Ruud Delwel started his career in 1983 in the lab of Bob Lowenberg, studying the in vitro behaviour of human acute myeloid leukemia cells in vitro. He obtained his PhD in 1990 (Cum Laude) and became a post doctoral fellow in the group of Dr. James Ihly, at the St. Jude’s Children’s Research Hospital in Memphis, Tennessee Leiden, and carried out retroviral insertional mutagenesis to discover novel disease genes in AML. He discovered the EVI1 gene to be one of the most severe disease genes in mouse leukemia’s and in human. When back in the Netherlands, ErasmusMC, he moved on studying the biological consequences of altered gene expression in human and murine AML.
His two major breakthrough studies are 1) The discovery that human AML can be classified based on unique gene expression signatures and on specific gene methylation profiles. These studies led to the uncover of a subset of unique AML cases with aberrant expression of the EVI1 gene. Further in depth analysis revealed a unique mechanism of enhancer deregulation in a subset of human EVI1-AMLs. Ruud Delwel and his team have been able to combine patient analysis with molecular studies using in vitro and in vivo modelling to improve our insight into molecular aspects of acute myeloid leukemia. These studies and the proposal that followed on these studies have been awarded by the Dutch Cancer Society or "Koningin Wilhelmina Fonds” with the "Koningin Wilhelmina Onderzoek prijs", or KWO Award.
- 2017: Jose Carreras Lecture/Price
- 2015: KWO Award
- 1994: Fellowship from the Royal Dutch Academy of Science (KNAW)
- Avellino, R., Havermans, M., Erpelinck, C., Sanders, M. A., Hoogenboezem, R., van de Werken, H. J., ... & Delwel, R. (2016). An autonomous CEBPA enhancer specific for myeloid-lineage priming and neutrophilic differentiation. Blood, 127(24), 2991-3003.
- Figueroa, M. E., Lugthart, S., Li, Y., Erpelinck-Verschueren, C., Christos, P. J., Mazumdar, M., ... & Delwel, R. (2008). Epigenetic signatures identify new clinically relevant subtypes and define gene regulatory patterns in patients with acute myeloid leukemia (AML). Cancer cell, 17(1),13-27
- Glass, J. L., Hassane, D., Wouters, B. J., Kunimoto, H., Avellino, R., Garrett-Bakelman, F. E., ... & Delwel, R. (2017). Epigenetic Identity in AML Depends on Disruption of Nonpromoter Regulatory Elements and Is Affected by Antagonistic Effects of Mutations in Epigenetic Modifiers. Cancer discovery, 7(8), 868-883.
- Gröschel, S., Sanders, M.A., Hoogenboezem, R., De Wit, E., Bouwman, B.A.M., Erpelinck, C., ... & Delwel, R. (2014). An oncogenic enhancer-rearrangement causes concomitant deregulation of EVI1 and GATA2 in leukemia. Cell, 157(2), 369-81.
- Gröschel, S., Schlenk, R. F., Engelmann, J., Rockova, V., Teleanu, V., Kühn, M. W., ... & Delwel, R. (2012). Deregulated expression of EVI1 defines a poor prognostic subset of MLL-rearranged acute myeloid leukemias: a study of the German-Austrian Acute Myeloid Leukemia Study Group and the Dutch-Belgian-Swiss HOVON/SAKK Cooperative Group. Journal of clinical oncology, 31(1), 95-103.