'From tumor suppression to tumor promotion: how do we deal with multitasking senescent cells?'

Abstract

Most used anti-cancer therapeutic approaches are based on targeting highly proliferative cells, thus often leading to side effects. We show that cells in vivo are induced to senescence upon treatment with standard chemotherapy drugs, and that these senescent cells contribute to chemotoxicity. We then focus on the elimination of chemotherapy-induced senescent cells or the use of alternative less toxic anti-cancer drugs.

About

Demaria obtained his PhD in Molecular Medicine at the University of Torino (Italy), under the supervision of Prof. Valeria Poli. In Poli's lab, he characterized the role of the transcription factor STAT3 as a master regulator of cancer cell survival and metabolism. Fascinated by the hypothesis that senescent cells present in the tumor microenvironment can promote cancer progression through protein secretion, he joined the laboratory of Prof. Judith Campisi at the Buck Institute for Research on Aging, in California (USA), in the summer of 2010. There, he used a newly developed mouse model to navigate through the complex phenotypes of senescent cells, and showed both positive and negative roles of cellular senescence in different physiological and pathological context. He also started to be interested in therapeutic approaches to target the negative aspect of senescent cells. He joined the European Research Institute for the Biology of Ageing (ERIBA) in September 2015 as the Principal Investigator of the laboratory 'Cellular Senescence and Age-related Pathologies'.