Ben Z. Stanger

This study shows that PARP11-induced MARylation and ubiquitination of MHC-I in cancer cells promotes immunosuppression, tumor growth, and resistance to therapies.

This study identifies SPTBN2 as a regulator of immunosuppressive tumor microenvironment and cross-resistance to therapies, showing its role in suppressing CAR T-cell efficacy.

This study identifies TMEM doorways as a mechanism for metastasis in PDAC, showing Tie2 macrophages facilitate intravasation and that targeting Tie2 improves survival in mouse models.

SUMMIT traces mitochondrial mutations in human tissues to identify spatially localized clones and their transcriptomic profiles.

This study shows that mitochondrial Ca2+ uptake via MCU promotes pancreatic cancer growth and metastasis by enhancing epithelial plasticity through EMT.

This study identifies a nuclear branched-chain amino acid catabolism pathway in pancreatic cancer that regulates histone propionylation and gene expression.

This study identifies a DNA methylation signature preserved during pancreatic carcinogenesis that distinguishes PDAC origins and influences tumor behavior.

The paper shows hypoxic fibroblasts in pancreas cancer use histone methylation and ROS-mediated NF-κB activation to produce growth factors that drive epithelial-mesenchymal transition in malignant cells.

This study shows that metabolic activity in cancer cells affects circadian rhythms, with hypermetabolic states linked to weaker circadian oscillations in both mouse and human tumor cells.

This study evaluates the therapeutic potential of RMC-7977, a broad-spectrum RAS inhibitor, in pancreatic ductal adenocarcinoma models, showing strong anti-tumor effects with minimal impact on normal tissues.