines; IL-1β; Neurotoxicity.

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