Yohan Bossé

The paper identifies regulatory variants associated with aortic valve disease and shows their impact on gene expression and disease mechanisms.

This study identifies three distinct evolutionary trajectories in lung adenocarcinomas using whole-genome sequencing, revealing that some never-smoking tumors follow smoking-like paths driven by KRAS mutations.

The paper identifies three subtypes of NS-LUAD using RNA-seq data and develops a 60-gene signature that predicts survival across subgroups.

This study examines real-time transcriptional responses to intermittent hypoxia in lung tissue of male mice, revealing cell-type-specific changes and mito-nuclear imbalance.

This study analyzes 1024 lung adenocarcinomas to identify evolutionary patterns and mutational mechanisms, revealing distinct trajectories linked to smoking, ancestry, and retrotransposition.

This paper evaluates polygenic risk scores (PRS) for CAD and blood lipids to predict CAD incidence in UK Biobank participants.

The paper identifies twelve novel genetic risk loci for lung cancer subtypes through multi-ancestry GWAS and shows smoking-independent genetic risk.

LaScaMolMR.jl enables efficient large-scale molecular Mendelian randomization studies by providing a fast, integrated Julia package for omic-wide MR analyses.

The paper identifies shared genetic variants between critically ill COVID-19 and idiopathic pulmonary fibrosis by integrating GWAS with context-specific eQTLs and transcriptomics.

This study compares scRNA-seq and snRNA-seq in lung samples, finding differences in cell type composition and biological insights between fresh and frozen tissues.

This paper uses Mendelian randomization to identify 49 blood proteins causally associated with calcific aortic valve disease, revealing immune and growth factor pathways involved in the disease.

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

This study uses trans-omic Mendelian randomization to identify genes, proteins, and metabolites associated with parental lifespan and potential drug targets for healthspan extension.

The paper uses multi-omics approaches to identify genes and plasma proteins associated with COVID-19, finding ABO plasma protein as a causal risk factor.

The paper identifies co-expressed genes with ACE2 and TMPRSS2 in lung tissue and finds many have drug interactions, suggesting potential targets for COVID-19 therapeutics.

This study uses Mendelian randomization to examine if ACE inhibitors or cardiometabolic risk factors affect lung ACE2 and TMPRSS2 expression or plasma ACE2 levels, finding no overall association.

This study identifies genetic loci and amino acid residues associated with immune response to viral infections using serological data from the UK Biobank.

This study uses Mendelian randomisation to show that higher serum CC-16 levels protect against COPD risk and progression, with genetic variants linked to CC-16 expression in lung tissue.

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

The paper identifies genetic links between impaired pulmonary function and increased lung cancer risk, showing causal relationships through Mendelian randomization and highlighting immune-related pathways.

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 identifies three new susceptibility genes for calcific aortic valve stenosis through GWAS and TWAS, highlighting roles in inflammation, mineralization, and blood vessel integrity.

This study investigates the association between elevated Lp(a) levels, parental lifespan, and long-term mortality risk using genetic and observational data.

This study shows genetic inhibition of PCSK9 lowers lipoprotein levels and reduces risk of CAD and CAVS, with PCSK9 present in calcified aortic valves and induced by oxidative stress.

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

The paper identifies 279 new genetic signals for lung function across multiple ancestries, showing associations with COPD and pleiotropic effects.

This study identifies over 50 new genetic loci associated with pulmonary function through a multiethnic meta-analysis of 90,715 individuals.

The paper identifies 12 novel COPD loci and candidate causal genes using GWAS and lung eQTL data from 129 risk loci.