Yongzhen Chen1, Fang Fang2, Kelley M Kidwell2,3, Kiran Vangipuram4, Lauren A Marcath5, Christina L Gersch3,6, James M Rae3,6, Daniel F Hayes3,6, Ellen M Lavoie Smith7, N Lynn Henry3,8, Andreas S Beutler9,10, Daniel L Hertz3,4. 1. College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA. 2. Department of Biostatistics, University of Michigan School of Public Health, Ann Arbor, MI 48109, USA. 3. University of Michigan Rogel Cancer Center, Ann Arbor, MI 48109. 4. Department of Clinical Pharmacy, University of Michigan College of Pharmacy, Ann Arbor, MI 48109, USA. 5. Department of Pharmacotherapy, Washington State University College of Pharmacy & Pharmaceutical Sciences, Pullman, WA 99164, USA. 6. Department of Internal Medicine, Division of Hematology/Oncology, University of Michigan Medical School, Ann Arbor, MI 48109, USA. 7. Department of Health Behavior & Biological Sciences, University of Michigan School of Nursing, Ann Arbor, MI 48109, USA. 8. Department of Internal Medicine, Division of Oncology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA. 9. Department of Anesthesiology, Mayo Clinic, Rochester, MN 55902, USA. 10. Department of Oncology, Mayo Clinic, Rochester, MN 55902, USA.
Abstract
Aim: This study explored whether inherited variants in genes causing the hereditary neuropathy condition Charcot-Marie-Tooth disease are associated with sensitivity to paclitaxel-induced peripheral neuropathy (PN). Patients & methods: Hereditary neuropathy genes previously associated with risk of paclitaxel-induced PN were sequenced in paclitaxel-treated patients. Eight putative genetic predictors in five hereditary neuropathy genes (ARHGEF10, SBF2, FGD4, FZD3 and NXN) were tested for association with PN sensitivity after accounting for systemic exposure and clinical variables. Results: FZD3 rs7833751, a proxy for rs7001034, decreased PN sensitivity (additive model, β = -0.41; 95% CI: -0.66 to -0.17; p = 0.0011). None of the other genetic predictors were associated with PN sensitivity. Conclusion: Our results support prior evidence that FZD3 rs7001034 is protective of PN and may be useful for individualizing paclitaxel treatment to prevent PN.
Aim: This study explored whether inherited variants in genes causing the hereditary neuropathy condition Charcot-Marie-Tooth disease are associated with sensitivity to paclitaxel-induced peripheral neuropathy (PN). Patients & methods: Hereditary neuropathy genes previously associated with risk of paclitaxel-induced PN were sequenced in paclitaxel-treated patients. Eight putative genetic predictors in five hereditary neuropathy genes (ARHGEF10, SBF2, FGD4, FZD3 and NXN) were tested for association with PN sensitivity after accounting for systemic exposure and clinical variables. Results:FZD3rs7833751, a proxy for rs7001034, decreased PN sensitivity (additive model, β = -0.41; 95% CI: -0.66 to -0.17; p = 0.0011). None of the other genetic predictors were associated with PN sensitivity. Conclusion: Our results support prior evidence that FZD3rs7001034 is protective of PN and may be useful for individualizing paclitaxel treatment to prevent PN.
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