Schwartz D.A.,Center for Genes
Proceedings of the American Thoracic Society | Year: 2010
Gene-environment interactions are the indisputable cause of most respiratory diseases. However,we still have very limited understanding of the mechanisms that guide these interactions. Although the conceptual approaches to environmental genomics were established several decades ago, the tools are only nowavailable to better define the mechanisms that underlie the interaction between these important etiologic features of lung disease. Epigenetic mechanisms can mediate the effect of the environment on thehuman genomeby controlling the transcriptional activity of specific genes, at specific points in time, in specific organs. In this article, we demonstrate the potential importance of epigenetic mechanisms in the development and progression of chronic obstructive pulmonary disease and asthma.
DiStefano J.K.,Center for Genes |
Gerhard G.S.,Temple University
Expert Review of Gastroenterology and Hepatology | Year: 2016
Liver biopsy is currently recognized as the most accurate method for diagnosing and staging nonalcoholic fatty liver disease (NAFLD). However, this procedure is typically performed when disease has progressed to clinically significant stages, thereby limiting early diagnosis of patients who are at high risk for development of liver- and cardiovascular-related morbidity and mortality. Recently, microRNAs (miRNAs), short, noncoding RNAs that regulate gene expression, have been associated with histological features of NAFLD and are readily detected in the circulation. As such, miRNAs are emerging as potentially useful noninvasive markers with which to follow the progression of NAFLD. In this article, we present the evidence linking circulating miRNAs with NAFLD and discuss the potential value of circulating miRNA profiles in the development of improved methods for NAFLD diagnosis and clinical monitoring of disease progression. © 2015 Taylor & Francis.
Walter N.D.,University of Colorado at Denver |
Strong M.,Center for Genes |
Ordway D.J.,Colorado State University |
Chan E.D.,University of Colorado at Denver
Respirology | Year: 2012
Multidrug (MDR)- and extensively drug-resistant (XDR) tuberculosis (TB) impose a heavy toll of human suffering and social costs. Controlling drug-resistant TB is a complex global public health challenge. Basic science advances including elucidation of the genetic basis of resistance have enabled development of new assays that are transforming the diagnosis of MDR-TB. Molecular epidemiological approaches have provided new insights into the natural history of TB with important implications for drug resistance. In the future, progress in understanding Mycobacterium tuberculosis strain-specific human immune responses, integration of systems biology approaches with traditional epidemiology and insight into the biology of mycobacterial persistence have potential to be translated into new tools for diagnosis and treatment of MDR- and XDR-TB. We review recent basic sciences developments that have contributed or may contribute to improved public health response. © 2012 Asian Pacific Society of Respirology.
Helling B.A.,Aurora University |
Yang I.V.,Aurora University |
Yang I.V.,Center for Genes
Current Opinion in Pulmonary Medicine | Year: 2015
Purpose of review Idiopathic pulmonary fibrosis (IPF) is a fatal disease with limited treatment options and extensive gene expression changes identified in the lung parenchyma. Multiple lines of evidence suggest that epigenetic factors contribute to dysregulation of gene expression in IPF lung. Most importantly, risk factors that predispose to IPF - age, sex, cigarette smoke, and genetic variants - all influence epigenetic marks. This review summarizes recent findings of association of DNA methylation and histone modifications with the presence of disease and fibroproliferation. Recent findings In addition to targeted studies focused on specific gene loci, genome-wide profiles of DNA methylation demonstrate widespread DNA methylation changes in IPF lung tissue and a substantial effect of these methylation changes on gene expression. Genetic loci that have been recently associated with IPF also contain differentially methylated regions, suggesting that genetic and epigenetic factors act in concert to dysregulate gene expression in IPF lung. Summary Although we are in very early stages of understanding the role of epigenetics in IPF, the potential for the use of epigenetic marks as biomarkers and therapeutic targets is high and discoveries made in this field will likely bring us closer to better prognosticating and treating this fatal disease. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Garantziotis S.,National Health Research Institute |
Schwartz D.A.,Center for Genes
Annual Review of Public Health | Year: 2010
Gene-environment interactions are the indisputable cause of most respiratory diseases. However, we still have very limited understanding of the mechanisms that guide these interactions. Although the conceptual approaches to environmental genomics were established several decades ago, the tools are only now available to better define the mechanisms that underlie the interactions among these important etiological features of lung disease. In this article, we summarize recent insights in the environmental genomics (ecogenomics) of common nonmalignant respiratory diseases (asthma, COPD, pulmonary fibrosis, and respiratory infections), describe the framework of gene-environment interactions that inform the pathogenesis of respiratory diseases, and propose future research directions that will help translate scientific advances into public health gains. Copyright © 2010 by Annual Reviews. All rights reserved.