Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA 02215, USA.
Mod Pathol. 2013 Apr;26(4):465-84. doi: 10.1038/modpathol.2012.214. Epub 2013 Jan 11.
Epigenetics acts as an interface between environmental/exogenous factors, cellular responses, and pathological processes. Aberrant epigenetic signatures are a hallmark of complex multifactorial diseases (including neoplasms and malignancies such as leukemias, lymphomas, sarcomas, and breast, lung, prostate, liver, and colorectal cancers). Epigenetic signatures (DNA methylation, mRNA and microRNA expression, etc) may serve as biomarkers for risk stratification, early detection, and disease classification, as well as targets for therapy and chemoprevention. In particular, DNA methylation assays are widely applied to formalin-fixed, paraffin-embedded archival tissue specimens as clinical pathology tests. To better understand the interplay between etiological factors, cellular molecular characteristics, and disease evolution, the field of 'molecular pathological epidemiology (MPE)' has emerged as an interdisciplinary integration of 'molecular pathology' and 'epidemiology'. In contrast to traditional epidemiological research including genome-wide association studies (GWAS), MPE is founded on the unique disease principle, that is, each disease process results from unique profiles of exposomes, epigenomes, transcriptomes, proteomes, metabolomes, microbiomes, and interactomes in relation to the macroenvironment and tissue microenvironment. MPE may represent a logical evolution of GWAS, termed 'GWAS-MPE approach'. Although epigenome-wide association study attracts increasing attention, currently, it has a fundamental problem in that each cell within one individual has a unique, time-varying epigenome. Having a similar conceptual framework to systems biology, the holistic MPE approach enables us to link potential etiological factors to specific molecular pathology, and gain novel pathogenic insights on causality. The widespread application of epigenome (eg, methylome) analyses will enhance our understanding of disease heterogeneity, epigenotypes (CpG island methylator phenotype, LINE-1 (long interspersed nucleotide element-1; also called long interspersed nuclear element-1; long interspersed element-1; L1) hypomethylation, etc), and host-disease interactions. In this article, we illustrate increasing contribution of modern pathology to broader public health sciences, which attests pivotal roles of pathologists in the new integrated MPE science towards our ultimate goal of personalized medicine and prevention.
表观遗传学作为环境/外源性因素、细胞反应和病理过程之间的接口。异常的表观遗传特征是复杂多因素疾病(包括肿瘤和恶性肿瘤,如白血病、淋巴瘤、肉瘤以及乳腺癌、肺癌、前列腺癌、肝癌和结直肠癌)的标志。表观遗传特征(DNA 甲基化、mRNA 和 microRNA 表达等)可作为风险分层、早期检测和疾病分类的生物标志物,以及治疗和化学预防的靶点。特别是,DNA 甲基化测定广泛应用于福尔马林固定、石蜡包埋的存档组织标本作为临床病理学检测。为了更好地理解病因因素、细胞分子特征和疾病演变之间的相互作用,“分子病理流行病学 (MPE)”领域作为“分子病理学”和“流行病学”的跨学科整合而出现。与包括全基因组关联研究 (GWAS) 在内的传统流行病学研究不同,MPE 基于独特的疾病原理,即每个疾病过程都与外显子组、表观基因组、转录组、蛋白质组、代谢组、微生物组和相互作用组与宏观环境和组织微环境的独特谱有关。MPE 可能代表 GWAS 的逻辑演进,称为“GWAS-MPE 方法”。尽管全基因组范围内的表观遗传关联研究引起了越来越多的关注,但目前它存在一个根本问题,即个体内的每个细胞都具有独特的、随时间变化的表观基因组。具有与系统生物学相似的概念框架,整体 MPE 方法使我们能够将潜在的病因因素与特定的分子病理学联系起来,并获得关于因果关系的新的发病机制见解。广泛应用表观基因组(例如,甲基组)分析将增强我们对疾病异质性、表观基因型(CpG 岛甲基化表型、LINE-1(长散布核苷酸元件-1;也称为长散布核元件-1;长散布元件-1;L1)低甲基化等)和宿主-疾病相互作用的理解。在本文中,我们说明了现代病理学对更广泛的公共卫生科学的贡献不断增加,这证明了病理学家在新的综合 MPE 科学中发挥着至关重要的作用,朝着我们个性化医学和预防的最终目标迈进。