Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Breast Cancer Res Treat. 2013 Nov;142(2):389-98. doi: 10.1007/s10549-013-2739-z. Epub 2013 Oct 29.
Pre-clinical and epidemiologic studies provide rationale for evaluating lipophilic statins for breast cancer prevention. We conducted a single-arm, biomarker modulation trial of lovastatin among women with increased risk of breast cancer. Eligibility criteria included a deleterious germline mutation in BRCA1, BRCA2, CDH1, or TP53; lifetime breast cancer risk of ≥20 % as estimated by the Claus model; or personal history of estrogen receptor and progesterone receptor-negative breast cancer. Participants received 40 mg of lovastatin orally twice daily for 6 months. We evaluated the following biomarkers before and after lovastatin use: breast duct cytology (primary endpoint), serum lipids, C-reactive protein, insulin-like growth factor-1, IGF binding protein-3, lipid peroxidation, oxidative DNA damage, 3-hydroxy-3-methylglutaryl CoA reductase genotype, and mammographic density. Thirty women were enrolled, and 26 (86.7 %) completed the study. For the primary endpoint of changes in breast duct cytology sampled by random periareolar fine needle aspiration, most participants [57.7 %, 95 % confidence interval (CI) 38.9-74.5 %] showed no change after lovastatin; 19.2 % (CI 8.1-38.3 %) had a favorable change in cytology, 7.7 % (95 % CI 1.0-25.3 %) had an unfavorable change, and 15.4 % (95 % CI 5.5-34.2 %) had equivocal results due to acellular specimens, usually after lovastatin. No significant changes were observed in secondary biomarker endpoints. The study was generally well-tolerated: 4 (13.3 %) participants did not complete the study, and one (3.8 %) required a dose reduction. This trial was technically feasible, but demonstrated no significant biomarker modulation; contributing factors may include insufficient sample size, drug dose and/or duration. The results are inconclusive and do not exclude a favorable effect on breast cancer risk.
临床前和流行病学研究为评估亲脂性他汀类药物预防乳腺癌提供了依据。我们进行了一项单臂、生物标志物调节试验,在乳腺癌风险增加的女性中使用洛伐他汀。入选标准包括 BRCA1、BRCA2、CDH1 或 TP53 的有害种系突变;根据 Claus 模型估计终生乳腺癌风险≥20%;或个人史雌激素受体和孕激素受体阴性乳腺癌。参与者每天口服洛伐他汀 40mg,每日两次,共 6 个月。我们在使用洛伐他汀前后评估了以下生物标志物:乳腺导管细胞学(主要终点)、血清脂质、C 反应蛋白、胰岛素样生长因子-1、IGF 结合蛋白-3、脂质过氧化、氧化 DNA 损伤、3-羟基-3-甲基戊二酰辅酶 A 还原酶基因型和乳腺密度。共纳入 30 名女性,26 名(86.7%)完成了研究。对于随机乳晕旁细针抽吸活检采集的乳腺导管细胞学变化的主要终点,大多数参与者[57.7%,95%置信区间(CI)38.9-74.5%]在洛伐他汀治疗后无变化;19.2%(CI 8.1-38.3%)的细胞学有良好变化,7.7%(95%CI 1.0-25.3%)的细胞学有不良变化,15.4%(95%CI 5.5-34.2%)的细胞学结果因细胞较少而不确定,通常在洛伐他汀治疗后。次要生物标志物终点未见明显变化。该研究总体上耐受性良好:4 名(13.3%)参与者未完成研究,1 名(3.8%)需要减少剂量。该试验在技术上是可行的,但未显示出明显的生物标志物调节作用;可能的影响因素包括样本量不足、药物剂量和/或持续时间。结果不确定,不能排除对乳腺癌风险的有利影响。