Iyer L, Ratain M J
Committee on Clinical Pharmacology, University of Chicago, Illinois 60637, USA.
Eur J Cancer. 1998 Sep;34(10):1493-9. doi: 10.1016/s0959-8049(98)00230-5.
Cancer chemotherapy is limited by significant inter-individual variations in responses and toxicities. Such variations are often due to genetic alterations in drug metabolising enzymes (pharmacokinetic polymorphisms) or receptor expression (pharmacodynamic polymorphisms). Pharmacogenetic screening prior to anticancer drug administration may lead to identification of specific populations predisposed to drug toxicity or poor drug responses. The role of polymorphisms in specific enzymes, such as thiopurine S-methyltransferases (TPMT), dihydropyrimidine dehydrogenase (DPD), aldehyde dehydrogenases (ALDH), glutathione S-transferases (GST), uridine diphosphate glucuronosyl-transferases (UGTs) and cytochrome P450 (CYP 450) enzymes in cancer therapy are discussed in this review.
癌症化疗受到个体间反应和毒性显著差异的限制。此类差异通常归因于药物代谢酶（药代动力学多态性）或受体表达（药效动力学多态性）的基因改变。在给予抗癌药物之前进行药物遗传学筛查，可能会识别出易发生药物毒性或药物反应不佳的特定人群。本文综述了特定酶的多态性在癌症治疗中的作用，如硫嘌呤S-甲基转移酶（TPMT）、二氢嘧啶脱氢酶（DPD）、醛脱氢酶（ALDH）、谷胱甘肽S-转移酶（GST）、尿苷二磷酸葡萄糖醛酸转移酶（UGT）和细胞色素P450（CYP 450）酶。
