Brian Matthew Wolpin

This study identifies Glis3 as a key transcription factor driving metastasis in PDAC by promoting a neural-like progenitor cell state.

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

This study identifies KEAP1 loss as a resistance mechanism to KRAS inhibitors in pancreatic and lung cancer and shows that combining glutamine inhibition with KRAS inhibitors can overcome this resistance.

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 study shows pancreatic cancer disrupts normal pancreatic function, leading to systemic nutrient depletion and muscle wasting, with autophagy in muscle playing a key role in nutrient redistribution to support tumor growth.

APEX infers cancer gene expression from plasma cfChIP-seq data, outperforming existing methods and enabling subtype classification and biomarker identification.

This study identifies mechanisms of resistance to tri-complex RAS inhibitors in patients with RAS-driven cancers, showing that resistance alterations disrupt the RAS:drug:CYPA tri-complex formation.

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.

This paper uses deep learning to predict pancreatic cancer risk from clinical disease trajectories in two large datasets, achieving higher accuracy than models without temporal information.

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 methylation patterns specific to intestinal epithelial cells to detect cell-free DNA in plasma, showing increased levels in advanced CRC compared to IBD and PDAC.