Infante-Rivard Claire
Department of Epidemiology, Biostatistics and Occupational Health, Faculty of Medicine, McGill University, 1130 Pine Avenue West, Montreal, Province of Québec, Canada, H3A 1A3.
Health Phys. 2003 Jul;85(1):60-4. doi: 10.1097/00004032-200307000-00012.
A model for childhood leukemia proposes that characteristic chromosomal translocations can arise in utero and that for most cases a second hit occurring postnatally will be necessary. Possible causal mechanisms for leukemias are environmental factors such as ionizing radiation from x rays and inherited susceptibility from polymorphisms in DNA repair genes. We performed a case-control study of childhood acute lymphoblastic leukemia measuring reported postnatal x rays in 701 cases aged 0-14 y and in as many population-based controls matched on age and sex. In addition we performed a case-only study in 207 cases to evaluate the interaction between x ray exposure and polymorphisms in DNA repair genes. There was an increase in risk of leukemia with number of x rays: the adjusted odds ratio for two or more x rays vs. none was 1.48 (95% confidence interval: 1.11-1.97). That risk was slightly higher among girls (odds ratio = 1.67). A polymorphism in the APE gene (ex 5) involved in the base excision repair system was suggestive of an increased risk among boys and a reduced risk among girls. HMLH1 (ex 8), a mismatch repair gene, was associated with reduction of risk among girls. Results from the genetic data are still preliminary and must be interpreted with caution especially because of the relatively small number of genotyped cases. However, ionizing radiation from x rays as well as polymorphisms in DNA repair genes are plausible risk factors for childhood leukemia and should be studied more.
一种儿童白血病模型提出，特征性染色体易位可能在子宫内发生，且对于大多数病例而言，出生后发生的第二次打击将是必要的。白血病可能的致病机制包括环境因素，如来自X射线的电离辐射，以及DNA修复基因多态性导致的遗传易感性。我们开展了一项儿童急性淋巴细胞白血病的病例对照研究，测量了701例0至14岁病例以及年龄和性别匹配的同样多的基于人群的对照者报告的出生后X射线暴露情况。此外，我们对207例病例进行了病例对照研究，以评估X射线暴露与DNA修复基因多态性之间的相互作用。白血病风险随X射线照射次数增加：两次或更多次X射线照射与无照射相比，校正后的比值比为1.48（95%置信区间：1.11 - 1.97）。女孩中的该风险略高（比值比 = 1.67）。参与碱基切除修复系统的APE基因（第5外显子）中的一种多态性提示男孩风险增加而女孩风险降低。错配修复基因HMLH1（第8外显子）与女孩风险降低有关。遗传数据的结果仍属初步，必须谨慎解读，特别是因为基因分型病例数量相对较少。然而，X射线的电离辐射以及DNA修复基因的多态性是儿童白血病可能的风险因素，应进一步开展研究。
