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Torben Glatz

Researcher at University of Freiburg

Publications -  58
Citations -  1038

Torben Glatz is an academic researcher from University of Freiburg. The author has contributed to research in topics: Perioperative & Medicine. The author has an hindex of 15, co-authored 52 publications receiving 779 citations. Previous affiliations of Torben Glatz include Ruhr University Bochum & University Medical Center Freiburg.

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ESOPEC: prospective randomized controlled multicenter phase III trial comparing perioperative chemotherapy (FLOT protocol) to neoadjuvant chemoradiation (CROSS protocol) in patients with adenocarcinoma of the esophagus (NCT02509286)

TL;DR: The ESOPEC trial compares perioperative chemotherapy according to the FLOT protocol to neoadjuvant chemoradiation according toThe CROSS protocol in multimodal treatment of non-metastasized recectable adenocarcinoma of the esophagus and the gastroesophageal junction to identify the superior protocol with regard to patient survival, treatment morbidity and quality of life.
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Pancreatic cancer: Circulating Tumor Cells and Primary Tumors show Heterogeneous KRAS Mutations.

TL;DR: Genetic characterization, including mutations such as KRAS, may prove useful for prognosis and understanding of tumor biology, and is compared to Kirsten rat sarcoma viral oncogene homolog mutations in pancreatic CTC and corresponding tumors.
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First-line endoscopic treatment with over-the-scope clips significantly improves the primary failure and rebleeding rates in high-risk gastrointestinal bleeding: A single-center experience with 100 cases

TL;DR: The data show for the first time that FLET with OTSC might be the best predictor to successfully prevent rebleeding of gastrointestinal bleeding compared to SLET.
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Peroxisome-proliferator-activated receptors gamma and peroxisome-proliferator-activated receptors beta/delta and the regulation of interleukin 1 receptor antagonist expression by pioglitazone in ischaemic brain.

TL;DR: The restoration of the equilibrium between I1-1β and IL-1ra in ischaemic brain tissue limits IL- 1β signalling, reduces inflammatory responses and is an important mechanism by which thiazolidinediones improve the recovery from ischaemia stroke.