TRANSLATIONAL CANCER RESEARCH
PRE-MALIGNANT STATES | p53 PATHOBIOLOGY | CLONAL HETEROGENEITY
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?
How do cancer-causing mutations co-operate? Why and how is clonal heterogeneity established and maintained during the course of the disease? What are the mechanisms of chemotherapy resistance?
What are the functional consequences of TP53 mutations - the most frequently mutated gene in cancer?
We are intrigued by these and other questions pertaining to basic and translational cancer research. We generate novel in vitro and in vivo models of pre-malignancies and overt cancer. We use human genetics data, precise CRISPR-based genome editing, classical molecular biology as well as large-scale functional genomics to elucidate disease mechanisms and to identify cancer vulnerabilities.
Our ultimate goal is to improve outcomes in cancer patients.