Celia Berkers

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.

Research in the Berkers group focusses on metabolomics: studying the small molecule metabolite profile of cells using mass spectrometry. My group employs a mechanistic metabolomics strategy. By performing metabolic tracer studies using a variety of stable-isotope nutrients and combining such studies with targeted metabolism-oriented proteomics studies, we aim to gain mechanistic insight into cellular metabolism. We apply our metabolomics tools to two biomedical frameworks: metabolism-mediated drug resistance and immuno-metabolism. 

https://www.uu.nl/medewerkers/CRBerkers

Presentation

Unravelling metabolic communication in cancer.

Metabolic reprogramming is observed across many cancer types and widely recognised as a hallmark of cancer, essential for rapid tumour growth and proliferation. Cancer cells rewire their cellular metabolism to fulfil their higher need for energy, building blocks for biosynthetic pathways and to help maintain their redox balance. As cancer cells can become reliant on specific metabolic reprogramming, it poses a vulnerability that can be exploited for therapy.

Metabolic reprogramming can be driven by both genetic alterations and environmental factors. Other cells in the tumour microenvironment engage in metabolic crosstalk and cross-feeding with cancer cells. Such metabolic communication is highly adaptable and tailored to the tumour’s needs, supporting tumour growth and processes such as metastasis and drug resistance.

In this talk, I will present our metabolomics-compatible co-culture systems that we developed to unravel metabolic communication in the tumour microenvironment. Using examples from both hepatocellular carcinoma and multiple myeloma, I will discuss how these model systems allow for metabolomics, stable-isotope tracing and multi-omics studies to reveal signals and downstream metabolic pathways involved in this metabolic crosstalk as well as novel metabolic targets that may ultimately improve therapy.