Liability of the Voltage-Gated Sodium Channel Gene SCN2A R19K Polymorphism to Oxaliplatin-Induced Peripheral Neuropathy
Liability of the Voltage-Gated Sodium Channel Gene SCN2A R19K Polymorphism to Oxaliplatin-Induced Peripheral Neuropathy
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DOI:
10.1159/000236049
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发表时间:
2009-01-01
期刊:
影响因子:
3.5
通讯作者:
Kalofonos, Haralabos P.
中科院分区:
文献类型:
--
作者:
Argyriou, Andreas A.;Antonacopoulou, Anna G.;Kalofonos, Haralabos P.
Aim: It was the aim of this study to test the hypothesis that the voltage-gated sodium channel gene SCN2A R19K polymorphism confers liability to oxaliplatin-induced peripheral neuropathy (OXLIPN). Methods: Sixty-two patients with advanced colorectal cancer were genotyped, using allele-specific primers and SYBR green in real-time polymerase chain reaction. All patients had received adjuvant oxalipla-tin-based chemotherapy. The severity of OXLIPN was defined by means of the clinical total neuropathy score. Following the discontinuation of treatment, 36/62 patients (58.1%) developed OXLIPN. Grade I neurotoxicity was revealed in 14 (38.9%) patients and grade II neurotoxicity in 22 (61.1%) patients. Results: From patients without OXLIPN (n = 26), 80.8% (n = 21) were homozygous for G, 19.2% (n = 5) were heterozygous (AG) and none was homozygous for A. The corresponding percentages for patients developing any grade of OXLIPN (n = 36) were similar. Likewise, among patients experiencing OXLIPN, insignificant differences in R19K genotypes were revealed between those with grade I versus grade II neurotoxicity. Conclusion: Our study failed to provide evidence to support a causal relationship between the SCN2A R19K polymorphism and OXLIPN. Copyright (C) 2009 S. Karger AG, Basel