Principal Investigators Prof. Dr. Schmid ⎮ Dr. Einwächter

Laboratory members

• Dr. med. Henrik Einwächter (PI)
• Prof. Dr. med. Roland M. Schmid (PI)
• Anke Bettenbrock, BTA
• Min-Chun Chen, M.Sc.
• Nirav Chhabra, Postdoc
• Bailing Li, MMed
• Leeanne Mundle, M.Sc.
• Mathilde Neuhofer, MTLA
• Niran Oezdemir, M.Sc.
• Mahnoosh Ostadreza, MB&B Master
• Sankaranarayanan Ramasubramanian, Postdoc
• Dr. med. vet. Marie-Christin Schilloks

Former members

• Hande Asimgil, PhD
• Lisa Baumgärtner, M.Sc.
• Andrea Boltendahl, BTA
• Ramona Böhm, Postdoc
• Anja Motz, BTA
• Thorsten Neuß, M.Sc.
• Kerstin Pfister, cand. med.
• Mariana Rickmann, PhD
• Christin Ruoff, M.Sc.
• Andrea Stroppiana, Veterinarian
• Chao Wu, MMed

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.

1. 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.
2. 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.
3. von Burstin J, Eser S, Paul MC, Seidler B, Brandl M, Messer M, von Werder A, Schmidt A, Mages J, Pagel P, Schnieke A, Schmid RM, Schneider G, Saur D. E-cadherin regulates metastasis of pancreatic cancer in vivo and is suppressed by a SNAIL/HDAC1/HDAC2 repressor complex. Gastroenterology (2009) 137(1):361-71.
4. 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.
5. 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.
6. 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.

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