Research

• Stiewe Group Mutations in the p53-encoding gene TP53 are observed in approximately half of all cancer patients, and germline mutations in human or mouse p53 invariably lead to cancer early in life. Different from other tumor suppressor genes, TP53 shows an unusual preference for missense mutations that result in the production of a full-length protein with single amino acid changes.
• Timofeev Group Cancer development is driven by activated oncogenes and loss of tumor suppressors. While the addiction of tumors to oncogenes is well-established and provides the rationale for oncogene-targeted therapies, it is less clear whether tumors likewise depend on the absence of tumor suppressors.
• Wanzel Group The success of cancer therapy is limited by the development of resistance to systemic therapy approaches. Among the most widely used anti-cancer drugs are the platinum compounds such as cisplatin. The cytotoxic activity of these compounds is dependent on their ability to induce DNA interstrand crosslinks, which impede replication and transcription and are therefore particularly deleterious.
• Gremke Group Based on novel insights in tumor biology within the last years, a plethora of different molecular cancer targeted therapies (e.g. CDK4/6- and PI3Kinase-Inhibitors) have entered clinical practice and improved the therapy of HR+, HER2- and PIK3CAmut metastasized breast cancer. However, the phenotypic plasticity and inherent genomic instability allow tumors, to rapidly evolve drug resistant subclones as a cause of intrinsic or acquired therapy resistance and eventually lead to tumor relapse and therapy failure.