Translational Sciences Section, Jonsson Comprehensive Cancer Center, School of Nursing, University of California, Los Angeles, 700 Tiverton Ave, 3-264 Factor Building, Los Angeles, CA, 90095, USA.
Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Sci Rep. 2021 Jan 13;11(1):1058. doi: 10.1038/s41598-020-80197-1.
Molecular and genetic immune-related pathways connected to breast cancer and lifestyles in postmenopausal women are not fully characterized. In this study, we explored the role of pro-inflammatory cytokines such as C-reactive protein (CRP) and interleukin-6 (IL-6) in those pathways at the genome-wide level. With single-nucleotide polymorphisms (SNPs) in the biomarkers and lifestyles together, we further constructed risk profiles to improve predictability for breast cancer. Our earlier genome-wide association gene-environment interaction study used large cohort data from the Women's Health Initiative Database for Genotypes and Phenotypes Study and identified 88 SNPs associated with CRP and IL-6. For this study, we added an additional 68 SNPs from previous GWA studies, and together with 48 selected lifestyles, evaluated for the association with breast cancer risk via a 2-stage multimodal random survival forest and generalized multifactor dimensionality reduction methods. Overall and in obesity strata (by body mass index, waist, waist-to-hip ratio, exercise, and dietary fat intake), we identified the most predictive genetic and lifestyle variables. Two SNPs (SALL1 rs10521222 and HLA-DQA1 rs9271608) and lifestyles, including alcohol intake, lifetime cumulative exposure to estrogen, and overall and visceral obesity, are the most common and strongest predictive markers for breast cancer across the analyses. The risk profile that combined those variables presented their synergistic effect on the increased breast cancer risk in a gene-lifestyle dose-dependent manner. Our study may contribute to improved predictability for breast cancer and suggest potential interventions for the women with the risk genotypes and lifestyles to reduce their breast cancer risk.
分子和遗传免疫相关途径与绝经后妇女的乳腺癌和生活方式有关,但尚未完全阐明。在这项研究中,我们在全基因组水平上探讨了促炎细胞因子(如 C 反应蛋白(CRP)和白细胞介素 6(IL-6))在这些途径中的作用。我们将生物标志物和生活方式中的单核苷酸多态性(SNP)结合起来,进一步构建风险模型,以提高乳腺癌的预测能力。我们之前的全基因组关联基因-环境相互作用研究使用了来自妇女健康倡议数据库的基因型和表型研究的大型队列数据,鉴定了与 CRP 和 IL-6 相关的 88 个 SNP。在这项研究中,我们添加了来自之前全基因组关联研究的另外 68 个 SNP,以及 48 个选定的生活方式,通过两阶段多模态随机生存森林和广义多因素降维方法评估其与乳腺癌风险的关联。总体而言,在肥胖分层(根据体重指数、腰围、腰臀比、运动和饮食脂肪摄入)中,我们确定了最具预测性的遗传和生活方式变量。两个 SNP(SALL1 rs10521222 和 HLA-DQA1 rs9271608)和生活方式,包括饮酒、雌激素终生累积暴露、整体和内脏肥胖,是跨分析中最常见和最强的乳腺癌预测标志物。结合这些变量的风险模型表现出基因-生活方式剂量依赖性协同作用,增加了乳腺癌风险。我们的研究可能有助于提高乳腺癌的预测能力,并为具有风险基因型和生活方式的女性提供潜在的干预措施,以降低其乳腺癌风险。