Editorial Material
Cell & Tissue Engineering
Michael Karl Melzer, Alexander Kleger
Summary: In this study, Jiang and colleagues investigate the function of Tff2+ transit-amplifying progenitor cells in the pancreatic acinar compartment of mice using various lineage-tracing approaches. The findings provide insights into the role of these progenitor cells in maintaining steady-state homeostasis and suppressing tumor development, as well as uncovering heterogeneity in acinar cells.
Article
Oncology
Vishaka Gopalan, Arashdeep Singh, Farid Rashidi Mehrabadi, Li Wang, Eytan Ruppin, H. Efsun Arda, Sridhar Hannenhalli
Summary: This study identifies edge epithelial cell states with oncogenic transcriptional activity in human organs without oncogenic mutations, with a particular focus on pancreatic ductal adenocarcinoma (PDAC). It also highlights the increase in the fraction of acinar cells with age in the pancreas, as well as the significantly higher presence of AE-like cells in human pancreatitis samples.
Article
Medicine, Research & Experimental
Sarah Merz, Markus Breunig, Michael Karl Melzer, Sandra Heller, Sandra Wiedenmann, Thomas Seufferlein, Matthias Meier, Jana Krueger, Medhanie A. Mulaw, Meike Hohwieler, Alexander Kleger
Summary: This study aims to guide human pluripotent stem cells into multipotent pancreatic progenitors, which serve as a common precursor population that can mature into acinar, ductal, and functional beta-cells. It provides a basis for studying developmental processes and deciphering early cancer formation in a cell type-specific context.
Article
Cardiac & Cardiovascular Systems
Davide Maselli, Gloria Garoffolo, Giada Andrea Cassanmagnago, Rosa Vono, Matthijs S. Ruiter, Anita C. Thomas, Paolo Madeddu, Maurizio Pesce, Gaia Spinetti
Summary: Mechanical stress promotes molecular phenotypic switching of saphenous vein progenitors and increases their responsiveness to extracellular environment alterations.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2022)
Article
Oncology
Mohamad Assi, Younes Achouri, Axelle Loriot, Nicolas Dauguet, Hajar Dahou, Jonathan Baldan, Maxime Libert, Jean S. Fain, Carmen Guerra, Luc Bouwens, Mariano Barbacid, Frederic P. Lemaigre, Patrick Jacquemin
Summary: The study demonstrates that pancreatic acinar cells become less sensitive to tumorigenesis induced by oncogenic Kras mutations after birth, due to low expression of KRAS and its effectors. Pancreatitis induces the expression of KRAS and its effectors, requiring the activity of EGFR. Expression of C-RAF in adult pancreas is essential for pancreatic tumorigenesis.
Article
Cell & Tissue Engineering
Markus Breunig, Jessica Merkle, Martin Wagner, Michael K. Melzer, Thomas F. E. Barth, Thomas Engleitner, Johannes Krumm, Sandra Wiedenmann, Christian M. Cohrs, Lukas Perkhofer, Gaurav Jain, Jana Kruger, Patrick C. Hermann, Maximilian Schmid, Tamara Madacsy, Arpad Varga, Joscha Griger, Ninel Azoitei, Martin Mueller, Oliver Wessely, Pamela G. Robey, Sandra Heller, Zahra Dantes, Maximilian Reichert, Cagatay Guenes, Christian Bolenz, Florian Kuhn, Jozsef Maleth, Stephan Speier, Stefan Liebau, Bence Sipos, Bernhard Kuster, Thomas Seufferlein, Roland Rad, Matthias Meier, Meike Hohwieler, Alexander Kleger
Summary: The study successfully differentiated hPSCs into pancreatic duct-like organoids (PDLOs) with features of human pancreatic ducts, and observed specific growth, structural, and molecular characteristics induced by different oncogenes. Transplanted PDLOs with oncogenic KRAS alone developed dysplastic lesions or cancer, while those with KRAS and CDKN2A loss formed dedifferentiated pancreatic ductal adenocarcinomas. PDLOs with mutant GNAS led to intraductal papillary mucinous neoplasia-like structures. The research highlights the potential of PDLOs for studying pancreatic plasticity, dysplasia, and cancer formation in vitro and in vivo.
Article
Medical Laboratory Technology
Toshi Ghosh, Patricia T. Greipp, Darlene Knutson, Sara Kloft-Nelson, Sarah Jenkins, Taofic Mounajjed, Samar Said, Stefano La Rosa, Alessandro Vanoli, Fausto Sessa, Bita Naini, Andrew Bellizzi, Lizhi Zhang, Sarah E. Kerr, Rondell P. Graham
Summary: Comprehensive genomic profiling has revealed the presence of potentially targetable BRAF fusions in approximately 20% of pancreatic carcinomas with acinar differentiation. This study also identified BRAF V600E mutations in approximately 5% of cases. These findings have significant implications for targeted therapy in pancreatic cancer.
ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
(2022)
Article
Medicine, Research & Experimental
Martina Pauk, Vera Kufner, Viktorija Rumenovic, Ivo Dumic-Cule, Vladimir Farkas, Milan Milosevic, Tatjana Bordukalo-Niksic, Slobodan Vukicevic
Summary: The study found that adult Bmp6(-/-) mice showed progressive iron deposits in the exocrine pancreas, leading to pancreatic degeneration and injury, while blood glucose levels and islet structure remained unaffected, and insulin secretion was normal.
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
(2021)
Article
Multidisciplinary Sciences
Yulong Gong, Bingyuan Yang, Dingdong Zhang, Yue Zhang, Zihan Tang, Liu Yang, Katie C. Coate, Linlin Yin, Brittney A. Covington, Ravi S. Patel, Walter A. Siv, Katelyn Sellick, Matthew Shou, Wenhan Chang, E. Danielle Dean, Alvin C. Powers, Wenbiao Chen
Summary: Insufficient glucagon signalling leads to hyperaminoacidemia and stimulates the proliferation of glucagon-producing alpha cells. The study reveals that the amino acid sensitive calcium sensing receptor (CaSR) is necessary for alpha cell proliferation through Gq signalling during hyperaminoacidemia.
NATURE COMMUNICATIONS
(2023)
Article
Oncology
Chiara Modica, Martina Olivero, Francesca Zuppini, Melissa Milan, Cristina Basilico, Elisa Vigna
Summary: This study explores the molecular mechanisms of the MET/HGF signaling pathway in the interaction between pancreatic cancer cells and the tumor microenvironment. Through large-scale gene expression analysis, tenascin C was identified as a key gene involved in sustaining the malignant phenotype. Further research demonstrates the modulation of tenascin C by MET activation, suggesting a role in tumor-stroma interplay during pancreatic tumor progression.
Article
Oncology
Megan M. Harper, Miranda Lin, Shadi A. Qasem, Reema A. Patel, Michael J. Cavnar, Prakash K. Pandalai, Mei Gao, Joseph Kim
Summary: This study describes a previously unreported mechanism of PD-1/MET interaction and the oncogenic functionality of PD-1 in pancreatic cancer. The researchers found that PD-1 can induce epithelial-to-mesenchymal transition (EMT) and regulate growth, migration, and invasion in pancreatic cancer cells. Targeting PD-1 and MET together resulted in substantial tumor cell cytotoxicity and growth inhibition. These findings highlight the importance of targeting the PD-1 axis in pancreatic cancer treatment.