Palmer R G, Smith-Burchnell C A, Dore C J, Denman A M
Br J Rheumatol. 1986 Nov;25(4):376-9. doi: 10.1093/rheumatology/25.4.376.
Cells with mutations at the hypoxanthine-guanine phosphoribosyl transferase (HPRT) locus may be detected in vitro by their resistance to the toxic effects of thioguanine. We have assessed HPRT mutants in peripheral blood lymphocytes of patients with connective tissue diseases who have been treated for long periods with cytotoxic drugs. The results from patients treated with cyclophosphamide were abnormal suggesting the presence of drug-induced mutations. The results from patients treated with chlorambucil or azathioprine did not differ from controls--either these drugs have not induced mutations or, more likely, the technique is not sufficiently sensitive to detect them. These possibilities are discussed. Specific mutations induced by cytotoxic drugs in patients with connective tissue diseases have not been previously recorded.
次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶（HPRT）位点发生突变的细胞可在体外通过其对硫鸟嘌呤毒性作用的抗性来检测。我们评估了长期接受细胞毒性药物治疗的结缔组织病患者外周血淋巴细胞中的HPRT突变体。接受环磷酰胺治疗的患者结果异常，提示存在药物诱导的突变。接受苯丁酸氮芥或硫唑嘌呤治疗的患者结果与对照组无差异——要么这些药物未诱导突变，要么更有可能的是，该技术不够灵敏，无法检测到这些突变。对这些可能性进行了讨论。此前尚未记录到结缔组织病患者中细胞毒性药物诱导的特定突变。
