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 2009 S. Karger AG, Basel.