prof. Susanne Sebens

Inflammatory Carcinogenesis

Our group intends to elucidate the cellular and molecular interactions promoting tumorigenesis related to chronic inflammation. In the focus of our research is the pancreatic ductal adenocarcinoma, a tumor with a still dismal prognosis and being characterized by a pronounced inflammatory stroma. Stromal cells (e.g. fibroblasts, macrophages, T cells) present already during chronic inflammation promote malignant transformation of epithelial cells, a process which proceeds later on in tumors. Upon these continuous interactions epithelial and tumor cells acquire migratory and invasive abilities, genetic and epigenetic alterations and evade the attack by the immune system. Having left the primary tumor, disseminated tumor cells have to face and survive various conditions in order to grow out to metastases, particularly when reached the secondary organ. However, the impact of the stromal microenvironment of the secondary organ on metastasized tumor cells is only poorly understood and one focus of our current research. Since the tumor microenvironment (of both the primary and secondary context) is an essential determinant of chemoresistance, we aim at understanding the underlying mechanisms in order to improve therapeutic concepts.

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Prof. Susanne Sebens

Kiel University

Tel.: +49 (0) 431-500-30501

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Selected Publications

  • Rahn S, Zimmermann V, Viol F, Knaack H, Stemmer K, Peters L, Lenk L, Ungefroren H, Saur D, Schäfer H, Helm O, Sebens S. (2018) Diabetes as risk factor for pancreatic cancer: hyperglycemia promotes epithelial-mesenchymal transition and stem cell properties in pancreatic ductal epithelial cells. Cancer Letters 415:129-150
  • Ammerpohl O, Hattermann K, Held-Feindt J, Röcken C, Schäfer H, Schem C, Schewe D, Schulenburg H, Sebens S, Synowitz M, Tiwari S, Traulsen A, Trauzold A, Valerius T, Wesch W (for the Kiel Oncology Network in alphabetical order, corresponding author: Susanne Sebens) (2017) Dormancy: an evolutionary key phenomenon in cancer development. In "Ecology and evolution of cancer", ISBN: 978-0-12-804310-3
  • Lenk L, Pein M, Will O, Gomez B, Viol F, Hauser C, Egberts J-H, Gundlach J-P, Tiwari S, Weiskirchen R, Rose-John S, Röcken C, Mikulits W, Wenzel P, Schneider G, Saur D, Schäfer H, Sebens S. (2017) The hepatic microenvironment essentially determines tumor cell dormancy and metastatic outgrowth of pancreatic ductal adenocarcinoma. OncoImmunology 7(1):e1368603
  • Helm O, Held-Feindt J, Grage-Griebenow E, Reiling N, Ungefroren U, Vogel I, Krüger U, Becker T, Ebsen M, Röcken C, Kabelitz D, Schäfer H, Sebens S (2014) Tumor associated macrophages exhibit pro- and anti-inflammatory properties by which they impact on pancreatic tumorigenesis. Int J Cancer.135(4):843-61
  • Geismann C, Morscheck M, Koch D, Bergmann F, Ungefroren H, Arlt A, Tsao MS, Bachem MG, Altevogt P, Sipos B, Fölsch UR, Schäfer H, Müerköster SS (2009) Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor b1- and Slug-dependent: role in malignant transformation of pancreatic cancer. Cancer Res 69(10): 4517-4526
  • Sebens Müerköster S, Lust J, Arlt A, Häsler R, Witt M, Sebens T, Schreiber S, Fölsch UR, Schäfer H (2006) Acquired chemoresistance in pancreatic carcinoma cells – induced secretion of IL-1beta and NO lead to inactivation of caspases. Oncogene 25(28): 3973-3981