Marc Mesnil

Professor
PhD, International Agency for Research on Cancer, France
Institute of Cellular Physiology and Biology, University of Poitiers

In 1989, Dr. Marc Mesnil obtained his PhD under the supervision of Dr. Yamasaki at the International Agency for Research on Cancer (Lyon, France) where he studied the involvement of gap junctions in carcinogenesis. He then pursued post-doctoral studies in the laboratory of Dr. Gilula at the Scripps Research Institute (La Jolla, California) where he confirmed that loss of gap junctional intercellular communication is a characteristic of cancer cells. From 1991, he went back to Dr. Yamasaki’s laboratory where he studied how gap junctions mediate anti-proliferation effect and also how they could be used to enhance the cytotoxicity of anticancer compounds by permitting their intercellular diffusion.

In 2000, Dr. Mesnil joined Dr. Giaume at the Collège de France (Paris, France) to study the effect of inflammation on astrocytic gap junctions; after a short time he was appointed as professor at the University of Poitiers (France). He developed a CNRS team focused on the study of gap junction involvement in brain tumor invasion and in metastatic bone targeting of prostate cancer cells. He is currently author and co-author of about 76 peer-reviewed articles.

Primary Recipient Awards

French Scholars Lecture Series, Marc Mesnil, 2014

Marc Mesnil

Lecture: "The history of a family of membrane channel proteins, the connexins (from intercellular communication, related pathologies and beyond)
Gap junctional intercellular communication has been known for long to be involved in cancer and more recently in a growing list of human pathologies. A special emphasis will be presented on the involvement of such communication and their structural proteins, the connexins, in human physiology and pathologies (cancer and others).

The presentation will be made from an historic point of view in order to show the evolution of our knowledge in this particular topic during the past four decades. In particular, it will be shown how earlier simple conclusions regarding gap junctions and disease were replaced by much more complex interpretations due to advances in genomics, imaging and bioinformatics. Moreover, it will be presented how this type of communication was first considered as a tumor suppressor before being involved, through its structural proteins (connexins), in the invasive steps and thus dissemination of cancer cells.