Prof. Celia Berkers, Professor Metabolomics Faculty of Science and Vetenary Medicine, Utrecht University
Celia Berkers studied chemistry at Utrecht University, where she graduated with honours in 2003. She started her PhD at the Harvard Medical School in Boston and continued her research at the Netherlands Cancer Institute in Amsterdam. Berkers received her PhD degree with honors in 2010 and was awarded the Antoni van Leeuwenhoek Prize 2010 for most promising young scientist. She then moved to the Beatson Institute for Cancer Research in Glasgow, where she did a post-doc in the laboratory of Prof. Karen Vousden, supported by a Rubicon fellowship from NWO. In 2013, Dr Berkers joined the Biomolecular Mass Spectrometry and Proteomics Department at Utrecht University as an independent group leader and was awarded a VENI grant from NWO-CW. In 2014, she was awarded the Heineken Young Scientists Award for Biochemistry and Biophysics by the Royal Netherlands Academy of Arts and Sciences. Berkers was appointed full professor at the Faculties of Vetenary Medicine and Science in 2018 and is a member of the Young Academy of the Royal Academy, a group of 50 top young scientists and scholars in the Netherlands.
Metabolism-mediated drug resistance
Metabolic rewiring is increasingly acknowledged to play a role in the sensitivity of cancer cells to anti-cancer therapies. We use metabolomics to find targetable metabolic changes in drug-resistant cells, to study the metabolic mode of action of drugs, or to obtain insight into adverse drug effects. In particular, we investigate proteasome inhibitors, which hold great promise for the treatment of cancer, but are associated with adverse effects and the occurrence of resistance. By characterizing the pathways that cells use to adapt to the action of proteasome inhibitors, we aim to reveal novel therapeutic targets for combination treatment and open up possibilities to treat resistant patients.
Immune responses depend on the balance between two types of T cells: conventional T cells (Tconv), that kill infected or tumor cells, and regulatory T cells (Treg), that inhibit the response of conventional T cells to self- and foreign antigens and are thereby critical to inhibit autoimmunity. Treg and Tconv share many features, including co-stimulatory and cytokine receptors, but differ significantly in their metabolic features. In an Institute for Chemical Immunology project we develop metabolomics strategies to map metabolic differences between these different T cells. Ultimately, we aim to identify metabolic targets that can be exploited to selectively modulate T-cell activity.