Our long-term goal is to understand how networks of biochemical reactions cooperate to the maintenance of cellular functional states and cellular homeostasis. More specifically, we are studying how biochemical networks encode cellular decisions underlying cell and tissue homeostasis and how oncogenes contribute to early tumour initiation and promotion by reprogramming these processes. We study how cells attempt to repair DNA damage, how mutations arising from DNA lesions induce loss of homeostatic control and how we can improve our early detection of cancer, focusing on the following research areas:
- The study of checkpoint signalling and the DNA damage response (DDR) with a particular interest in their heterogeneous response among a clonal population of cells;
- The study of how oncogenic signalling triggers cancer-associated phenotypes by reprogramming signalling and metabolic networks while avoiding cell-autonomous and non-cell-autonomous tumour suppressive mechanisms;
- The translation of the technologies and knowledge developed for these studies to early detection and intervention;
- A transdisciplinary programme of research aimed to establish a ‘live single-cell systems biology of cellular function and cell decision’.
In our laboratory, we are currently studying KRAS signalling in the context of pancreatic and colorectal cancers.
For a description of our work on cancer in plain English, see the home page.
You can navigate through different projects in this area, using the links embedded in the text, the main navigation menu at the top the page, or the ‘Cancer Biology’ menu at the right-hand side of the page.