Stefan J. Erkeland
Department of Hematology
Room 1330 D
Erasmus University Medical Center
Dr. Molenwaterplein 50
3015 GE Rotterdam, the Netherlands
Phone: +31 (0)10 704 30 34
Work experience since graduating
• P.I. position at Hematology Department, ErasmusMC Rotterdam, Rotterdam, The Netherlands (December 2007- ).
• Post-doc at Hematology Department, ErasmusMC Rotterdam, Rotterdam, TheNetherlands, fixed-term (KWF-fellowship, May 2007- November 2007).
• Post-doc at the Center of Cancer Research (CCR), Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts, USA (KWF-fellowship, june 2005-april 2007).
PhD-student at the Hematology Department, Erasmus University Rotterdam, Rotterdam, The Netherlands (October 1999- April 2005).
Research technician at the Hematology Department, Erasmus University Rotterdam, Rotterdam, The Netherlands (February – September 1999).
Research technician at the Department of Molecular Cell Biology/Leadd BV, Leiden University, Leiden, The Netherlands (December 1996- January 1999)
Research technician at the Department of Cell Biology, Dutch Cancer Institute (NKI), Amsterdam, The Netherlands, (January – November 1996).
Honors and awards
University: Erasmus University Rotterdam
Starting date: 01/10/99
Completion date: 27/04/05
Supervisor (‘Promotor’): Prof. Dr. I.P. Touw and Prof. Dr. B. Löwenberg
Title of thesis: Identification, Function and Clinical Relevance of Mouse Myeloid Leukemia Genes
College of Higher Education: Hogeschool West-Brabant
Completion Date: 21/06/95
Main subject: Biochemistry
Brief summary of research over last five years
During my PhD training, I studied acute myeloid leukemia (AML).We found that retroviral insertional mutagenesis in mice with Graffi-1.4 leukemia virus (Gr-1.4) is a powerful strategy to identify novel genes involved in murine AML. Investigation of newly identified Gr-1.4 targets such as Yin Yang-1, Thioredoxin interacting protein and WD40-repeat domain and SOCS box-containing protein-2, suggested a role for these proteins in leukemic transformation of normal murine and human myeloid progenitor cells. We found that genes directly flanked by the virus integration site have the highest probability to be significantly deregulated in subsets of human AML. Moreover, we found that the combinatorial approach of gene expression profiling of human AML samples and gene tagging screens in mice allows identification of new networks and genes involved in the pathogenesis of human leukemia.
During my postdoctoral training, I studied the role for miRNAs in cancer. In this period we developed retroviral and lentiviral vectors to express miRNAs in mammalian cells. For example, to investigate the functions of miRNAs and tumor suppressor genes in cancer, we recently developed a doxycyclin (DOX)-regulated lentiviral expression vector that highly induces miRNAs expression. Both in vitro and allo-transplantation experiments in nude mice showed DOX-dependent tumor suppressing activity of the miRNA Let7g. To investigate the role of miRNAs in cancer we generated a miRNA expression library containing over 200 single miRNAs and clusters in a MSCV based retrovirus vector MIG-Cre. Currently, we are using this library to identify new transforming miRNAs in mouse AML using pre-leukemic mouse models.