Die Rolle der Glykogen Synthase Kinase 3β in der Regulation von DNS-Schäden und Chemotherapieresistenz im Pankreaskarzinom
by Anna Eleonora Angelika Tirilomi-Mascher née Tirilomi
Date of Examination:2024-09-25
Date of issue:2024-09-24
Advisor:Prof. Dr. Volker Ellenrieder
Referee:Prof. Dr. Volker Ellenrieder
Referee:Prof. Dr. Philipp Ströbel
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Abstract
English
Pancreatic carcinoma is one of the most aggressive solid tumour types and is characterized by pronounced molecular heterogeneity. Research is continuing into molecularly definable subgroups that are suitable for targeted, individualized treatment. In particularly aggressive subgroups of pancreatic cancer, glycogen synthase kinase 3β (GSK3β) has been identified, which is associated with tumor cell proliferation, de-differentiation, progression and resistance to chemotherapy. An oncogenic effect of GSK3β has been demonstrated in multiple tumor entities. Using established murine and human cell lines as well as primary cell lines isolated from PDX tumors (patient-derived xenografts), the role of glycogen synthase kinase 3β in the regulation of DNA damage was investigated.
Keywords: pancreatic cancer; GSK3β; chemotherapy; chemotherapy resistance
Schlagwörter: Pankreaskarzinom; GSK3β; Chemotherapie; Chemotherapieresistenz