Furberg Helena, Millikan R C, Geradts J, Gammon M D, Dressler L G, Ambrosone C B, Newman B
Derald H. Ruttenberg Cancer Center, Mt. Sinai School of Medicine. New York, New York 10029, USA.
Cancer Epidemiol Biomarkers Prev. 2002 Sep;11(9):829-35.
Findings from studies of cigarette smoking and low-dose ionizing radiation exposure and breast cancer are unclear. Laboratory studies indicate that both exposures can cause DNA damage, potentially increasing cancer risk if such mutations occur in growth control genes, such as p53. We examined the potential etiologic heterogeneity of breast cancer by evaluating whether associations between cigarette smoking and low-dose ionizing radiation and breast cancer differed by p53 protein expression status. Data were obtained from the Carolina Breast Cancer Study, a population-based, case-control study conducted among African-American and white women ages 20-74 years. Questionnaire data were available from 861 women with incident, primary invasive breast cancer and 790 community-based controls. p53 immunostaining was performed on tissue from 683 women with breast cancer; 46% were classified as p53+. Two separate unconditional logistic regression models were used to calculate odds ratios (ORs) for p53+ and p53- breast cancer, as compared with controls, in relation to smoking and low-dose ionizing radiation exposure. Smoking was not differentially associated with p53+ or p53- breast cancer, even when duration, dose, and passive smoking status were considered. Exposure to individual sources of radiation did not differ for p53+ and p53- breast cancers. However, ORs for combined exposure to chest X-rays and occupational radiation were higher for p53+ [OR, 2.2; 95% confidence interval (CI), 1.0-5.3] than p53- breast cancer (OR, 1.2; 95% CI, 0.5-3.4). Combined exposure to radiation from other medical sources as well as occupational exposure was also higher for p53+ (OR, 3.7; 95% CI, 0.8-16.8) than for p53- breast cancer (OR, 1.7; 95% CI, 0.3-10.5). Although preliminary, our results suggest that exposure to multiple sources of low-dose ionizing radiation may contribute to the development of p53+ breast cancer.
关于吸烟、低剂量电离辐射暴露与乳腺癌之间关系的研究结果尚不清楚。实验室研究表明,这两种暴露都可导致DNA损伤,如果此类突变发生在生长控制基因(如p53)中,则可能增加癌症风险。我们通过评估吸烟和低剂量电离辐射与乳腺癌之间的关联是否因p53蛋白表达状态而异,来研究乳腺癌潜在的病因异质性。数据来自卡罗来纳乳腺癌研究,这是一项针对年龄在20 - 74岁的非裔美国女性和白人女性开展的基于人群的病例对照研究。我们获取了861例原发性浸润性乳腺癌患者及790例社区对照的问卷数据。对683例乳腺癌患者的组织进行了p53免疫染色;46%被归类为p53阳性。使用两个独立的非条件逻辑回归模型,计算与对照组相比,p53阳性和p53阴性乳腺癌患者在吸烟和低剂量电离辐射暴露方面的比值比(OR)。即使考虑吸烟持续时间、剂量和被动吸烟状态,吸烟与p53阳性或p53阴性乳腺癌之间的关联也无差异。p53阳性和p53阴性乳腺癌患者接触单个辐射源的情况并无不同。然而,p53阳性乳腺癌患者(OR,2.2;95%置信区间[CI],1.0 - 5.3)联合暴露于胸部X线和职业辐射的OR高于p53阴性乳腺癌患者(OR,1.2;95% CI,0.5 - 3.4)。p53阳性乳腺癌患者(OR,3.7;95% CI,0.8 - 16.8)联合暴露于其他医疗源辐射以及职业辐射的情况也高于p53阴性乳腺癌患者(OR,1.7;95% CI,0.3 - 10.5)。尽管是初步结果,但我们的研究结果表明,暴露于多种低剂量电离辐射源可能促使p53阳性乳腺癌的发生。