Stefan N. Constantinescu
Senior Group Leader
I am a Member of the Ludwig Institute for Cancer Research, Professor and Head of the Cell Signaling Pole at the Université catholique de Louvain’s de Duve Institute in Brussels, and Director of Research (Honorary) at the Fonds National de la Recherche Scientifique (FRS-FNRS), Belgium. I teach advanced molecular biology to biomedical students and cell biology to medical students, and I serve on review panels such as the European Research Council’s panels for advanced grants. I am a full Member of the Royal Academy of Medicine of Belgium and was elected for 2021-2024 as President of the Federation of European Academies of Medicine (FEAM).
I was initially trained as a medical doctor, worked briefly in paediatric oncology and paediatric AIDS, then switched to basic research after obtaining my PhD. I trained as a postdoctoral fellow with Professor Harvey F. Lodish at Whitehead Institute for Biomedical Research at MIT, Cambridge, MA.
My research is focused on understanding the structure and function of cytokine receptors and their associated proteins, JAKs (Janus kinases) in normal blood formation and in disease. We aim to elucidate the molecular basis of blood cancers, especially chronic myeloproliferative neoplasms (MPNs) such as Polycythaemia Vera, Essential Thrombocythemia and Myelofibrosis, as well as secondary acute myeloid leukaemia that derive from their progression.
In 2021, I started a second group at Ludwig Oxford to study the link between signalling, epigenetic regulators, chromatin dynamics and differentiation in blood cancers and leukaemia. While we have elucidated how several driver mutants induce myeloid blood cancers, we recently observed that driver mutants in myeloid cancers regulate the function of epigenetic regulators. Given the incredible importance of epigenetic regulation for normal differentiation, and the high prevalence of epigenetic mutations in blood cancers, my group will focus on a systematic study of signalling and epigenetic regulation during oncogenesis in chronic myeloid cancers and their progression to secondary acute myeloid leukaemia, a very severe condition.
CALR mutant protein rescues the response of MPL p.R464G variant associated with CAMT to eltrombopag.
Basso-Valentina F. et al, (2021), Blood
Functional Consequences of Mutations in Myeloproliferative Neoplasms
Constantinescu SN. et al, (2021), HemaSphere