Prof. Roland M. Schmid | Dr. Henrik Einwächter Research Group

Our research group is working on the molecular basis of pancreatic carcinogenesis and tumor survival, investigating the role of tumor-relevant mutations using transgenic and knock-in mice; one focus is on the link between oxidative stress, chronic inflammatory processes and tumor development.

Team

Team

Former members

  • Hande Asimgil, PhD
  • Lisa Baumgärtner, M.Sc.
  • Ramona Böhm, Postdoc
  • Judit Desztics, M.Sc./Dipl.-Ing.
  • Bailing Li, MMed
  • Anja Motz, BTA
  • Leeanne Mundle, M.Sc.
  • Thorsten Neuß, M.Sc.
  • Kerstin Pfister, cand. med.
  • Mariana Rickmann, PhD
  • Christin Ruoff, M.Sc.
  • Dr. med. vet. Marie-Christin Schilloks
  • Andrea Stroppiana, Tierarzt
  • Chao Wu, MMed
Research area

The major research objectives of our laboratory are to understand the molecular mechanisms of pancreatic carcinogenesis and tumor maintenance. We use transgenic and knockout approaches to investigate the role of cancer-relevant mutations in mice. Our group focuses on the role of reactive oxygen species in chronic inflammation and the link between inflammation and tumor development.

Chronic pancreatitis

Patients suffering from chronic pancreatitis are at increased risk of developing pancreatic cancer. We have established genetic models of chronic pancreatitis. These models are used to investigate the role of inflammation in pancreatic tumor development as well as to test preventive and therapeutic approaches.

Tumor maintenance

Tumor viability is maintained by more genetic alterations than have initially led to tumor development. Identifying these changes will help to understand the cooperative effect of multiple oncogenic changes. Approaches include identification of critical cellular components and characterization of their functions using molecular, cellular and genetic methods.

Selected publications
  • Einwachter H, Li B, Aichler M, Rickmann M, Chhabra NF, Oellinger R, Brielmeier M, Schmid RM. A Redundant System of Thioredoxin and Glutathione Is Essential for Pancreatic Acinar Integrity. Cell Mol Gastroenterol Hepatol 2025;19:101627
  • Ramasubramanian S, Ollinger R, Eberhagen C, Zischka H, Schmid RM, Einwachter H. Mitochondrial superoxide dismutase controls metabolic plasticity in pancreatic cancer. Cell Commun Signal 2025;23:524.
  • Neuss T, Chen MC, Wirges N, Usluer S, Oellinger R, Lier S, Dudek M, Madl T, Jastroch M, Steiger K, Schmitz W, Einwachter H, Schmid RM. Metabolic Reprogramming Is an Initial Step in Pancreatic Carcinogenesis That Can Be Targeted to Inhibit Acinar-to-Ductal Metaplasia. Cancer Res 2024;84:2297-312.
  • Mazur P, Einwächter H, Lee M, Sipos B, Nakhai H, Rad R, Zimber-Strobl U, Strobl L, Radtke F, Kloeppel G, Schmid RM, Siveke J. Notch2 is required for PanIN progression and development of pancreatic ductal adenocarcinoma. Proc Natl Acad Sci USA (2010) 107(30):13438-43.
  • Siveke JT, Lubeseder-Martellato C, Lee M, Mazur PK, Nakhai H, Radtke F, Schmid RM. Notch signaling is required for exocrine regeneration after acute pancreatitis. Gastroenterology (2008) 134(2):544-55.
  • Siveke JT, Einwächter H, Sipos B, Lubeseder-Martellato C, Klöppel G, Schmid RM. Concomitant pancreatic activation of Kras(G12D) and Tgfa results in cystic papillary neoplasms reminiscent of human IPMN. Cancer Cell (2007) 12(3):266-79.
  • Algül H, Treiber M, Lesina M, Nakhai H, Saur D, Geisler F, Pfeifer A, Paxian S, Schmid RM. Pancreas-specific RelA/p65 truncation increases susceptibility of acini to inflammation-associated cell death following cerulein pancreatitis. J Clin Invest (2007) 117(6):1490-501.
Thesis projects

Please send your applications by email.