After graduated as a biochemical engineer from the National Institutes of Science and Technology (INSA) in Fran (Lyon) in 1991, I completed my PhD thesis in Biology at the CEA Grenoble and graduated from the Université Joseph Fourier of Grenoble in 1996. I pursued my research at Pharmacology and Toxicoloy Institute, laboratory of Prof. Bernard Thorens, in Lausanne, where I studied the role of the glucagon-like peptide-1 receptor in the beta-cell glucose competence. Then, I moved to the Faculty of Medicine at Geneva in 1998, working on the gap junction communication in beta cells in the laboratory of Prof. Paolo Meda. In 2003, I joined the Surgery Department of the University of Geneva, in the lab of Prof. Léo Buhler, Visceral Surgery Unit, studying the pancreatic islets vascularization. Since 2009, I was in charge of the basic research projects of the Thoracic and Endocrine Surgery Unit in Geneva, supervised by Prof. Frédéric Triponez. We established several pre-clinical human models (in vitro, ex vivo, in vivo) of mesothelioma and lung cancers. Currently, we are focusing on the translation of basic research to clinical application by means of ex vivo culture of human lung tumors to test anti-cancer drug efficacy, including immunotherapy. I am actively teaching for more than 20 years at Bachelor, Masters and post-graduate levels.

Our research focuses on two major axes, the role of the inflammation in the development of mesothelioma and lung cancers, and the establishment of pre-clinical tumor models. We provided strong evidence that chronic inflammation induced by asbestos led to a tumor-promoting environment activating MIF/CD74 signaling, YAP/TAZ signaling and RNA editing, prior to mesothelioma development. Macrophages and mesothelioma precursor cells (MPC) accumulated in the inflammatory environment, facilitating tumorigenesis, suggesting that MPC may function as mesothelioma stem cells (MSC). Mesothelioma-associated macrophages (MAM) shared some phenotypes with MPC/MSC and could play roles in mesothelioma development. We observed that the monocyte-derived macrophages, recruited in a CCR2-dependent manner, played a predominant role in the development of mesothelioma. In contrast, tissue-resident macrophages originating from embryonic sources, may be more efficient in activating the T cell response, having a protective effect. MAM derived from circulating monocytes could thus be an important target for immunotherapy in clinical trials, particularly in combination with immune checkpoint blockade.

We established several pre-clinical models (in vitro, in ovo, ex vivo and in vivo) of human mesothelioma and lung cancers to study, on one hand, the role of the inflammation on tumorigenesis, and on the other hand the functional and mechanistic effects of treatments. We plan to adapt our spheroid model in clinic to characterize the efficacy of anti-cancer drugs for patient diagnosed with lung cancer.