摘要
目的研究胃癌患者SLCO1B3基因多态性与多西他赛化疗引起的骨髓抑制的相关性。方法共纳入61例接受多西他赛化疗的胃癌患者,采用飞行时间质谱法检测SLCO1B3基因多态性,研究不同SLCO1B3基因分型与骨髓抑制风险发生的相关性。结果 SLCO1B3 AA型42例(68.9%),AG型16例(26.2%),GG型有3例(4.9%)。Logistic回归分析发现,不同SLCO1B3基因型与骨髓抑制发生风险之间无统计学差异[共显性遗传模型:杂合子(AG)vs.野生型(AA),优势比(OR)=0.341,95%置信区间(95%CI):0.101-1.156;纯合子(GG)vs.(AA),OR=0.375,95%CI:0.031-4.465;显性遗传模型:(AG+GG)vs.AA,OR=0.346,95%CI=0.110-1.087;隐性遗传模型:GG vs.(AG+AA),OR=0.500,95%CI=0.043-5.823]。进一步对患者各临床特征与骨髓抑制发生风险之间进行统计学分析,结果发现二者之间也不存在相关性。结论 SLCO1B3基因多态性不能作为预测本组人群多西他赛化疗相关骨髓抑制的基因预测指标。
Objective To study the association between SLCO1B3 gene polymorphism and docetaxel-induced myelosuppression in patients with gastric cancer. Methods A total of 61 patients with gastric cancer who received docetaxel chemotherapy were enrolled in this study. The SLCO1B3 gene polymorphism was detected by time-of-flight mass spectrometry,and the correlation between different SLCO1B3 genotyping and myelosuppression risk was studied. Results There were 42 cases（ 68. 9%） of STCO1B3 AA type,16 cases（ 26. 2%） of AG type and 3 cases（ 4. 9%） of GG type. Logistic regression analysis showed that there was no significant difference between the different SLCO1B3 genotype and the risk of myelosuppression. [Codominant genetic model： heterozygote（ AG） vs. wild type（ AA）,odds ratio（ OR） = 0. 341,95% confidence interval（ 95%CI） ： 0. 101-1. 156; homozygote（ GG） vs.（ AA）,OR = 0. 375,95% CI： 0. 031-4. 465; dominant genetic model：（ AG ＋ GG）vs. AA,OR = 0. 346,95% CI = 0. 110-1. 087; recessive genetic model： GG vs.（ AG ＋ AA）,OR = 0. 500,95% CI = 0. 043-5. 823]. Further analysis of the clinical characteristics of patients and the risk of myelosuppression between the statistical analysis found that there is no correlation between the two. Conclusion SLCO1B3 gene polymorphism can not be used as a predictor of gene prediction of docetaxel-associated myelosuppression in this group.
出处
《临床合理用药杂志》
2017年第26期5-7,共3页
Chinese Journal of Clinical Rational Drug Use
基金
江苏省医药协会奥赛康临床药学研究项目(No:KY201379)
