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Maarten van Lohuizen group

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Maarten van Lohuizen

Head of Division, Group Leader

Personal details

Experience

Maarten van Lohuizen studied Biology at the University of Amsterdam and received his Ph.D. in 1992 (cum laude, supervisors Dr. A. Berns and Prof dr. P. Borst) from the same University. During his thesis work, he demonstrated the power of using retroviruses in genetic screens to identify cooperating oncogenes in cancer-predisposed mice.

After staying on for one year as a postdoc, he joined the group of Prof. Dr. Ira Herskowitz, University of California at San Francisco, USA, for his postdoctoral training. Here, he was involved in analysis of a novel cell cycle checkpoint mechanism and in studying regulation of the Yeast MAP-kinase signaling pathway. In 1995 he returned to The Netherlands Cancer Institute as an assistant professor in the division of Molecular Carcinogenesis, to take up studying his old favorite: mechanisms of epigenetic silencing by mammalian Polycomb-group protein complexes and their role in cancer, when deregulated. After his tenure in 2000, he joined the division of Molecular Genetics in 2001, of which he was appointed head of division in 2002. Inaddition, in 2001 he became a part time professor on the subject of regulation of Cell Cycle control and Oncogenesis atUtrechtUniversityMedicalSchooland was appointed as a member of the Centre for Biomedical Genetics in 2003 and as EMBO member in2004. In2007 he became part time professor at the University of Amsterdam Medical School (AMC) with the profile: Biology and epigenetic regulation of normal and cancer stem cells. 

His group has made important contributions on the functional analysis of epigenetic gene silencing mechanisms by Polycomb-group protein complexes, which play crucial roles in controlling development and cell fate and when deregulated, contribute to cancer formation. Recent work has also focused on the regulation of enzymatic activities of the Polycomb protein complexes by posttranslational modifications and its implications for cancer and DNA repair processes. Using Glioblastoma mouse models and cancer-initiating cancer stem cell lines derived from human Glioblastomas his group is performing in vivo shRNAi library screening to identify critical Polycomb targets and try to define synthetic-lethal interactions. In addition these models are being used to define new combination therapies involving epigenetic mechanisms. 

His group has also developed a cancer systems biology approach using high-throughput genome-wide genetic screens in cell-based assays and in cancer-prone mice combined with new bioinformatic tools (in collaboration with Prof. Dr. A. Berns and Prof. Dr. A. Bradley, The Sanger Center, UK) to identify new genes that contribute to cancer and classify them in functional groups/signaling pathways. By using the DamID technique, his group has recently comprehensively mapped all Polycomb target genes in the Drosophila genome (in collaboration with the group of Bas van Steensel. Follow-up work using for the first time in vivo genome wide 4C in Drosophila larval brains revealed dynamic interactions between Polycomb domains. In addition, his group has recently demonstrated a crucial role for Bmi1/Pc-G protein complexes in maintaining hemapoietic, neuronal, breast epithelial and embryonal stem cell fate and has implicated the Sonic Hedgehog (Shh) morphogen as a regulator of Bmi1 expression in neuronal precursor cells. Unraveling the role of Bmi1/Pc-G in stem cell fate versus differentiation decisions and the consequence of this for cancer (stem) cell biology is currently a major focus of his group.

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