Maarten van Lohuizen
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.
In 1993 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 at Utrecht University Medical School and was appointed as a member of the Centre for Biomedical Genetics in 2003 and as EMBO member in 2004. In 2007 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. He has been elected as member of Academia Europaea in 2015 and as senior group leader of Oncode Institute in 2017. 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 and CRISPR library screening to identify critical Polycomb targets and try to define synthetic-lethal interactions. Other focus is on the roles of Polycomb deregulation in Lung cancer and in Mesothelioma. Next to genetic screening these models are being used in drug screens to define new combination therapies involving epigenetic mechanisms.