Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Zahra Dantes
Based on 5 articles published since 2010
(Why 5 articles?)
||||

Between 2010 and 2020, Zahra Dantes wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article SUMO pathway inhibition targets an aggressive pancreatic cancer subtype. 2020

Biederstädt, Alexander / Hassan, Zonera / Schneeweis, Christian / Schick, Markus / Schneider, Lara / Muckenhuber, Alexander / Hong, Yingfen / Siegers, Gerrit / Nilsson, Lisa / Wirth, Matthias / Dantes, Zahra / Steiger, Katja / Schunck, Kathrin / Langston, Steve / Lenhof, H-P / Coluccio, Andrea / Orben, Felix / Slawska, Jolanta / Scherger, Anna / Saur, Dieter / Müller, Stefan / Rad, Roland / Weichert, Wilko / Nilsson, Jonas / Reichert, Maximilian / Schneider, Günter / Keller, Ulrich. ·Medical Clinic and Policlinic III, Klinikum rechts der Isar, Technical University Munich, München, Germany. · Medical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany. · Department of Hematology, Oncology and Tumor Immunology, Campus Benjamin Franklin, Charité - Universitätsmedizin Berlin, Berlin, Germany. · Center for Bioinformatics, Saarland Informatics Campus, Saarland University, Saarbrücken, Germany. · Saarbrücken Graduate School of Computer Science, Saarland Informatics Campus, Saarland University, Saarbrücken, Germany. · Institute of Pathology, Technical University Munich, München, Germany. · Department of Surgery, Sahlgrenska Cancer Center, Gothenburg University, Gothenburg, Sweden. · German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany. · Goethe University, Medical School, Institute of Biochemistry II, Frankfurt, Germany. · Oncology Drug Discovery Unit, Takeda Pharmaceuticals International Co, Cambridge, Massachusetts, USA. · Institute for Translational Cancer Research and Experimental Cancer Therapy, Technical University Munich, München, Germany. · Institute of Molecular Oncology and Functional Genomics, Technical University Munich, München, Germany. · Medical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany guenter.schneider@tum.de ulrich.keller@charite.de. · Department of Hematology, Oncology and Tumor Immunology, Campus Benjamin Franklin, Charité - Universitätsmedizin Berlin, Berlin, Germany guenter.schneider@tum.de ulrich.keller@charite.de. ·Gut · Pubmed #32001555.

ABSTRACT: OBJECTIVE: Pancreatic ductal adenocarcinoma (PDAC) still carries a dismal prognosis with an overall 5-year survival rate of 9%. Conventional combination chemotherapies are a clear advance in the treatment of PDAC; however, subtypes of the disease exist, which exhibit extensive resistance to such therapies. Genomic MYC amplifications represent a distinct subset of PDAC with an aggressive tumour biology. It is clear that hyperactivation of MYC generates dependencies that can be exploited therapeutically. The aim of the study was to find and to target MYC-associated dependencies. DESIGN: We analysed human PDAC gene expression datasets. Results were corroborated by the analysis of the small ubiquitin-like modifier (SUMO) pathway in a large PDAC cohort using immunohistochemistry. A SUMO inhibitor was used and characterised using human and murine two-dimensional, organoid and in vivo models of PDAC. RESULTS: We observed that MYC is connected to the SUMOylation machinery in PDAC. Components of the SUMO pathway characterise a PDAC subtype with a dismal prognosis and we provide evidence that hyperactivation of MYC is connected to an increased sensitivity to pharmacological SUMO inhibition. CONCLUSION: SUMO inhibitor-based therapies should be further developed for an aggressive PDAC subtype.

2 Article Cholinergic Signaling via Muscarinic Receptors Directly and Indirectly Suppresses Pancreatic Tumorigenesis and Cancer Stemness. 2018

Renz, Bernhard W / Tanaka, Takayuki / Sunagawa, Masaki / Takahashi, Ryota / Jiang, Zhengyu / Macchini, Marina / Dantes, Zahra / Valenti, Giovanni / White, Ruth A / Middelhoff, Moritz A / Ilmer, Matthias / Oberstein, Paul E / Angele, Martin K / Deng, Huan / Hayakawa, Yoku / Westphalen, C Benedikt / Werner, Jens / Remotti, Helen / Reichert, Maximilian / Tailor, Yagnesh H / Nagar, Karan / Friedman, Richard A / Iuga, Alina C / Olive, Kenneth P / Wang, Timothy C. ·Department of General, Visceral and Transplantation Surgery, Hospital of the University of Munich, Munich, Germany; German Cancer Consortium (DKTK), Partner Site Munich; and German Cancer Research Center (DKFZ), Heidelberg, Germany. · Division of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. · Department of Surgery, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki, Japan. · Department of Oncology, IRCCS San Raffaele Scientific Institute, Milan, Italy. · Department of Medicine II, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany. · Division of Oncology, Department of Medicine and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. · Perlmutter Cancer Center, New York University Langone Medical Center, New York, New York. · Department of Pathology, and Molecular Medicine and Genetics Center, The Fourth Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. · Department of Gastroenterology, Graduate School of Medicine, the University of Tokyo, Tokyo, Japan. · Department of Internal Medicine III, Hospital of the University of Munich, Munich, Germany; German Cancer Consortium (DKTK), Partner Site Munich; and German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Pathology and Cell Biology, Columbia University Medical Center, New York, New York. · Biomedical Informatics Shared Resource of the Herbert Irving Comprehensive Cancer Center and Department of Biomedical Informatics, Columbia University Medical Center, New York, New York. · Department of Pathology and Cell Biology and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. · Division of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. tcw21@columbia.edu. ·Cancer Discov · Pubmed #30185628.

ABSTRACT: In many solid tumors, parasympathetic input is provided by the vagus nerve, which has been shown to modulate tumor growth. However, whether cholinergic signaling directly regulates progression of pancreatic ductal adenocarcinoma (PDAC) has not been defined. Here, we found that subdiaphragmatic vagotomy in LSL-

3 Article Mutant KRAS-driven cancers depend on PTPN11/SHP2 phosphatase. 2018

Ruess, Dietrich A / Heynen, Guus J / Ciecielski, Katrin J / Ai, Jiaoyu / Berninger, Alexandra / Kabacaoglu, Derya / Görgülü, Kivanc / Dantes, Zahra / Wörmann, Sonja M / Diakopoulos, Kalliope N / Karpathaki, Angeliki F / Kowalska, Marlena / Kaya-Aksoy, Ezgi / Song, Liang / van der Laan, Eveline A Zeeuw / López-Alberca, María P / Nazaré, Marc / Reichert, Maximilian / Saur, Dieter / Erkan, Mert M / Hopt, Ulrich T / Sainz, Bruno / Birchmeier, Walter / Schmid, Roland M / Lesina, Marina / Algül, Hana. ·Mildred-Scheel-Chair of Tumor Metabolism, Internal Medicine II, Klinikum rechts der Isar, Technische Universität München, Munich, Germany. · Department of Surgery, Faculty of Medicine, Medical Center-University of Freiburg, Freiburg, Germany. · Cancer Research Program, Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, Germany. · Medicinal Chemistry, Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Berlin, Germany. · Koç University School of Medicine, Istanbul, Turkey. · Department of Biochemistry, Autónoma University of Madrid, School of Medicine, Instituto de Investigaciones Biomédicas "Alberto Sols", Madrid, Spain. · Mildred-Scheel-Chair of Tumor Metabolism, Internal Medicine II, Klinikum rechts der Isar, Technische Universität München, Munich, Germany. hana.alguel@mri.tum.de. ·Nat Med · Pubmed #29808009.

ABSTRACT: The ubiquitously expressed non-receptor protein tyrosine phosphatase SHP2, encoded by PTPN11, is involved in signal transduction downstream of multiple growth factor, cytokine and integrin receptors

4 Article MTOR inhibitor-based combination therapies for pancreatic cancer. 2018

Hassan, Zonera / Schneeweis, Christian / Wirth, Matthias / Veltkamp, Christian / Dantes, Zahra / Feuerecker, Benedikt / Ceyhan, Güralp O / Knauer, Shirley K / Weichert, Wilko / Schmid, Roland M / Stauber, Roland / Arlt, Alexander / Krämer, Oliver H / Rad, Roland / Reichert, Maximilian / Saur, Dieter / Schneider, Günter. ·Medical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, 81675 München, Germany. · Institute of Pathology, Heinrich-Heine University and University Hospital Düsseldorf, 40225 Düsseldorf, Germany. · Department of Nuclear Medicine, Klinikum rechts der Isar, Technical University Munich, 81675 München, Germany. · German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), 69120 Heidelberg, Germany. · Department of Surgery, Klinikum rechts der Isar, Technical University of Munich, 81675 München, Germany. · Molecular Biology, Centre for Medical Biotechnology (ZMB), University Duisburg-Essen, 45141 Essen, Germany. · Institute of Pathology, Technische Universität München, 81675 München, Germany. · Molecular and Cellular Oncology/ENT, University Medical Center Mainz, Langenbeckstrasse 1, Mainz 55131, Germany. · Laboratory of Molecular Gastroenterology and Hepatology, 1st Department of Internal Medicine, University Hospital Schleswig-Holstein, Kiel, Germany. · Department of Toxicology, University of Mainz Medical Center, Mainz 55131, Germany. · Division of Gastroenterology and Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ·Br J Cancer · Pubmed #29384525.

ABSTRACT: BACKGROUND: Although the mechanistic target of rapamycin (MTOR) kinase, included in the mTORC1 and mTORC2 signalling hubs, has been demonstrated to be active in a significant fraction of patients with pancreatic ductal adenocarcinoma (PDAC), the value of the kinase as a therapeutic target needs further clarification. METHODS: We used Mtor floxed mice to analyse the function of the kinase in context of the pancreas at the genetic level. Using a dual-recombinase system, which is based on the flippase-FRT (Flp-FRT) and Cre-loxP recombination technologies, we generated a novel cellular model, allowing the genetic analysis of MTOR functions in tumour maintenance. Cross-species validation and pharmacological intervention studies were used to recapitulate genetic data in human models, including primary human 3D PDAC cultures. RESULTS: Genetic deletion of the Mtor gene in the pancreas results in exocrine and endocrine insufficiency. In established murine PDAC cells, MTOR is linked to metabolic pathways and maintains the glucose uptake and growth. Importantly, blocking MTOR genetically as well as pharmacologically results in adaptive rewiring of oncogenic signalling with activation of canonical extracellular signal-regulated kinase and phosphoinositide 3-kinase-AKT pathways. We provide evidence that interfering with such adaptive signalling in murine and human PDAC models is important in a subgroup. CONCLUSIONS: Our data suggest developing dual MTORC1/TORC2 inhibitor-based therapies for subtype-specific intervention.

5 Article β2 Adrenergic-Neurotrophin Feedforward Loop Promotes Pancreatic Cancer. 2018

Renz, Bernhard W / Takahashi, Ryota / Tanaka, Takayuki / Macchini, Marina / Hayakawa, Yoku / Dantes, Zahra / Maurer, H Carlo / Chen, Xiaowei / Jiang, Zhengyu / Westphalen, C Benedikt / Ilmer, Matthias / Valenti, Giovanni / Mohanta, Sarajo K / Habenicht, Andreas J R / Middelhoff, Moritz / Chu, Timothy / Nagar, Karan / Tailor, Yagnesh / Casadei, Riccardo / Di Marco, Mariacristina / Kleespies, Axel / Friedman, Richard A / Remotti, Helen / Reichert, Maximilian / Worthley, Daniel L / Neumann, Jens / Werner, Jens / Iuga, Alina C / Olive, Kenneth P / Wang, Timothy C. ·Department of General, Visceral and Transplantation Surgery, Hospital of the University of Munich, 81377 Munich, Germany; Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Oncology, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan. · Department of Medicine II, Klinikum Rechts der Isar, Technische Universität München, 81675 Munich, Germany. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Internal Medicine III, Hospital of the University of Munich, 81377 Munich, Germany. · Department of General, Visceral and Transplantation Surgery, Hospital of the University of Munich, 81377 Munich, Germany. · Institute for Cardiovascular Prevention, University of Munich, 80336 Munich, Germany. · Department of Internal Medicine and Surgery (DIMEC), Alma Mater Studiorum, University of Bologna, Sant'Orsola-Malpighi Hospital, 40138 Bologna, Italy. · Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Sant'Orsola-Malpighi Hospital, 40138 Bologna, Italy. · Biomedical Informatics Shared Resource, Herbert Irving Comprehensive Cancer Center, Department of Biomedical Informatics, Columbia University Medical Center, New York, NY 10032, USA. · Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Medicine, University of Adelaide, Adelaide, SA 5005, Australia. · Department of Pathology, Hospital of the University of Munich, 81377 Munich, Germany. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA. Electronic address: tcw21@columbia.edu. ·Cancer Cell · Pubmed #29249692.

ABSTRACT: Catecholamines stimulate epithelial proliferation, but the role of sympathetic nerve signaling in pancreatic ductal adenocarcinoma (PDAC) is poorly understood. Catecholamines promoted ADRB2-dependent PDAC development, nerve growth factor (NGF) secretion, and pancreatic nerve density. Pancreatic Ngf overexpression accelerated tumor development in LSL-Kras