Johnson Kevin C, Houseman E Andres, King Jessica E, Christensen Brock C
Department of Epidemiology, Geisel School of Medicine at Dartmouth, Lebanon, NH, 03756, USA.
Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Lebanon, NH, 03756, USA.
Breast Cancer Res. 2017 Jul 10;19(1):81. doi: 10.1186/s13058-017-0873-y.
The underlying biological mechanisms through which epidemiologically defined breast cancer risk factors contribute to disease risk remain poorly understood. Identification of the molecular changes associated with cancer risk factors in normal tissues may aid in determining the earliest events of carcinogenesis and informing cancer prevention strategies.
Here we investigated the impact cancer risk factors have on the normal breast epigenome by analyzing DNA methylation genome-wide (Infinium 450 K array) in cancer-free women from the Susan G. Komen Tissue Bank (n = 100). We tested the relation of established breast cancer risk factors, age, body mass index, parity, and family history of disease, with DNA methylation adjusting for potential variation in cell-type proportions.
We identified 787 cytosine-guanine dinucleotide (CpG) sites that demonstrated significant associations (Q value <0.01) with subject age. Notably, DNA methylation was not strongly associated with the other evaluated breast cancer risk factors. Age-related DNA methylation changes are primarily increases in methylation enriched at breast epithelial cell enhancer regions (P = 7.1E-20), and binding sites of chromatin remodelers (MYC and CTCF). We validated the age-related associations in two independent populations, using normal breast tissue samples (n = 18) and samples of normal tissue adjacent to tumor tissue (n = 97). The genomic regions classified as age-related were more likely to be regions altered in both pre-invasive (n = 40, P = 3.0E-03) and invasive breast tumors (n = 731, P = 1.1E-13).
DNA methylation changes with age occur at regulatory regions, and are further exacerbated in cancer, suggesting that age influences breast cancer risk in part through its contribution to epigenetic dysregulation in normal breast tissue.
从流行病学角度定义的乳腺癌风险因素导致疾病风险的潜在生物学机制仍未得到充分了解。识别正常组织中与癌症风险因素相关的分子变化,可能有助于确定癌变的最早事件,并为癌症预防策略提供依据。
在此,我们通过对来自苏珊·科曼组织库的无癌女性(n = 100)进行全基因组DNA甲基化分析(Infinium 450K芯片),研究了癌症风险因素对正常乳腺表观基因组的影响。我们测试了已确定的乳腺癌风险因素、年龄、体重指数、生育状况和家族病史与DNA甲基化之间的关系,并对细胞类型比例的潜在差异进行了校正。
我们鉴定出787个胞嘧啶-鸟嘌呤二核苷酸(CpG)位点,这些位点与受试者年龄显示出显著关联(Q值<0.01)。值得注意的是,DNA甲基化与其他评估的乳腺癌风险因素没有强烈关联。与年龄相关的DNA甲基化变化主要是乳腺上皮细胞增强子区域(P = 7.1E - 20)以及染色质重塑因子(MYC和CTCF)结合位点处的甲基化增加。我们使用正常乳腺组织样本(n = 18)和肿瘤组织旁正常组织样本(n = 97)在两个独立人群中验证了与年龄相关的关联。被归类为与年龄相关的基因组区域在乳腺原位癌(n = 40,P = 3.0E - 03)和浸润性乳腺癌(n = 731,P = 1.1E - 13)中更有可能发生改变。
随着年龄增长,DNA甲基化变化发生在调控区域,并且在癌症中进一步加剧,这表明年龄部分地通过对正常乳腺组织表观遗传失调的影响来影响乳腺癌风险。