Unlimited In Vitro Expansion of Adult Bi-Potent Pancreas Progenitors through the Lgr5/R-Spondin Axis Wnt signaling is inactive and Lgr5 is not expressed under physiological conditions in the adult pancreas. However, scientists now report that the Wnt pathway is robustly activated upon injury by partial duct ligation, concomitant with the appearance of Lgr5 expression in regenerating pancreatic ducts. [EMBO J] Full Article | Press Release Transcription Factor ZBED6 Affects Gene Expression, Proliferation, and Cell Death in Pancreatic Beta Cells Scientists investigated whether the recently discovered transcription factor, zinc finger BED domain-containing protein 6 (ZBED6), is expressed in insulin-producing cells and, if so, to what extent it affects beta cell function. [Proc Natl Acad Sci USA] Abstract | Full Article Alternative Splicing and Differential Expression of the Islet Autoantigen IGRP between Pancreas and Thymus Contributes to Immunogenicity of Pancreatic Islets but Not Diabetogenicity in Humans Investigators tested whether specific splice variation in islets versus thymus correlates with loss of tolerance to islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) in type 1 diabetes. [Diabetologia] Abstract Pancreatic Duct Ligation after Almost Complete Beta-Cell Loss: Exocrine Regeneration but No Evidence of Beta-Cell Regeneration There has been great interest in the extent of beta-cell regeneration after pancreatic duct ligation (PDL) and whether alpha-to beta-cell conversion might account for beta-cell regeneration after near-complete beta-cell loss. To assess these questions, scientists established a PDL-model in adult male rats after almost complete beta-cell depletion achieved by giving a single high dose of streptozocin in the fasted state. [Endocrinology] Abstract Nkx6.1 Is Essential for Maintaining the Functional State of Pancreatic Beta Cells Given that Nkx6.1 levels are reduced in human type 2 diabetic beta cells, this study lends support to the concept that loss of beta cell features could contribute to the pathogenesis of diabetes. [Cell Rep] Abstract | Full Article | Graphical Abstract PANCREATIC CANCER Genetic Inactivation of Nupr1 Acts as a Dominant Suppressor Event in a Two-Hit Model of Pancreatic Carcinogenesis Scientists investigated the role of Nupr1 in pancreatic ductal adenocarcinoma progression beyond pancreatic intraepithelial neoplastic lesions in Pdx1-cre;LSL-KrasG12D;Ink4a/Arffl/fl(KIC) mice. [Gut] Abstract Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors Scientists used human pancreatic cancer cells both in vitro and in vivo to demonstrate the role of NAD synthesis and degradation in tumor cell metabolism and growth. They demonstrated that pharmacological and genetic targeting of Nampt, the key enzyme in the NAD salvage synthesis pathway, inhibits cell growth and survival of pancreatic cancer cells. [Clin Cancer Res] Abstract | Full Article Combination of siRNA-Directed Kras Oncogene Silencing and Arsenic-Induced Apoptosis Using a Nanomedicine Strategy for the Effective Treatment of Pancreatic Cancer Down-regulation of the mutant Kras gene by siRNA caused defective abilities of proliferation, clonal formation, migration, and invasion of pancreatic cancer cells, as well as cell cycle arrest at the G0/G1 phase, which substantially enhanced the apoptosis-inducing effect of arsenic administration. [Nanomedicine] Abstract miR-204 Mediated Loss of Myeloid Cell Leukemia-1 Results in Pancreatic Cancer Cell Death Using pancreatic cancer cell lines, researchers have shown that miR-204, a putative regulator of Mcl-1, is repressed in cancer cell lines compared to normal cells. [Mol Cancer] Abstract | Full Article Downregulation of Gas5 Increases Pancreatic Cancer Cell Proliferation by Regulating CDK6 Researchers assayed the expression level of gas5 in pancreatic cancer tissues and define the role of gas5 in the regulation of pancreatic cancer cell proliferation. They verified that the expression level of gas5 is significantly decreased in pancreatic cancer tissues compared with normal control. [Cell Tissue Res] Abstract |