We thank Apellániz-Ruiz and colleagues (1) for their interest in our study (2) and for their thoughtful comments.
Both maximum taxane-related sensory neuropathy (TRSN) and cumulative dose TRSN analysis have been conducted under an additive genetic model, as described in our article (2), for three single-nucleotide polymorphisms (SNP; rs7349683, rs301927, and rs209709). We have now performed both analyses under a recessive model for these SNPs.
The SNP rs7349683 in EPHA5 was associated with decreased risk of both maximum TRSN (T-allele homozygote, OR, 0.57; 95% CI, 0.38–0.87; P = 0.009) and cumulative TRSN (T-allele homozygote, HR, 0.68; 95% CI, 0.48–0.97; P = 0.035). This is consistent with the results previously reported (1).
However, rs301927 in EPHA6 was associated with decreased risk of both maximum TRSN (A-allele homozygote, OR, 0.68; 95% CI, 0.52–0.89; P = 0.004) and cumulative TRSN (A-allele homozygote, HR, 0.71; 95% CI, 0.57–0.88; P = 0.002). This association had a discordant direction of effect to the results reported in the article (1). We found no evidence of association for rs209709 in EPHA8 under a recessive model (P = 0.97 for maximum TRSN and P = 0.94 for cumulative TRSN).
See the original Letter to the Editor, p. 3092
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.