Nelson Dusetti

The methionine cycle sustains the mesenchymal phenotype of tumor cells and drives PDA progression

This study identifies the methionine cycle as a driver of mesenchymal traits in PDA, showing that targeting SAHH reduces metastasis and improves survival.

Chromosomal instability drives continual flux in cancer genomes

This study shows that chromosomal instability (CIN) drives rapid genome changes in cancer cells, generating new copy number alterations each cell cycle and increasing genomic complexity.

Transcriptomic FOLFIRINOX sensitivity signatures stratify overall survival and reveal directional reclassification after neoadjuvant FOLFIRINOX in borderline resectable and locally advanced pancreatic cancer

This paper evaluates transcriptomic FOLFIRINOX sensitivity signatures in neoadjuvant pancreatic cancer, finding they predict survival and show directional reclassification after treatment.

Co-translational O-glycosylation driven by GALNTs spatial reprogramming fosters pancreatic cancer growth

The paper shows that GALA, a process relocating GALNTs to the ER, enables co-translational O-glycosylation in pancreatic cancer, expanding the O-glycoproteome and promoting tumor growth.

A Luminal-Basal Stratification of the Native Human Pancreatic Duct is Differentially Represented in Pancreatic Cancers

This study identifies spatially distinct cell populations in human pancreatic ducts and shows that ASCP better preserves native cell identities compared to PDAC.

SG33, a vaccine strain of myxoma virus with oncolytic potential, exploits macropinocytosis and clathrin-mediated endocytosis for entry into pancreatic cancer cells.

This study identifies the entry mechanisms of SG33, an oncolytic myxoma virus, into pancreatic cancer cells, showing it uses macropinocytosis and clathrin-mediated endocytosis.

A genome-wide CRISPR-Cas9 screen identifies TGN46 as a host determinant for H-1PV susceptibility in pancreatic adenocarcinoma.

The paper identifies TGN46 as a host factor critical for H-1PV infection in pancreatic cancer cells through a CRISPR-Cas9 screen and functional analyses.

A TARGETED COMBINATION THERAPY ACHIEVES EFFECTIVE PANCREATIC CANCER REGRESSION AND PREVENTS TUMOR RESISTANCE

This paper shows that combining three KRAS signaling pathway inhibitors effectively regresses pancreatic tumors and prevents resistance in preclinical models.

Exploiting TGF-β-mediated Stromal Programming in Homologous Recombination-Deficient Pancreatic Cancer

This study shows that ATM-deficient pancreatic cancers reprogram the tumor microenvironment via TGF-β-driven myCAF enrichment, and targeting this stromal axis with chemotherapy improves therapeutic efficacy.

KRAS Inhibition Reverses Chemotherapy Resistance Promoted by Therapy-Induced Senescence-like in Pancreatic Ductal Adenocarcinoma

This study shows that KRAS inhibition can reverse chemotherapy resistance in PDAC by targeting therapy-induced senescence-like cells, with ERK pathway involvement.

SMAP: exploiting high-throughput sequencing data of patient derived xenografts

SMAP improves sequencing analysis of xenografts by accurately mapping reads to both host and graft genomes and enhancing fusion transcript detection.