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My work on antitrypsin deficiency led to work to identify genetic and protein biomarkers for the stratification of individuals with chronic obstructive pulmonary disease (COPD). I was the founder and co-lead PI of the International COPD Genetics Network that demonstrated that airway wall thickening and emphysema make independent contributions to airflow obstruction in COPD (Am. J. Resp. Crit. Care Med. 2008;178:500-5) and that was used to undertake the first genome wide association study (GWAS) in COPD. This identified single nucleotide polymorphisms (SNPs) in the nicotinic acetylcholine receptor/IREB2, HHIP and FAM13A (PLoS Genet. 2009;5:e1000421; Nat. Genet. 2010;42:200-202). These findings have now been replicated in multiple other cohorts of individuals with COPD by different investigators. The results help to explain why some people who smoke develop lung disease whilst others do not and may provide targets for new therapies for this condition. I served on the steering committee of the ECLIPSE study that recruited approximately 3000 individuals from 42 centres to identify novel endpoints for COPD. We showed that exacerbations are a stable phenotype in COPD (N. Engl. J. Med. 2010;363;1128- 1138) and that C-16 predicts decline in FEV1 (N. Engl. J. Med 2011;365:1184-1192). Exacerbations are now routinely used as an endpoint for clinical trials of new therapies for COPD.
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Methods in molecular biology (Clifton, N.J.) (2024): 41-55
Gastro Hep Advances (2024)
FEBS JOURNAL (2024)
ACTA PHYSIOLOGICA (2023): 9-9
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HEPATOLOGYno. 5 (2023): E118-E118
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Britta Handyside,Lening Zhang,Katina Ngo,Ryan Murphy,Joseph Chen,Nicole Galicia,Olivia Gorostiza,Glenn Pacheco,Lin Xie, Donald Mackenzie, Heidi Jones,Brian Heglar,
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