Global gene expression profiles reveal pathways related to the pathogenesis of chronic obstructive pulmonary disease.
Academic Article
Overview
abstract
Extract: Chronic obstructive pulmonary disease (COPD) is a slowly progressive, and irreversible disorder characterized by airway obstruction, which is a significant cause of morbidity, mortality and health care costs. COPD is a collective term describing two separate chronic lung diseases: emphysema and chronic bronchitis, which have a common culprit -- the cigarette. Cigarette smoke has been generally accepted as the primary factor in the development of COPD; cigarette use accounts for about 80% to 90% of COPD cases in the United States. However, only 15 to 20% of smokers develop clinically significant symptoms of COPD, which suggests there may be a genetic susceptibility to the development of the disease. The genes that determine this genetic susceptibility to cigarette smoking and disease progression to COPD are poorly understood. Individual genes or groups of genes that are expressed differently in smokers with and without COPD can be determined by comparing their corresponding global gene expression profiles. Two approaches, microarray and serial analysis of gene expression (SAGE), are currently used for simultaneous and rapid analysis of the expression levels of thousands of genes in a given cell population. Microarray, involving the binding of labeled nucleic acids targets to immobilized probes, is a relatively rapid and widely used technique. However, microarray is a closed method, meaning that it only measures expression levels of already collected nucleic acids sequences.
