Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

What causes cancer? And how? These seemingly simple questions are surprisingly hard to answer. For example, we know that exposure to UV light or tobacco smoke can cause damage in the DNA in our cells. This damage can turn into DNA mutations, which may then cause cancer. The first goal of our group is to research the different sources of DNA mutations – and the mechanisms of how exactly these mutagenic processes work. We believe that by understanding these mechanisms, we can (a) learn how to avoid mutations and prevent cancer, and (b) apply this knowledge for effective personalised treatment (by discovering cancer vulnerabilities based on the mutational mechanisms).

DNA mutations can be bad because they can cause cancer (as well as many other diseases). However, DNA mutations happen in all our cells throughout our life – and most of them are in fact harmless. One of the big questions in cancer research has therefore been: how can we tell apart the dangerous DNA mutations from the harmless ones? The second goal of our group is development of computational methods that use “big data” to discover the dangerous cancer-driving DNA mutations. In particular, we focus on the non-coding parts of the genome, which still remain largely unexplored.

Finally, while a lot of cancer research has focused on DNA mutations, more recent research revealed that they play just one part in the origin of cancer. Some of these alternative mechanisms lie in the so called “epigenome” – reversible marks on and around the DNA that regulate which genes are turned “on” and “off”. Many of these epigenomic marks are dramatically altered in cancer. Moreover, the reversibility of epigenome helps the cells to adapt to changes, which can lead to resistance to therapy.  In the third goal of our group, we try to understand how these epigenomic alterations contribute to cancer. Understanding these mechanisms is important for overcoming the therapy resistance and development of epigenome-targeting drugs.


Graphical abstract showing the external factors that can lead to cancer. This is split into two sections: mutagenesis, where the 1st question looks at mechanisms; and epigenomics, where the third question asks about the mechanisms of this. The second question asked in the research overview is represented by the two original factors coming together in an arrow towards cancer, labelled with the question 'Drivers?'.