Erasmus Medical Center
Rotterdam, Zuid-Holland, Netherlands
Pim French has been recruited to the Neuro-Oncological Laboratory (dept Neurology, Erasmus MC, Rotterdam, the Netherlands) as a molecular biologist with a strong background in molecular screens with subsequent functional analysis of candidates. My lab is part of the ErasmusMC Cancer Center and the recently established ‘hersentumorcentrum’ and has strong collaborations with the neuro-oncology clinic, the European Organization for Research and Treatment of Cancer (EORTC, member of the EORTC-brain tumor group steering committee). The lab has many (inter-) national research collaborations.
One of the goals of our lab is to identify clinically relevant subgroups of glioma which has evolved from discovery screens to validation on randomized phase III clinical trial material. The importance of our work is illustrated by our finding that only specific molecular subtypes of glioma benefit from adjuvant PCV chemotherapy. We are currently analyzing material from additional large randomized clinical trials and include EORTC-22033, TAVAREC, Intellance II and CATNON trials.
To improve the dismal prognosis of glioma patients, it is imperative to better understand the pathobiology of gliomas. Our lab therefore performs functional analysis on genes involved in glioma-genesis. Currently we developing appropriate model systems (including cell lines, zebrafish and xenografts) in which we are studying the functional consequences of causal cancer genes IDH1 and EGFR. This fundamental understanding of glioma-biology will ultimately enable the development of novel treatment strategies for patients. Our lab has also recently established a facility that allows high-throughput, high-content functional and drug screens within the Erasmus MC cancer institute (ctsf.erasmusmc.nl). This facility enables functional research on causal cancer genes and affected pathways. We are using this facility to perform phenotypic screens to identify effective combinations of drugs and to determine the mechanism of resistance to EGFR inhibitors in gliomas.
