Gene expression alterations associated with progression of emphysema and small airway disease in smokers with COPD
Gil, Julie Zeskind
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Chronic Obstructive Pulmonary Disease (COPD) is a disease of reduced lung function. It is the fourth leading cause of death in the US. In the US it is primarily caused by smoking, yet only 10-20% of smokers will develop COPD. The exact molecular and genetic mechanisms contributing to the disease are unknown. Current therapies reduce symptoms but cannot halt the lung function decline. COPD is comprised of two subphenotypes - emphysema (alveolar destruction) and small airway disease (airway-wall thickening). The relative combination of airway disease and emphysema is heterogeneous between patients. The degree of disease is heterogeneous within each patient. This study takes two unique approaches to gain insights into the molecular processes that contribute to airway thickening and alveolar destruction. First, it utilizes the regional heterogeneity in each patient as a surrogate for disease progression. Second, it examines the airway disease and emphysematous components separately. [TRUNCATED]
Thesis (Ph.D.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at firstname.lastname@example.org. Thank you.