Nicolas Skuli INSERM Researcher, Principal Investigator, PhD Oncology

Course and current status

- Currently: Visiting Researcher, Johns Hopkins University, Department of Neurosurgery, Hunterian Brain Tumor Laboratory, Pr. Henry Brem and Dr. Betty Tyler, Baltimore, USA

Currently: Principal Investigator, Senior Associate Professor, CR1, INSERM U1037, Toulouse, France

- 2012-2015: Principal Investigator, Junior Associate Professor, CR2, INSERM U1037, Toulouse, France

- 2011-2012: Research Associate, Celeste Simon Lab, University of Pennsylvania, Howard Hughes Medical Institute, Philadelphia, USA

- 2008-2011: Post-doctoral Fellow, Celeste Simon Lab, University of Pennsylvania, Howard Hughes Medical Institute, Philadelphia, USA

- 2004-2008: PhD in Oncology, INSERM U563, Toulouse, France

- 2003-2004: Master degree  in Immunology and  Cell and Developmental Biology, Institut Claudius Regaud, Toulouse, France

Scientific summary

Expertise: Hypoxia, Hypoxia Inducible Factors, Angiogenesis, Radiobiology, Gliomas Stem Cells, Gliomas.

Research Summary: Glioblastomas (GBM) are extremely aggressive and hypoxic brain tumors. These tumors often relapse despite an initial treatment combining chemotherapy and radiotherapy. Hypoxia and Hypoxia Inducible Factors (HIF-1 and HIF-2) are the main transcription factors involved in cell response and adaptation under low oxygen conditions and contribute to the resistance to anti-cancer therapeutics. Studying the mechanisms of resistance, particularly in gliomas, and identifying new targets to improve therapeutics is crucial. During my PhD, I demonstrated the role of cell adhesion pathways in the control of tumor hypoxia and radioresistance in GBM cells, which involves integrins and the RhoB/Akt/GSK-3b axis. My postdoctoral studies led me to focus on hypoxia and the HIFs within Pr Celeste Simon laboratory. I showed that despite the fact that HIF-1 and HIF-2 share common functions, HIF-1 and HIF-2 also have unique features in endothelial cells and hematopoietic stem cells. I developed different mouse models in order to demonstrate the specific role of either HIF-1 or HIF-2 in these different cell types. I am currently working on a new factor identified as a specific regulator of HIF-2: Int6 also known as Eif3e (subunit “e” of the translation initiation factor Eif3). Overexpression of Int6/Eif3e in patients with gliomas significantly increases the survival of these patients. My research aims to determine how Int6 overexpression can influence survival of patients with GBM, potentially through the regulation of HIF-2 or other factors, such as Glioma Stem Cells (GSC), involved in the aggressiveness of these tumors. This research should allow us to identify new therapeutic options to improve the treatment of glioma patients.

Image d’exemple