F. Notta

Single-cell analysis of an engineered organoid-based model of pancreatic cancer identifies hypoxia as a contributing factor in the determination of transcriptional subtypes

This study uses single-cell transcriptomics to show that hypoxia in organoid models influences transcriptional subtypes in pancreatic cancer.

p73 activates transcriptional signatures of basal lineage identity and ciliogenesis in pancreatic ductal adenocarcinoma

This study shows p73 activates basal lineage and ciliogenesis genes in PDAC, suggesting its role in lineage plasticity and tumor progression.

Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression

The paper investigates how 9p21.3 deletions in cancer disable both cell intrinsic and extrinsic tumor suppression by co-deleting CDKN2A/B and type I interferons, leading to immune evasion and metastasis.

In vivo CRISPR screens reveal SCAF1 and USP15 as novel drivers of pancreatic cancer

This study uses in vivo CRISPR screens to identify USP15 and SCAF1 as novel tumor suppressors in pancreatic cancer, with potential therapeutic implications.

A primary patient-derived model for investigating functional heterogeneity within the human Leukemic Stem Cell Compartment

Spatially confined sub-tumor microenvironments orchestrate pancreatic cancer pathobiology

This study identifies spatially confined sub-tumor microenvironments in PDAC that drive distinct tumor progression outcomes.

MYC controls metastatic heterogeneity in pancreatic cancer

This study identifies MYC as a key driver of metastatic heterogeneity in pancreatic cancer by linking its activity to increased metastasis through TAM recruitment.

Developmental and MAPK-responsive transcription factors drive distinct malignant subtypes and genetic dependencies in pancreatic cancer

The paper identifies three developmental lineages in pancreatic cancer driven by master regulators and shows their association with MAPK activity and therapeutic vulnerabilities.

NOX4 links metabolic regulation in pancreatic cancer to endoplasmic reticulum redox vulnerability and dependence on PRDX4

This study identifies NOX4 as a link between metabolic deregulation and ER-specific redox vulnerability in PDAC, suggesting PRDX4 as a therapeutic target for pancreatic cancer.