Advances in polymorphisms of genes associated with oxaliplatin-induced peripheral neurotoxicity
- VernacularTitle:奥沙利铂所致周围神经毒性相关基因多态性研究进展
- Author:
Yu CUI
1
;
Menglu LI
1
;
Shan XU
2
Author Information
1. College of Pharmacy，Dalian Medical University，Liaoning Dalian 116000，China;Dept. of Pharmacy，the Third Affiliated Hospital of Nanjing Medical University （Changzhou Second People’s Hospital），Jiangsu Changzhou 213000，China
2. Dept. of Pharmacy，the Third Affiliated Hospital of Nanjing Medical University （Changzhou Second People’s Hospital），Jiangsu Changzhou 213000，China
- Publication Type:Journal Article
- Keywords:
oxaliplatin;
peripheral neurotoxicity;
genetic polymorphisms;
transporter genes;
metabolic enzymes;
DNA repair
- From:
China Pharmacy
2026;37(1):130-136
- CountryChina
- Language:Chinese
-
Abstract:
Peripheral neurotoxicity represents one of the most severe dose-limiting adverse reactions associated with oxaliplatin， with genetic polymorphisms playing a significant role in oxaliplatin-induced peripheral neuropathy （OIPN）. OIPN can be categorized as acute or chronic based on onset timing. The former presents clinically as sensory abnormalities or even motor disorders， while the latter presents clinically as limb sensory disorders that persist， numbness or pain in the hands and feet. The transporter genes OCT2， OCTN2， and NHE1 may be implicated in OIPN； drug-metabolizing enzyme gene GSTP1 Ile105Val， DPYD rs1801265， voltage-gated sodium channel （NaV） gene SCN4A rs2302237， SCN9A rs6746030， SCN10A rs12632942， and other associated genes such as HLA-G rs1610696， rs371194629 and CCNH rs2230641， rs3093816 are associated with severe OIPN. Conversely， DNA repair-related gene XRCC1 rs23885， NaV gene SCN9A rs3750904， rs12478318 and rs6754031 are associated with reduced OIPN risk. In the future， the genetic research findings on OIPN can be translated into clinical applications， ultimately achieving individualized precision medicine for patients.
