Susanne Sebens

ORCID: 0000-0001-6582-0083
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About
Contact & Profiles
Research Areas
  • Pancreatic and Hepatic Oncology Research
  • Cancer Cells and Metastasis
  • Cancer Immunotherapy and Biomarkers
  • Genomics, phytochemicals, and oxidative stress
  • Immune cells in cancer
  • Cancer Genomics and Diagnostics
  • Immune Cell Function and Interaction
  • Monoclonal and Polyclonal Antibodies Research
  • Cancer, Hypoxia, and Metabolism
  • Epigenetics and DNA Methylation
  • Phagocytosis and Immune Regulation
  • Pancreatitis Pathology and Treatment
  • Immunotherapy and Immune Responses
  • T-cell and B-cell Immunology
  • CAR-T cell therapy research
  • Cell Adhesion Molecules Research
  • Cancer Research and Treatments
  • Synthesis and Biological Evaluation
  • Chemokine receptors and signaling
  • Pancreatic function and diabetes
  • Lung Cancer Treatments and Mutations
  • NF-κB Signaling Pathways
  • GDF15 and Related Biomarkers
  • Proteoglycans and glycosaminoglycans research
  • Caveolin-1 and cellular processes

University Hospital Schleswig-Holstein
2016-2025

University of Lübeck
2016-2025

Kiel University
2016-2025

Clinical Research Center Kiel
2011-2023

Universität Hamburg
2022

University Medical Center Hamburg-Eppendorf
2022

Genesis Foundation
2014-2015

Laboratory of Molecular Genetics
2012

Schmerzklinik Kiel
2006-2012

SUPERA Park of Innovation and Technology of Ribeirão Preto
2012

Recent advances in tumor biology have revealed that a detailed analysis of the complex interactions cells with their adjacent microenvironment (tumor stroma) is mandatory order to understand various mechanisms involved growth and development metastasis. The mutual between cellular non-cellular components (extracellular matrix = ECM) will eventually lead loss tissue homeostasis promote progression. Thus, genetically altered ECM on one hand reactive non-neoplastic other essentially control...

10.1186/1478-811x-9-18 article EN cc-by Cell Communication and Signaling 2011-01-01

Pancreatic ductal adenocarcinoma (PDAC) still ranking 4th in the order of fatal tumor diseases is characterized by a profound stroma with high numbers tumor-associated macrophages (TAMs). Driven environmental factors, monocytes differentiate into M1- or M2-macrophages, latter commonly regarded as being protumorigenic. Because detailed analysis TAMs human PDAC development lacking, freshly isolated PDAC-derived were analyzed for their phenotype and impact on epithelial-mesenchymal-transition...

10.1002/ijc.28736 article EN International Journal of Cancer 2014-01-23

The ability of human γδ T cells from healthy donors to kill pancreatic ductal adenocarcinoma (PDAC) in vitro and vivo immunocompromised mice requires the addition T-cell-stimulating antigens. In this study, we demonstrate that isolated patients with PDAC tumor infiltrates lyse after selective stimulation phosphorylated We determined absolute numbers T-cell subsets patient whole blood applied a real-time cell analyzer measure their cytotoxic effector function over prolonged time periods....

10.1158/0008-5472.can-13-0675 article EN Cancer Research 2014-01-22

FOXO3 is consistently annotated as a human longevity gene. However, functional variants and underlying mechanisms for the association remain unknown. Here, we perform resequencing of locus single-nucleotide variant (SNV) genotyping in three European populations. We find two SNVs, rs12206094 rs4946935, to be most significantly associated with further characterize them functionally. experimentally validate silico predicted allele-dependent binding transcription factors (CTCF, SRF) SNVs....

10.1038/s41467-017-02183-y article EN cc-by Nature Communications 2017-12-06

An enhanced expression of human epidermal growth factor receptor 2 (HER2, ErbB2) often occurs in an advanced stage breast, ovarian, gastric or esophageal cancer and pancreatic ductal adenocarcinoma (PDAC). Commonly, HER2 is associated with poor clinical outcome chemoresistance ovarian breast patients. Treatment humanized anti-HER2 monoclonal antibodies such as trastuzumab pertuzumab has improved the patients HER2-positive-metastatic cancer, but not all benefit. In this study, bispecific...

10.3389/fimmu.2018.00814 article EN cc-by Frontiers in Immunology 2018-04-19

Abstract The application of evolutionary and ecological principles to cancer prevention treatment, as well recognizing a selection force in nature, has gained impetus over the last 50 years. Following initial theoretical approaches that combined knowledge from interdisciplinary fields, it became clear using eco‐evolutionary framework is key importance understand cancer. We are now at pivotal point where accumulating evidence starts steer future directions discipline allows us underpin...

10.1111/eva.13190 article EN cc-by Evolutionary Applications 2020-12-31

Progression of pancreatic ductal adenocarcinoma (PDAC) is largely the result genetic and/or epigenetic alterations in transforming growth factor-beta (TGF-β)/Smad signalling pathway, eventually resulting loss TGF-β-mediated arrest and an increase cellular migration, invasion, metastasis. These responses to TGF-β are mediated solely or partially through canonical Smad pathway which commences with activation receptor-regulated Smads (R-Smads) Smad2 Smad3 by type I receptor. However, little...

10.1186/1476-4598-10-67 article EN cc-by Molecular Cancer 2011-01-01

Expression of L1 cell adhesion molecule (L1CAM) is associated with poor prognosis in a variety human carcinomas including breast, ovarian and pancreatic ductal adenocarcinoma (PDAC). Recently we reported that L1CAM induces sustained nuclear factor kappa B (NF-κB) activation by augmenting the autocrine production interleukin 1 beta (IL-1β), process dependent on interaction integrins. In present study, demonstrate transforming growth β1 (TGF-β1) treatment breast carcinoma (MDA-MB231) PDAC...

10.1093/carcin/bgs220 article EN Carcinogenesis 2012-07-04

Pancreatic ductal adenocarcinoma (PDAC) is characterized by an extensive stroma being also present in chronic pancreatitis (CP). Using immunohistochemistry, the of CP and PDAC was comprehensively analyzed correlated with epithelial/carcinoma-related alterations clinicopathological patient characteristics. While there were no significant differences between regarding distribution CD3+ T cells α-SMA+ fibroblasts, proportions CD4+ CD8+ significantly lower numbers CD25+(CD4+) FoxP3+(CD4+)...

10.1371/journal.pone.0094357 article EN cc-by PLoS ONE 2014-05-05

Patients with highly malignant glioblastomas have a short median survival time mainly due to aggressive relapses after therapeutic treatment. Beside others, they achieve their progressive character via epithelial-to-mesenchymal transition (EMT). However, comprehensive investigations on EMT in paired primary-recurrent glioblastoma pairs are presently not available. Thus, our present study we examined the expression profile of different EMT-markers 17 matched primary and recurrent by qPCR...

10.3892/ijo.2015.2944 article EN International Journal of Oncology 2015-03-31

Nrf2 and TGF-β1 both affect tumorigenesis in a dual fashion, either by preventing carcinogen induced carcinogenesis suppressing tumor growth, respectively, or conferring cytoprotection invasiveness to cells during malignant transformation. Given the involvement of adaptation epithelial persistent inflammatory stress, e.g. pancreatic duct epithelium chronic pancreatitis, crosstalk between can be envisaged. By using premalignant human (HPDE) ductal adenocarcinoma cell line Colo357, we could...

10.1371/journal.pone.0132978 article EN cc-by PLoS ONE 2015-07-30

Although nuclear factor E2-related factor-2 (Nrf2) protects from carcinogen-induced tumorigenesis, underlying the rationale for using Nrf2 inducers in chemoprevention, this antioxidative transcription may also act as a proto-oncogene. Thus, an enhanced activity promotes formation and chemoresistance of colon cancer. One mechanism causing persistent activation is adaptation epithelial cells to oxidative stress during chronic inflammation, e.g. colonocytes inflammatory bowel diseases,...

10.1074/jbc.m113.490920 article EN cc-by Journal of Biological Chemistry 2013-12-06

// Hendrik Ungefroren 1,2 , Susanne Sebens 3 Klaudia Giehl 4 Ole Helm Stephanie Groth 2,7 Fred Fändrich 2 Christoph Röcken 5 Bence Sipos 6 Lehnert 1 Frank Gieseler First Department of Medicine, University Hospital Schleswig-Holstein (UKSH), Campus Lübeck, Germany Clinic for Applied Cellular (UKSH) Kiel, Institute Experimental Group Inflammatory Carcinogenesis, Molecular Oncology Solid Tumors, Internal Medicine V, Justus-Liebig-University Giessen, Pathology, General Pathology and...

10.18632/oncotarget.1696 article EN cc-by Oncotarget 2013-12-23

Chronic pancreatitis (CP) is a risk factor of pancreatic ductal adenocarcinoma (PDAC) and characterized by pronounced desmoplastic reaction with CD4+ T cells accounting for the majority stromal cell infiltrate. Epithelial-mesenchymal-transition (EMT) critical process metastasis which epithelial/carcinoma become enabled to disseminate probably prior tumor formation. To investigate whether induce EMT in human epithelial cells, premalignant H6c7 were mono- or co-cultured CD4+CD25+CD127-CD49d-...

10.1080/2162402x.2014.1000083 article EN OncoImmunology 2015-01-22

The metabolism of seaweeds depends on environmental parameters, the availability nutrients, and biotic/abiotic stresses; therefore, their chemical composition fluctuates throughout year. This study investigated seasonal variations in metabolome Baltic Sea brown alga Fucus vesiculosus its potential relation to bioactivity profile. By using a definitive screening design (DSD) combined with pressurised liquid extraction (PLE), an optimised protocol was developed extract algal biomass monthly...

10.3390/md16120503 article EN cc-by Marine Drugs 2018-12-13

Metabolite exchange between stromal and tumor cells or among themselves accompanies metabolic reprogramming in cancer including pancreatic adenocarcinoma (PDAC). Some import utilize lactate for oxidative energy production (reverse Warburg-metabolism) the presence of these “reverse Warburg“ associates with a more aggressive phenotype worse prognosis, though underlying mechanisms are poorly understood. We now show that PDAC (BxPc3, A818-6, T3M4) expressing lactate-importer monocarboxylate...

10.3390/cancers12030581 article EN Cancers 2020-03-03
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