M. Pasca di Magliano

The paper analyzes donor pancreata to define the transcriptomic signature and microenvironment of early pre-neoplastic lesions, finding PanIN lesions are common in healthy individuals and show transcriptional similarity to cancer cells.

This study shows Notch signaling in tumor-associated macrophages promotes immunosuppression in pancreatic cancer, and blocking it enhances immune therapy effectiveness.

This study shows that ammonia accumulation in the colorectal cancer microenvironment promotes T cell exhaustion and treatment resistance, and that reducing ammonia improves immunotherapy efficacy.

This study shows hypoxia drives an inflammatory phenotype in pancreatic cancer-associated fibroblasts, promoting tumor IL1 expression and iCAF formation in hypoxic regions.

This study identifies metabolic markers and pathways in pancreatic tumor-associated macrophages using multi-omic analysis and in vitro models.

This study shows that extrinsic KRAS signaling reprograms pancreatic fibroblasts to create an inflammatory microenvironment that supports tumor growth.

This study identifies uridine as a novel nutrient for pancreatic cancer cells through uridine phosphorylase 1, showing its role in survival and metabolism under glucose deprivation.

The paper identifies consistently expressed genes in pancreatic ductal adenocarcinoma (PDAC) to prioritize therapeutic targets and biomarkers.

This study shows that loss of ATF3 reduces pancreatic cancer progression by limiting acinar-to-ductal metaplasia and enhancing regeneration, but KRASG12D can bypass ATF3's requirement in some contexts.

This study shows that the pancreatic tumor microenvironment compensates for loss of GOT2 by providing pyruvate, maintaining redox homeostasis and tumor growth in vivo.

The paper identifies two metabolic subclasses in pancreatic cancer cells and shows asparagine's role in supporting proliferation under mitochondrial stress, suggesting a new therapeutic strategy.

This study identifies KMT2D as a tumor suppressor in pancreatic cancer, linking TGF-β signaling to the non-canonical activin A pathway through miR-147b and showing its role in cancer cell plasticity and metastasis.

This study shows that inhibiting GOT1 in pancreatic cancer primes cells for ferroptosis by promoting autophagy-mediated release of labile iron.

This study identifies integrin β1 signaling as a mediator of MEK inhibitor resistance in pancreatic cancer organoids, suggesting combination therapy targeting both pathways.

This study shows macrophages in pancreatic cancer release pyrimidines that inhibit gemcitabine therapy by competing with the drug for uptake and metabolism, and reducing macrophage burden improves treatment response.