Sean Rudd

An important treatment for cancer patients, especially patients with acute leukemia, are so-called antimetabolites. These act by disrupting important processes in the cell such as DNA synthesis and thereby killing cancer cells. But it is currently difficult to predict when these therapies will work and when they will fail. This is what we want to deal with. Through a multidisciplinary approach combining biochemistry, cancer biology, experimental disease models and advanced technology, we seek to understand the molecular mechanisms of how antimetabolites work and to use this knowledge to develop more effective treatments. For example, we have identified an enzyme that protects cancer cells against antimetabolites and reduces the effect of the treatments. We are developing strategies to turn off this enzyme in cancer cells, which we hope to use clinically to improve current cancer treatments. The goal of our research is to increase the understanding of how antimetabolite treatments kill cancer cells and use this knowledge to develop more effective chemotherapy for leukemia patients

Cancer is one of the most common causes of death in the world. Each year, over 60,000 individuals, of which 300 are children, are diagnosed with cancer and these numbers are expected to increase in the future. An important treatment for these patients are so-called anti-metabolites that work by disrupting important processes in the cell such as DNA synthesis and thus killing cancer cells. We have identified an enzyme, SAMHD1, which protects cancer cells against the effect of these anti-metabolites and thereby reduces the effect of the treatments. Our research focuses on the enzyme SAMHD1 and the role it plays in the breakdown of anti-metabolite treatments used for a range of cancers including blood cancers. Through a multidisciplinary approach that combines biochemistry, cancer biology and experimental disease models, we seek to understand how SAMHD1 affects the degradation of these drugs. In addition, we are developing strategies to inactivate SAMHD1 in cancer cells which we hope to use clinically to improve current cancer treatments. The goal of our research is to develop new, more effective cancer treatments. Anti-metabolite-based chemotherapy represents a very important treatment option for today's cancer patients and our research has identified SAMHD1 as an important barrier to their therapeutic effect. By increasing the understanding of how this happens, we hope to be able to use SAMHD1 as an important biomarker to predict how patients respond to treatment. Furthermore, we hope to exploit this process to develop strategies to inactivate SAMHD1 and thus increase the efficacy of today's anti-metabolite treatments.