Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, VIC, Australia.
Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, VIC, Australia.
Breast Cancer Res. 2022 Sep 6;24(1):59. doi: 10.1186/s13058-022-01554-8.
DNA methylation in blood may reflect adverse exposures accumulated over the lifetime and could therefore provide potential improvements in the prediction of cancer risk. A substantial body of research has shown associations between epigenetic aging and risk of disease, including cancer. Here we aimed to study epigenetic measures of aging and lifestyle-related factors in association with risk of breast cancer.
Using data from four prospective case-control studies nested in three cohorts of European ancestry participants, including a total of 1,655 breast cancer cases, we calculated three methylation-based measures of lifestyle factors (body mass index [BMI], tobacco smoking and alcohol consumption) and seven measures of epigenetic aging (Horvath-based, Hannum-based, PhenoAge and GrimAge). All measures were regression-adjusted for their respective risk factors and expressed per standard deviation (SD). Odds ratios (OR) and 95% confidence intervals (CI) were calculated using conditional or unconditional logistic regression and pooled using fixed-effects meta-analysis. Subgroup analyses were conducted by age at blood draw, time from blood sample to diagnosis, oestrogen receptor-positivity status and tumour stage.
None of the measures of epigenetic aging were associated with risk of breast cancer in the pooled analysis: Horvath 'age acceleration' (AA): OR per SD = 1.02, 95%CI: 0.95-1.10; AA-Hannum: OR = 1.03, 95%CI:0.95-1.12; PhenoAge: OR = 1.01, 95%CI: 0.94-1.09 and GrimAge: OR = 1.03, 95%CI: 0.94-1.12, in models adjusting for white blood cell proportions, body mass index, smoking and alcohol consumption. The BMI-adjusted predictor of BMI was associated with breast cancer risk, OR per SD = 1.09, 95%CI: 1.01-1.17. The results for the alcohol and smoking methylation-based predictors were consistent with a null association. Risk did not appear to substantially vary by age at blood draw, time to diagnosis or tumour characteristics.
We found no evidence that methylation-based measures of aging, smoking or alcohol consumption were associated with risk of breast cancer. A methylation-based marker of BMI was associated with risk and may provide insights into the underlying associations between BMI and breast cancer.
血液中的 DNA 甲基化可能反映一生中积累的不利暴露,因此可能会提高癌症风险预测的准确性。大量研究表明,表观遗传衰老与疾病风险之间存在关联,包括癌症。本研究旨在研究与乳腺癌风险相关的表观遗传衰老和与生活方式相关的因素。
本研究使用了来自三个欧洲血统参与者队列中四个前瞻性病例对照研究的嵌套数据,共包括 1655 例乳腺癌病例,我们计算了三种基于甲基化的生活方式因素(体重指数 [BMI]、吸烟和饮酒)和七种基于表观遗传的衰老指标(Horvath 基础、Hannum 基础、PhenoAge 和 GrimAge)。所有指标均根据各自的危险因素进行回归调整,并以标准差(SD)表示。使用条件或无条件逻辑回归计算比值比(OR)和 95%置信区间(CI),并使用固定效应荟萃分析进行汇总。亚组分析按采血时的年龄、从采血到诊断的时间、雌激素受体阳性状态和肿瘤分期进行。
在汇总分析中,没有一种基于表观遗传的衰老指标与乳腺癌风险相关:Horvath“年龄加速”(AA):每 SD 的 OR=1.02,95%CI:0.95-1.10;AA-Hannum:OR=1.03,95%CI:0.95-1.12;PhenoAge:OR=1.01,95%CI:0.94-1.09;GrimAge:OR=1.03,95%CI:0.94-1.12,在调整白细胞比例、体重指数、吸烟和饮酒的模型中。调整后的 BMI 预测因子与乳腺癌风险相关,每 SD 的 OR=1.09,95%CI:1.01-1.17。酒精和吸烟的甲基化预测因子的结果与零关联一致。风险似乎不会因采血时的年龄、诊断时间或肿瘤特征而有实质性差异。
我们没有发现基于甲基化的衰老、吸烟或饮酒指标与乳腺癌风险相关的证据。BMI 的基于甲基化的标志物与风险相关,可能为 BMI 与乳腺癌之间的潜在关联提供见解。