(Boston) – Chronic obstructive pulmonary disease (COPD) is a disease caused by smoking that reduces lung function and causes difficulty breathing. It is the third leading cause of death in the world. Current treatments for COPD only affect the symptoms, not the progression. Identifying who will get COPD before they get it is key to knowing how to catch the disease at an early stage.
Researchers at Boston University School of Medicine (BUSM) have identified a panel of genes that are active in smokers and ex-smokers who experience faster loss of lung function over time. They believe these genes could be useful in predicting which people are most at risk for tobacco-related lung function decline.
“Our finding that airway genes change before a rapid decline in lung function should give COPD patients a lot of hope. A test like this could help doctors identify those at risk for COPD beforehand. they do not catch it, and help scientists find new treatments to stop the disease before it gets worse, âexplained corresponding author Katrina Steiling, MD, MSc, assistant professor of medicine at BUSM.
Smoking and smoking-related illnesses create changes in the airways and lungs. These changes can be detected using a procedure called bronchoscopy, where a small flexible camera inserted through the nose or mouth is used to collect cells with brushes on the sides of the airways. The researchers tested the airway brushings of 134 people who were current or former smokers. They found changes in the activity of specific genes in people who continued to have their lung function worsening more rapidly several years after that initial airway brushing. Some of these genes were more active in people who were losing lung function quickly, while others were less active in those people.
According to the researchers, further study of these genes could provide clues to the causes of the rapid decline in lung function that could be used to develop new treatments to prevent the development of COPD. âBeing able to identify those most at risk for worsening lung function could also facilitate clinical trials of drugs for COPD, by enriching trials testing new drugs for those most at risk of disease. ‘benefit,’ added co-author Beth Becker, PhD, a recent graduate of BU’s bioinformatics program.
This study further shows another use of the âairway injury fieldâ hypothesis. “Smoking causes changes in the cells of the lungs and airways. Because the changes in the airways are similar to those that occur deep inside the lungs, the airway cell test can be used. to detect diseases deep in the lungs, “added Marc Lenburg, PhD, professor of medicine and pathology and laboratory medicine at BUSM.
These results are published online in the journal Thorax.
Funding for this study was provided by the National Institutes of Health / National Heart, Lung, and Blood Institute (ROI HL095388 and ROI HL 118542-01) and the Dutch Longfonds Foundation (126.96.36.199JO).
Note to editors:
GO reports unrelated personal expenses from AstraZeneca and grants from Janssen Pharmaceuticals. PSH reports unrelated grants from Boehringer Lngelheim and the Galapagos. MvdB reports independent research grants from GlaxoSmithKline, TEVA Pharmaceuticals and Chiesi. AS reports equity from the unrelated founders of Metera Pharmaceuticals as well as grants and personal fees from Janssen Research and Development. KS reports CHEST Foundation grants, Lungevity Foundation Early Detection Award untied grants, and UpToDate royalties. MEL reports the equity of the unrelated founders of Metera Pharmaceuticals and the unrelated grants of Janssen Research and Development. WT reports unrelated personal charges from pfizer, GSK, Roche Diagnostics / Ventana, Merck Sharp Dohme, Novartis, Lilly Oncology, Boehringer lngelheim, AstraZeneca, Bristol-Myers-Squibb and AbbVie. KS, MEL and AS have issued U.S. Patent 9,677,138. EJB, KS, MEL and AS have a pending patent (Application No. 62/916,431).
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