Jason W. Hoskins

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 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.

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.