At the laboratory, we study the cellular and molecular fates of tissues in response to anti-cancer therapies that induce DNA damage (radiotherapy, chemotherapy, PARP inhibitor, etc.). In particular, we are interested in cellular senescence, which is a tumor suppressor mechanism that can be activated in normal as well as cancerous cells following these anti-cancer therapies. Although beneficial in the short term (by blocking proliferation), senescent cells can pose a risk of treatment resistance and relapse, particularly due to their properties of high resistance to apoptosis and production of a pro-inflammatory secretome (senescence-associated secretory phenotype = SASP). Therefore, it is important to find ways to eliminate senescent cells (by senolytic agents) or specifically manipulate their harmful properties, especially SASP.
Our projects are focused on:

• Better understanding the different stages of the process leading to the establishment of senescence and SASP expression in response to DNA damage in normal and cancerous cells.
• Finding new molecular targets to manipulate and decrease the pro-inflammatory SASP without preventing the proliferation arrest of senescence.
• Evaluating the cellular senescence response in patients during DNA damage-inducing therapies in prostate and ovarian cancers.
• Improving and finding new combinations of therapeutic agents targeting senescent cells.