Laufey Thora Amundadottir

The paper fine-maps GWAS risk variants for PDAC and identifies candidate target genes through chromatin conformation capture, finding functional interactions and eQTLs at specific loci.

This study identifies novel genetic risk loci for pancreatic ductal adenocarcinoma in African ancestry individuals through admixture mapping and GWAS.

This study identifies rs9581943 as a causal variant in a PDAC GWAS signal, showing it reduces PDX1 expression and impairs stress buffering in exocrine pancreatic cells.

The paper identifies functional variants and VNTRs at the 5p15.33 locus using fine-mapping, MPRA, and CRISPRi screens, revealing their role in cancer susceptibility through antagonistic pleiotropy.

The paper identifies rs3769823 as a functional variant near CASP8 influencing its expression in a cell-type specific manner and associated with multiple cancers.

This paper shows a CTRB2 deletion variant increases pancreatic cancer risk by causing ER stress and inflammation in mice, using a new genetic model.

The paper fine-maps a PDAC GWAS signal at chr1p36.33 and identifies KLHL17 as a target gene regulated by JunB/D, with potential implications for inflammation and PDAC risk.

The paper develops a method to prioritize enhancers linked to pancreas disease risk by integrating chromatin interactions, machine learning, and single-cell perturbation assays.

This paper identifies shared and unique chromatin accessibility and 3D interactions of SUD loci, implicating non-neural cell types like pancreatic β-cells and showing a causal link between T2D and AUD.

The paper uses a multi-layered approach combining GWAS, spatial autocorrelation, and Hi-C to identify novel genetic variants associated with pancreatic cancer susceptibility.

This study assesses polygenicity and risk prediction using common variants across 14 cancers, finding varying numbers of susceptibility variants and risk score effectiveness.

The paper identifies cell-type specific eQTLs in primary melanocytes, revealing novel melanoma susceptibility genes and associations with GWAS loci.