What are the functional consequences of TP53 mutations – the most frequently mutated gene in cancer?

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How do pre-malignant cells arise? How do they escape the safeguard mechanisms that have evolved to prevent cancer initiation? What are the selective pressures that drive the expansion of pre-malignant clones in blood and bone marrow?

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How do leukemia-causing mutations co-operate over time? How do these mutations shape disease evolution and treatment failure? What are the mechanisms of chemotherapy and immunotherapy resistance, and how can we exploit them therapeutically?

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We are intrigued by these and other questions at the interface of basic and translational cancer research, with a particular focus on TP53-mutant clonal hematopoiesis and myeloid malignancies.

 

We generate novel in vitro and in vivo models of clonal hematopoiesis and overt leukemia, and integrate human genetics and longitudinal patient cohort data with precise CRISPR-based genome editing, classical molecular biology and large-scale functional genomics to elucidate disease mechanisms and identify actionable leukemia vulnerabilities.

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Our ultimate goal is to translate mechanistic insight into better therapies and improved outcomes for cancer patients.

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The BOETTCHER LAB is located in the Department of Medical Oncology and Hematology at the University Hospital Zurich and the University of Zurich.

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