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Pancreatic Neoplasms: HELP
Articles by Alexander J. Kind
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Alexander Kind wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Genetically Engineered Pigs to Study Cancer. 2020

Kalla, Daniela / Kind, Alexander / Schnieke, Angelika. ·Chair of Livestock Biotechnology, School of Life Sciences, Technische Universität München, 85354 Freising, Germany. ·Int J Mol Sci · Pubmed #31940967.

ABSTRACT: Recent decades have seen groundbreaking advances in cancer research. Genetically engineered animal models, mainly in mice, have contributed to a better understanding of the underlying mechanisms involved in cancer. However, mice are not ideal for translating basic research into studies closer to the clinic. There is a need for complementary information provided by non-rodent species. Pigs are well suited for translational biomedical research as they share many similarities with humans such as body and organ size, aspects of anatomy, physiology and pathophysiology and can provide valuable means of developing and testing novel diagnostic and therapeutic procedures. Porcine oncology is a new field, but it is clear that replication of key oncogenic mutation in pigs can usefully mimic several human cancers. This review briefly outlines the technology used to generate genetically modified pigs, provides an overview of existing cancer models, their applications and how the field may develop in the near future.

2 Article A next-generation dual-recombinase system for time- and host-specific targeting of pancreatic cancer. 2014

Schönhuber, Nina / Seidler, Barbara / Schuck, Kathleen / Veltkamp, Christian / Schachtler, Christina / Zukowska, Magdalena / Eser, Stefan / Feyerabend, Thorsten B / Paul, Mariel C / Eser, Philipp / Klein, Sabine / Lowy, Andrew M / Banerjee, Ruby / Yang, Fangtang / Lee, Chang-Lung / Moding, Everett J / Kirsch, David G / Scheideler, Angelika / Alessi, Dario R / Varela, Ignacio / Bradley, Allan / Kind, Alexander / Schnieke, Angelika E / Rodewald, Hans-Reimer / Rad, Roland / Schmid, Roland M / Schneider, Günter / Saur, Dieter. ·Department of Internal Medicine II, Klinikum rechts der Isar, Technische Universität München, München, Germany. · German Cancer Research Center (DKFZ), Division for Cellular Immunology, Heidelberg, Germany. · Gene Center and Department of Biochemistry, Center for Integrated Protein Science CIPSM, Ludwig-Maximilians-Universität München, München, Germany. · Moores Cancer Center, Division of Surgical Oncology, University of California San Diego, La Jolla, California, USA. · Wellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridge, UK. · Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina, USA. · Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina, USA. · Helmholtz Zentrum München, Research Unit Comparative Medicine, Neuherberg, Germany. · MRC Protein Phosphorylation Unit, University of Dundee, Dundee, UK. · Instituto de Biomedicina y Biotecnología de Cantabria (CSIC-UC-Sodercan), Departamento de Biología Molecular, Universidad de Cantabria, Santander, Spain. · Livestock Biotechnology, Technische Universität München, Freising, Germany. · German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany. ·Nat Med · Pubmed #25326799.

ABSTRACT: Genetically engineered mouse models (GEMMs) have dramatically improved our understanding of tumor evolution and therapeutic resistance. However, sequential genetic manipulation of gene expression and targeting of the host is almost impossible using conventional Cre-loxP-based models. We have developed an inducible dual-recombinase system by combining flippase-FRT (Flp-FRT) and Cre-loxP recombination technologies to improve GEMMs of pancreatic cancer. This enables investigation of multistep carcinogenesis, genetic manipulation of tumor subpopulations (such as cancer stem cells), selective targeting of the tumor microenvironment and genetic validation of therapeutic targets in autochthonous tumors on a genome-wide scale. As a proof of concept, we performed tumor cell-autonomous and nonautonomous targeting, recapitulated hallmarks of human multistep carcinogenesis, validated genetic therapy by 3-phosphoinositide-dependent protein kinase inactivation as well as cancer cell depletion and show that mast cells in the tumor microenvironment, which had been thought to be key oncogenic players, are dispensable for tumor formation.

3 Article Selective requirement of PI3K/PDK1 signaling for Kras oncogene-driven pancreatic cell plasticity and cancer. 2013

Eser, Stefan / Reiff, Nina / Messer, Marlena / Seidler, Barbara / Gottschalk, Kathleen / Dobler, Melanie / Hieber, Maren / Arbeiter, Andreas / Klein, Sabine / Kong, Bo / Michalski, Christoph W / Schlitter, Anna Melissa / Esposito, Irene / Kind, Alexander J / Rad, Lena / Schnieke, Angelika E / Baccarini, Manuela / Alessi, Dario R / Rad, Roland / Schmid, Roland M / Schneider, Günter / Saur, Dieter. ·Department of Internal Medicine 2, Technische Universität München, Ismaningerstr. 22, 81675 München, Germany. ·Cancer Cell · Pubmed #23453624.

ABSTRACT: Oncogenic Kras activates a plethora of signaling pathways, but our understanding of critical Ras effectors is still very limited. We show that cell-autonomous phosphoinositide 3-kinase (PI3K) and 3-phosphoinositide-dependent protein kinase 1 (PDK1), but not Craf, are key effectors of oncogenic Kras in the pancreas, mediating cell plasticity, acinar-to-ductal metaplasia (ADM), and pancreatic ductal adenocarcinoma (PDAC) formation. This contrasts with Kras-driven non-small cell lung cancer, where signaling via Craf, but not PDK1, is an essential tumor-initiating event. These in vivo genetic studies together with pharmacologic treatment studies in models of human ADM and PDAC demonstrate tissue-specific differences of oncogenic Kras signaling and define PI3K/PDK1 as a suitable target for therapeutic intervention specifically in PDAC.