Katelyn E. Connelly

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.

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.