Early researcher

Sven De Pourcq


My academic career started at the University of Antwerp studying biomedical sciences. I majored in molecular and cellular mechanisms of disease due to my fascination with molecular mechanisms of cancer and my keen interest in stem cells. During my studies I did several internships at the University of Antwerp, the longest one focussing on unravelling corticosteroid sensitivity/resistance and epigenetic mechanisms in Multiple Myeloma together with the team of Wim Vanden Berghe.

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I obtained my degree during my internship abroad at the University of Saarland (Genetics Department) joining the team of Jörn E. Walter. Here I improved my wet-lab and in silico skills with a focus on DNA-methylation. It was then that I became absolutely convinced I wanted to start a career in research and pursue a PhD. Shortly after I came into contact with my current research project within the INTERCEPT-MDS network and subsequently I joined the laboratory of Myelodysplastic Syndromes with Valeria Santini as supervisor.

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I have always been fascinated by the mechanisms involved in cancer and had a particular interest in (epi)genetics as soon as I started my academic career. Therefore, I would often read about these subjects and voluntarily joined a laboratory aligning with my interest during my studies.

As of today I am part of a small but very ambitious and capable group with a long standing history in myelodysplastic syndrome (MDS) research focusing on the effects of hypomethylating agents (HMAs). Although the widespread use of HMAs has played a pivotal role in MDS treatment, there is an extensive need for improvement as acquired or primary resistance to HMAs is inevitable and remains ambiguous.

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I want to determine whether patients undergoing HMA-based combination therapies have altered DNA methylation in stem –and progenitor cell populations by using a high-throughput technique called Enhanced Reduced Representation Bisulfite Sequencing (ERRBS) for assessment of DNA methylation at base pair resolution. We use this technique because it has more extensive inclusion of intergenic regions, effective epigenetic patterning and handling of highly heterogenic samples/diseases.

I strive for clinical implementation of these results to be used for identification and exploitation of new drug targets, hopefully leading to an improvement of current therapies.

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