Miles Parkes

The paper identifies molecular signatures of Crohn's disease using scRNA-seq data from terminal ileal biopsies, highlighting key cell types and pathways involved in disease pathogenesis.

This study identifies 619 IBD risk signals, resolves 81 high-confidence variants, and prioritizes 664 candidate effector genes using GWAS, eQTL, and exome sequencing.

This study uses exome and genome sequencing to identify 68 genes directly associated with inflammatory bowel disease, providing clearer genetic insights and therapeutic targets.

The paper maps cell-type-specific eQTLs in IBD patients to identify effector genes and mechanisms linking genetic risk to disease.

This study uses single-cell RNA sequencing to analyze immune cell transcriptional profiles in mucosal and circulatory compartments of Crohn's disease patients, revealing tissue-specific inflammation signatures and identifying circulating T cells with mucosal-like features.

The paper analyzes somatic mutations in colonic crypts of IBD patients and controls, finding higher mutation rates and clonal expansions in IBD-affected tissue.

This study identifies HLA-DQA1*05 as a genetic risk factor for anti-drug antibody development in Crohn's disease patients treated with anti-TNF therapies.

This paper introduces iSNP, a workflow to identify patient-specific pathogenic pathways in ulcerative colitis by integrating SNP profiles with regulatory networks.

This paper develops and validates a 17-gene qPCR classifier in whole blood that stratifies IBD patients into prognostic subgroups without requiring cell separation.

This study uses whole genome sequencing to explore the genetic architecture of inflammatory bowel diseases, identifying a risk variant in ADCY7 for ulcerative colitis but finding limited contribution of low-frequency variants to heritability.

This study identifies 26 new genetic loci associated with inflammatory bowel disease, including integrin genes linked to immune activation and disease risk.

This study fine-maps 94 inflammatory bowel disease loci to identify 45 causal variants with high confidence, providing insights into their functional impacts on disease mechanisms.