Philippe Joubert

This study identifies ZNF768 as a regulator of E2F1 expression, which drives G0/G1 transition and cell cycle progression, with implications for cancer progression.

This study examines ecDNA in lung cancer, finding it in 18.9% of patients and associating it with worse survival and genomic instability.

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

This paper develops a deep learning model to predict molecular alterations in never-smoker lung adenocarcinomas from histological images, achieving high accuracy for most features.

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

This study shows β-glucan reprograms neutrophils to induce disease tolerance against Influenza A virus by promoting a unique subset of neutrophils that limit tissue damage and enhance survival.

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 study identifies seven age-associated ECM proteins with increased expression in human lung tissue and demonstrates age-related differences in specific lung compartments.

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 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.

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

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