Le Dr. Marc Diederich de la Fondation Recherche sur le Cancer et les Maladies du Sang (Laboratoire de Biologie Moléculaire et Cellulaire du Cancer (LBMCC) Hopital Kirchberg, Luxembourg) présentera une conférence intitulée :

« Marine natural compounds as chemopreventive and chemotherapeutic agents »

LUNDI 14 MARS 2011 à 14h15 Amphi Martin Faculté de Médecine

CRI INSERM UMR 866 / IFR 100

Contact. N.Latruffe. Latruffe@u-bourgogne.fr 0380396236

Résumé

Natural compounds as inhibitors of inflammation and activators of cell death mechanisms.

Programmed cell death plays a critical role in the cellular housekeeping, and aberrant cell death regulation leads to body malformations and to numerous diseases, including various autoimmune diseases, cancer, stroke, infarctations, and neurodegenerative diseases. Research in the field of cell death has evolved at a very rapid pace over the last fifty years. It is now generally accepted that programmed cell death can be subdivided into three different categories: apoptosis (programmed cell death type I), autophagy (programmed cell death type II, or lysosomal cell death), and oncosis (programmed cell death type III, also referred to as necrosis). Apoptosis, in particular, has been studied in great depth and autophagy has recently sparked an enormous research interest. In the 1960ʼs to early 1980ʼs, at the same time as renowned biologists including Richard Lockshin and John Saunders, John Kerr, Alastair Currie, and Andrew Wyllie, and Sydney Brenner, Robert Horvitz, and John Sulston initiated their investigations into cell death, research groups lead by Paul Scheuer, John Faulkner, George Pettit, and other chemists pioneered the research field of natural products, with the aim to identify potent anticancer compounds amongst the toxins produced by marine organisms as a chemical defence mechanism against their predators. Since then, numerous marine natural products have been identified as modulators of cell death. Here, we discuss the mechanism of action of the major marine natural products reported as inducers of apoptosis, autophagy, or oncosis.