Biosketch

Marcel Spaargaren obtained his PhD in 1992 at the Hubrecht Institute and the University of Utrecht, Utrecht, the Netherlands. As recipient of a postdoctoral fellowship of the Dutch Cancer Society (KWF) he was a visiting scientist at ONYX Pharmaceuticals, Richmond CA, USA, and a postdoctoral researcher at the dept. of Physiological Chemistry, UMC Utrecht. In 1998 he was appointed assistant professor and staff member at the dept. of Pathology of the Academic Medical Center (AMC) of the University of Amsterdam (UvA).

Currently, he is associate professor at the dept. of Pathology of the Amsterdam UMC (location UvA) and board-member of the Lymphoma and Myeloma Center Amsterdam (LYMMCARE; lymmcare.nl). He is also leader of the theme on ‘Target & Therapy Discovery’ (Target & Therapy Discovery CCA (amsterdamumc.org) ) and member of the Research Board of the Cancer Center Amsterdam (CCA; cancer center amsterdam.nl ), dean of the Oncology Graduate School Amsterdam (OOA; ooa-graduateschool.org ), and chair of the society for Cancer Biology of the Dutch Cancer Society (KWF) (kwfcancerbiology.nl).

Research Interest

His research group has a long-standing interest in the molecular and cellular aspects of the pathogenesis of (mature) B-cell malignancies, in particular Non-Hodgkin Lymphoma (Diffuse Large B-cell Lymphoma and Mantle Cell Lymphoma), Chronic Lymphocytic Leukemia, Multiple Myeloma and Waldenström’s Macroglobulinemia, with a focus on signal transduction, cell adhesion and migration, and microenvironment-dependence, aiming for the discovery of novel therapeutic targets (e.g., by functional genomic CRISPR screens) and preclinical therapy development.

Specific interests:
- signal transduction
- cell proliferation and survival
- cell adhesion and migration
- tumor microenvironment-dependence

Favorite molecules:
- B-cell antigen receptor
- chemokines (e.g., CXCL12)
- HGF and MET
- WNT and beta-catenin
- heparan sulfate proteoglycans (e.g., Syndecan-1 and CD44)
- adhesion molecules (integrins and cadherins)
- kinases (e.g., Bruton’s tyrosine kinase and PI3K) and inhibitors (e.g., ibrutinib and idelalisib)
- transcription factors (e.g., FOXP1 and NFκB)
- BCL-2 family proteins (e.g., BCL-2 and MCL-1) and inhibitors (e.g., venetoclax)