Airway Gene Expression in Chronic Obstructive Pulmonary Disease

Overview

Journal Proc Am Thorac Soc

Specialty Pulmonary Medicine

Date 2009 Dec 17

PMID 20008878

Citations 21

Authors

Katrina Steiling

Marc E Lenburg

Avrum Spira

Affiliations

Soon will be listed here.

Abstract

Although cigarette smoking is the major cause of chronic obstructive pulmonary disease (COPD), only a subset of smokers develops this disease. There is significant clinical, radiographic, and pathologic heterogeneity within smokers who develop COPD that likely reflects multiple molecular mechanisms of disease. It is possible that variations in the individual response to cigarette smoking form the basis for the distinct clinical and molecular phenotypes and variable natural history associated with COPD. Using the biologic premise of a molecular field of airway injury created by cigarette smoking, this response to tobacco exposure can be measured by molecular profiling of the airway epithelium. Noninvasive study of this field effect by profiling airway gene expression in patients with COPD holds important implications for our understanding of disease heterogeneity, early disease detection, and identification of novel disease-modifying therapies.

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