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Pancreatic Neoplasms: HELP
Articles by Stefan Schreiber
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Stefan Schreiber wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial Neoadjuvant chemoradiation therapy with gemcitabine/cisplatin and surgery versus immediate surgery in resectable pancreatic cancer: results of the first prospective randomized phase II trial. 2015

Golcher, Henriette / Brunner, Thomas B / Witzigmann, Helmut / Marti, Lukas / Bechstein, Wolf-Otto / Bruns, Christiane / Jungnickel, Henry / Schreiber, Stefan / Grabenbauer, Gerhard G / Meyer, Thomas / Merkel, Susanne / Fietkau, Rainer / Hohenberger, Werner. ·Department of Surgery, University Hospital Erlangen, Krankenhausstr. 12, 91054, Erlangen, Germany, henriette.golcher@uk-erlangen.de. ·Strahlenther Onkol · Pubmed #25252602.

ABSTRACT: BACKGROUND: In nonrandomized trials, neoadjuvant treatment was reported to prolong survival in patients with pancreatic cancer. As neoadjuvant chemoradiation is established for the treatment of rectal cancer we examined the value of neoadjuvant chemoradiotherapy in pancreatic cancer in a randomized phase II trial. Radiological staging defining resectability was basic information prior to randomization in contrast to adjuvant therapy trials resting on pathological staging. PATIENTS AND METHODS: Patients with resectable adenocarcinoma of the pancreatic head were randomized to primary surgery (Arm A) or neoadjuvant chemoradiotherapy followed by surgery (Arm B), which was followed by adjuvant chemotherapy in both arms. A total of 254 patients were required to detect a 4.33-month improvement in median overall survival (mOS). RESULTS: The trial was stopped after 73 patients; 66 patients were eligible for analysis. Twenty nine of 33 allocated patients received chemoradiotherapy. Radiotherapy was completed in all patients. Chemotherapy was changed in 3 patients due to toxicity. Tumor resection was performed in 23 vs. 19 patients (A vs. B). The R0 resection rate was 48% (A) and 52% (B, P = 0.81) and (y)pN0 was 30% (A) vs. 39% (B, P = 0.44), respectively. Postoperative complications were comparable in both groups. mOS was 14.4 vs. 17.4 months (A vs. B; intention-to-treat analysis; P = 0.96). After tumor resection, mOS was 18.9 vs. 25.0 months (A vs. B; P = 0.79). CONCLUSION: This worldwide first randomized trial for neoadjuvant chemoradiotherapy in pancreatic cancer showed that neoadjuvant chemoradiation is safe with respect to toxicity, perioperative morbidity, and mortality. Nevertheless, the trial was terminated early due to slow recruiting and the results were not significant. ISRCTN78805636; NCT00335543.

2 Article TRAIL/NF-κB/CX3CL1 Mediated Onco-Immuno Crosstalk Leading to TRAIL Resistance of Pancreatic Cancer Cell Lines. 2018

Geismann, Claudia / Erhart, Wiebke / Grohmann, Frauke / Schreiber, Stefan / Schneider, Günter / Schäfer, Heiner / Arlt, Alexander. ·Laboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany. cgeismann@email.uni-kiel.de. · Laboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany. wiebke.erhart@uksh.de. · Laboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany. fraukethun@gmx.de. · Laboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany. s.schreiber@mucosa.de. · Institute of Clinical Molecular Biology, UKSH Campus Kiel, 24105 Kiel, Germany. s.schreiber@mucosa.de. · Technische Universität München, Klinikum Rechts der Isar, II. Medizinische Klinik, 81675 Munich, Germany. guenter.schneider@tum.de. · Laboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany. hschaef@1med.uni-kiel.de. · Institute of Experimental Cancer Research, UKSH Campus Kiel, 24105 Kiel, Germany. hschaef@1med.uni-kiel.de. · Laboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany. aarlt@1med.uni-kiel.de. ·Int J Mol Sci · Pubmed #29867042.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignant neoplasms and registers rising death rates in western countries. Due to its late detection in advanced stages, its extremely aggressive nature and the minimal effectiveness of currently available therapies, PDAC is a challenging problem in the clinical field. One characteristic of PDAC is a distinct desmoplasia consisting of fibroblasts, endothelial and immune cells as well as non-cellular components, contributing to therapy resistance. It is well established that the NF-κB signaling pathway controls inflammation, cancer progression and apoptosis resistance in PDAC. This study attempts to identify NF-κB target genes mediating therapy resistance of humane PDAC cell lines towards death ligand induced apoptosis. By using a genome wide unbiased approach the chemokine CX3CL1 was established as a central NF-κB target gene mediating therapy resistance. While no direct impact of CX3CL1 expression on cancer cell apoptosis was identified in co-culture assays it became apparent that CX3CL1 is acting in a paracrine fashion, leading to an increased recruitment of inflammatory cells. These inflammatory cells in turn mediate apoptosis resistance of PDAC cells. Therefore, our data dissect a bifunctional cross-signaling pathway in PDAC between tumor and immune cells giving rise to therapy resistance.

3 Article Role of CCL20 mediated immune cell recruitment in NF-κB mediated TRAIL resistance of pancreatic cancer. 2017

Geismann, Claudia / Grohmann, Frauke / Dreher, Anita / Häsler, Robert / Rosenstiel, Philip / Legler, Karen / Hauser, Charlotte / Egberts, Jan Hendrik / Sipos, Bence / Schreiber, Stefan / Linkermann, Andreas / Hassan, Zonera / Schneider, Günter / Schäfer, Heiner / Arlt, Alexander. ·Department of Internal Medicine I, Laboratory of Molecular Gastroenterology & Hepatology, UKSH-Campus Kiel, Kiel, Germany. · Institute of Clinical Molecular Biology, UKSH Campus Kiel, Germany. · Division of Molecular Oncology, Institute for Experimental Cancer Research, UKSH Campus Kiel, Kiel, Germany. · Department of Surgery, UKSH Campus Kiel, Kiel, German. · Institute of Pathology, University Hospital Tübingen, Tübingen, Germany. · Department of Internal Medicine I, Laboratory of Molecular Gastroenterology & Hepatology, UKSH-Campus Kiel, Kiel, Germany; Institute of Clinical Molecular Biology, UKSH Campus Kiel, Germany. · Clinic for Nephrology and Hypertension, Christian-Albrechts-University, Kiel, Germany. · Technische Universität München, Klinikum rechts der Isar, II. Medizinische Klinik, Munich, Germany. · Department of Internal Medicine I, Laboratory of Molecular Gastroenterology & Hepatology, UKSH-Campus Kiel, Kiel, Germany; Institute of Experimental Cancer Research, UKSH Campus Kiel, Germany. · Department of Internal Medicine I, Laboratory of Molecular Gastroenterology & Hepatology, UKSH-Campus Kiel, Kiel, Germany. Electronic address: aarlt@1med.uni-kiel.de. ·Biochim Biophys Acta Mol Cell Res · Pubmed #28188806.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) represents one of the deadliest cancers. From a clinical view, the transcription factor NF-κB is of particular importance, since this pathway confers apoptosis resistance and limits drug efficacy. Whereas the role of the most abundant NF-κB subunit p65/RelA in therapeutic resistance is well documented, only little knowledge of the RelA downstream targets and their functional relevance in TRAIL mediated apoptosis in PDAC is available. In the present study TRAIL resistant and sensitive PDAC cell lines were analyzed for differentially expressed RelA target genes, to define RelA downstream targets mediating TRAIL resistance. The most upregulated target gene was then further functionally characterized. Unbiased genome-wide expression analysis demonstrated that the chemokine CCL20 represents the strongest TRAIL inducible direct RelA target gene in resistant PDAC cells. Unexpectedly, targeting CCL20 by siRNA, blocking antibodies or by downregulation of the sole CCL20 receptor CCR6 had no effect on PDAC cell death or cancer cell migration, arguing against an autocrine role of CCL20 in PDAC. However, by using an ex vivo indirect co-culture system we were able to show that CCL20 acts paracrine to recruit immune cells. Importantly, CCL20-recruited immune cells further increase TRAIL resistance of CCL20-producing PDAC cells. In conclusion, our data show a functional role of a RelA-CCL20 pathway in PDAC TRAIL resistance. We demonstrate how the therapy-induced cross-talk of cancer cells with immune cells affects treatment responses, knowledge needed to tailor novel bi-specific treatments, which target tumor cell as well as immune cells.