Thomas M. Gress
University of Marburg
GeneCancerInternal medicineEndocrinologyPathologyOncologyMolecular biologyChemistryImmunologyPancreatitisPancreatic diseasePancreasNeuroendocrine tumorsPancreatic cancerCancer researchMedicineTranscription factorBiologyGastroenterologyCell biology
374Publications
82H-index
17.6kCitations
Publications 469
Newest
BACKGROUND AND AIMS The overall evidence on the association between gallbladder conditions (GBC: gallstones and cholecystectomy) and pancreatic cancer (PC) is inconsistent. To our knowledge, no previous investigations considered the role of tumour characteristics on this association. Thus, we aimed to assess the association between self-reported GBC and PC risk, by focussing on timing to PC diagnosis and tumour features (stage, location, and resection). METHODS Data derived from a European case-...
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#1Sami Matrood (University of Marburg)H-Index: 1
#7Damiano Librizzi (University of Marburg)H-Index: 10
Last. Zoltan Kender (University Hospital Heidelberg)H-Index: 7
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#7Mark Klein (University of Mainz)H-Index: 185
Emerging data demonstrate that the activity of immune cells can be modulated by microbial molecules. Here, we show that the short-chain fatty acids (SCFAs) pentanoate and butyrate enhance the anti-tumor activity of cytotoxic T lymphocytes (CTLs) and chimeric antigen receptor (CAR) T cells through metabolic and epigenetic reprograming. We show that in vitro treatment of CTLs and CAR T cells with pentanoate and butyrate increases the function of mTOR as a central cellular metabolic sensor, and inh...
6 CitationsSource
#1Elisabeth Hessmann (GAU: University of Göttingen)H-Index: 13
#2Günter Schneider (TUM: Technische Universität München)H-Index: 47
Last. Chiara FalcomatàH-Index: 2
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Abstract null null Pancreatic ductal adenocarcinoma (PDAC) remains a major challenge in cancer medicine. Given the increase in incidence and mortality, interdisciplinary research is necessary to translate basic knowledge into therapeutic strategies improving the outcome of patients. On the 4th and 5th of February 2021, three German pancreatic cancer research centers, the clinical research unit (CRU) 5002 from Gottingen, the collaborative research center (CRC) 1321 from Munich, and CRU325 from Ma...
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#1Anja Rinke (University of Marburg)H-Index: 22
#2Christoph J. Auernhammer (LMU: Ludwig Maximilian University of Munich)H-Index: 31
Last. Thomas M. Gress (University of Marburg)H-Index: 82
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Gastroenteropancreatic neuroendocrine neoplasia (GEPNEN) comprises clinically as well as prognostically diverse tumour entities often diagnosed at late stage. Current classification provides a uniform terminology and a Ki67-based grading system, thereby facilitating management. Advances in the study of genomic and epigenetic landscapes have amplified knowledge of tumour biology and enhanced identification of prognostic and potentially predictive treatment subgroups. Translation of this genomic a...
1 CitationsSource
Background Familial pancreatic carcinoma (FPC) is a rare hereditary tumor syndrome with a heterogeneous clinical phenotype. The study of FPC also contributes to a better understanding of the more common sporadic pancreatic ductal adenocarcinoma (PDAC). We report on the past 20 years' experience of the German National Case Collection for Familial Pancreatic Carcinoma (FaPaCa) of the German Cancer Aid (Deutsche Krebshilfe). Methods From 1999 onward, families in which at least two first-degree rela...
2 CitationsSource
#1Silke D. Werle (University of Ulm)H-Index: 2
#2Julian D. Schwab (University of Ulm)H-Index: 6
Last. Hans A. Kestler (University of Ulm)H-Index: 55
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Cofilin-1 (CFL1) overexpression in pancreatic cancer correlates with high invasiveness and shorter survival. Besides a well-documented role in actin remodeling, additional cellular functions of CFL1 remain poorly understood. Here, we unraveled molecular tumor-promoting functions of CFL1 in pancreatic cancer. For this purpose, we first show that a knockdown of CFL1 results in reduced growth and proliferation rates in vitro and in vivo, while apoptosis is not induced. By mechanistic modeling we we...
2 CitationsSource
#1Albert JobH-Index: 2
#2Marina TaturaH-Index: 1
Last. Eike GallmeierH-Index: 24
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Inhibition of the kinase ATR, a central regulator of the DNA damage response, eliminates subsets of cancer cells in certain tumors. As previously shown, this is at least partly attributable to synthetic lethal interactions between ATR and POLD1, the catalytic subunit of the polymerase δ. Various POLD1 variants have been found in colorectal cancer, but their significance as therapeutic targets for ATR pathway inhibition remains unknown. Using CRISPR/Cas9 in the colorectal cancer cell line DLD-1, ...
1 CitationsSource