Replication of Genetic Polymorphisms Reported to Be Associated with Taxane-Related Sensory Neuropathy in Patients with Early Breast Cancer Treated with Paclitaxel—Response

@article{Guo2015ReplicationOG,
  title={Replication of Genetic Polymorphisms Reported to Be Associated with Taxane-Related Sensory Neuropathy in Patients with Early Breast Cancer Treated with Paclitaxel—Response},
  author={Qi Guo and Jean E. Abraham and Carlos Caldas and Helena Earl and Paul D. P. Pharoah},
  journal={Clinical Cancer Research},
  year={2015},
  volume={21},
  pages={3094 - 3094}
}
We thank Apellaniz-Ruiz and colleagues ([1][1]) for their interest in our study ([2][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][ 
Current opinion on the pharmacogenomics of paclitaxel-induced toxicity
TLDR
Genes in paclitaxel’s pharmacokinetic pathways could not provide consistent results in any of its associated toxicities, and there is a need to dig deeper into toxicity-development mechanisms and personal vulnerability factors, rather than targeting only the genes suspected to affect drug exposure.

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Replication of Genetic Polymorphisms Reported to Be Associated with Taxane-Related Sensory Neuropathy in Patients with Early Breast Cancer Treated with Paclitaxel—Letter
TLDR
The pharmacogenetic study by Abraham and colleagues reporting SNPs associated with paclitaxel-induced neuropathy is an important clinical problem for taxanes, vinca-alkaloids, platinum compounds.
Replication of Genetic Polymorphisms Reported to Be Associated with Taxane-Related Sensory Neuropathy in Patients with Early Breast Cancer Treated with Paclitaxel
TLDR
Strong evidence is found that SNPs within genes in taxane pharmacokinetic and pharmacodynamic pathways contribute to TRSN risk, however, a large proportion of the inter-individual variability in TRSn remains unexplained.
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