Ian P. Hall

This study identifies three novel genetic signals associated with idiopathic pulmonary fibrosis using GWAS and clinically-curated datasets, highlighting potential drug targets like MUC1 and NTN4.

This study performs GWAS of IPF using dominant and recessive models, identifying five new genome-wide significant signals and genes, including PMF1 and EPN3, and observing increased PMF1 expression in IPF patients.

The paper investigates the effects of the ADRB2 Thr164Ile variant on lung function, plasma proteome, and other traits using UK Biobank data, finding associations with immune and lipid metabolism pathways but not COPD or asthma.

This study identifies three genetic variants with sex-specific effects on IPF susceptibility but finds no significant difference in predictive accuracy of polygenic risk scores between males and females.

This study investigates the association between HLA genetic variants and IPF risk using a meta-analysis of seven case-control studies, finding no consistent HLA region associations.

This study performs a GWAS on asthma exacerbations in the UK Biobank, identifying two novel genetic loci associated with exacerbation risk in individuals with asthma.

The paper identifies four novel genetic variants associated with IPF survival, including a PCSK6 variant, and suggests PCSK6 as a prognostic biomarker and therapeutic target.

This study identifies eight novel genetic signals associated with asthma-COPD overlap through a genome-wide association analysis involving multiple cohorts.

This study investigates the pleiotropic effects of SERPINA1 Z allele heterozygosity on various phenotypes using UK Biobank data, finding associations with height, gall bladder disease, heart disease, and lung function.

The paper identifies SNPs with sex-specific effects on lung function traits using UK Biobank data, finding a significant interaction at rs7697189 near HHIP.

This study identifies three new genetic loci associated with idiopathic pulmonary fibrosis and confirms 11 previously reported ones, highlighting mTOR signaling and mitotic spindle-assembly genes in disease susceptibility.

This study expands the genetic landscape of COPD by identifying 82 risk loci, revealing associations with lung function, cell types, and comorbidities.