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Hexosamine salvage through the enzyme N-acetylglucosamine kinase is stimulated in nutrient-limited conditions and supports pancreatic tumor growth.

Circulating myeloid cells invade the brain during pancreatic cancer, where they accumulate at a unique central nervous system interface and drive anorexia and muscle catabolism.

Structures of PKA in complex with wild type and mutant phospholamban show a mechanism underlying familial dilated cardiomyopathy.

Physiological and biochemical studies show that the treatment of a transgenic mouse model carrying recessive Ryr1 mutations with a combination of class II histone deacetylase inhibitors and DNA methyl transferase inhibitors significantly improves skeletal muscle function.

Stromal cell levels and localization of active α₅β₁-integrin are regulated by desmoplastic extracellular matrix control of α_vβ₅-integrin signaling, and predict clinical outcomes for pancreatic and renal cancer patients.

Results show that STAT3 and KRAS jointly regulate oncogenic dependency of mutant KRAS cancer cells.

Profiling spatially defined fibroblasts in the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment identifies high levels of podoplanin and hypoxia in tumor-proximal fibroblasts associated with bad prognosis, whilst inflammatory markers define more distal fibroblast regions and associate with better outcomes.

Lactate in pancreatic cancer micro-environment can lead to TET enzyme activation and loss of DNA methylation seen in cancer associated fibroblasts.

Pancreatic cancer-associated muscle atrophy is characterized by strong mitochondrial metabolic defects that are not limited to carbohydrate, protein, and redox metabolism, but also concern lipid and nucleic acid metabolisms.

Behavioral, pharmacological, optogenetic, electrophysiological and computational analyses suggest that the anterior dorsal striatum is a causal node in the network responsible for evidence accumulation.