SAD-A Kinase Controls Islet ß-Cell Size and Function as a Mediator of mTORC1 Signaling Researchers showed that global synapses of amphids defective kinase-A (SAD-A) deletion leads to defective glucose-stimulated insulin secretion and petite islets, which are reminiscent of the defects in mice with global deletion of ribosomal protein S6 kinase 1, a downstream target of mammalian target of rapamycin complex 1 (mTORC1). [Proc Natl Acad Sci USA] Abstract Efficient ß-Cell Regeneration by a Combination of Neogenesis and Replication Following ß-Cell Ablation and Reversal of Pancreatic Duct Ligation Investigators studied the effect of surgical reversal of the duct ligation, and found that that there was a wave of ß-cell replication following reversal. [Stem Cells] Abstract Induction of ß-Cell Replication by a Synthetic HNF4a Antagonist Scientists tested the hypothesis that a potent HNF4a antagonist might stimulate ß-cell replication. A bioavailable HNF4a antagonist was injected into normal mice and rabbits and ß-cell ablated mice and the effect on ß-cell replication was measured. [Stem Cells] Abstract Autoimmunity against INS-IGF2 Expressed in Human Pancreatic Islets Investigators determined expression of INS-IGF2 in human pancreatic islets and autoantibodies in newly diagnosed type 1 diabetes children and controls. [J Biol Chem] Abstract | Full Article Cerulein-Induced Acute Pancreatitis Is Associated with c-Jun NH(2)-Terminal Kinase 1-Dependent Ferritin Degradation and Iron-Dependent Free Radicals Formation Pancreatic acinar AR42J cells stimulated by cerulein showed increased labile iron pool that was accompanied by a decrease in the cellular ferritin-L level and an increase in the reactive oxygen species formation. [Pancreas] Abstract PANCREATIC CANCER Integration of Metabolomics and Transcriptomics Revealed a Fatty Acid Network Exerting Growth Inhibitory Effects in Human Pancreatic Cancer Scientists demonstrated that two saturated free fatty acids, palmitate and stearate significantly induced TRAIL expression, triggered apoptosis, and inhibited proliferation in pancreatic cancer cells. [Clin Cancer Res] Abstract Subtype Specific MEK – PI3 Kinase Feedback as a Therapeutic Target in Pancreatic Adenocarcinoma The authors investigated the consequences of MEK inhibition in a large pancreatic adenocarcinoma cell line panel. Inhibition of MEK activated PI3 kinase in an EGFR-dependent fashion and combinations of MEK and EGFR inhibitors synergistically induced apoptosis. [Mol Cancer Ther] Abstract Guggulsterone Decreases Proliferation and Metastatic Behavior of Pancreatic Cancer Cells by Modulating JAK/STAT and Src/FAK Signaling Investigators studied the effect of guggulsterone on pancreatic cancer cell growth, motility and invasion and elucidated the molecular mechanisms associated with its anti-tumor effects. [Cancer Lett] Abstract Generation of CTL Responses against Pancreatic Cancer In Vitro Using Dendritic Cells Co-Transfected with MUC4 and Survivin RNA Dendritic cells (DCs) co-transfected with two tumor associated-antigens mRNAs were found to induce stronger cytotoxic T lymphocyte (CTL) responses against pancreatic cancer target cells in vitro, compared with the DCs transfected with a single mRNA. [Vaccine] Abstract Proteinase-Activated Receptors Differentially Modulate In Vitro Invasion of Human Pancreatic Adenocarcinoma PANC-1 Cells in Correlation with Changes in the Expression of CDC42 Protein Scientists examined the role of proteinase-activated receptor-1 (PAR)s in a human pancreatic adenocarcinoma PANC-1 cell line phenotype in vitro. PAR-1 and PAR-2 knockdowns (KDs) were markedly less, whereas PAR-3 KDs were robustly more migratory and invasive than the controls. [Pancreas] Abstract |