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DTSTART:19960101T000000 END:STANDARD BEGIN:STANDARD TZNAME:GMT TZOFFSETFROM:+0100 TZOFFSETTO:+0000 DTSTART:19961027T020000 RRULE:FREQ=YEARLY;BYMONTH=10;BYDAY=-1SU END:STANDARD END:VTIMEZONE BEGIN:VEVENT DTSTAMP:20260511T010043Z DTSTART;VALUE=DATE-TIME:20210429T123000 DTEND;VALUE=DATE-TIME:20210429T133000 SUMMARY:BMS Divisional Webinar: Strategies to target senescence\, Profess or Jesus Gil\, Faculty of Medicine\, Institute to Clinical Sciences\, Im perial College TZID:Europe/London UID:20210429-8a1785d7785a70b00178db1cadb64f2a@warwick.ac.uk CREATED:20210416T143633Z DESCRIPTION:Abstract: Cellular senescence is a complex stress response pl aying a causal role in many age-related pathologies. Promising strategie s aimed at clearing senescent cells are potentially able to slow down th e ageing process. To identify novel senolytic compounds\, we have screen ed libraries comprising ~2\,000 small molecules using systems of oncogen e-induced and therapy-induced senescence. We have assessed the senolytic effect of these compounds in different cell types and in response to di fferent senescent inducers. Interestingly\, we observed that while some compounds have just selectivity to kill cells undergoing oncogene-induce d senescence\, others behaved as broad-spectrum senolytics. Here\, we wi ll show our progress on validation of one of these small molecules that displays conserved senolytic activity across different senescence models . So far\, our results suggest the on-target activity of this compound a nd members of its family. Additional experiments are being conducted to gain mechanistic insights into the underlying signaling pathways involve d. Moreover\, preliminary results show the ability of this compound to s electively kill senescent cells in vivo in the context of natural ageing \, therapy-induced senescence\, and oncogene-induced senescence. Overall \, our results suggest drug screens are a useful tool to identify new vu lnerabilities of senescent cells and highlight the broad potential of se nolysis as a therapeutic strategy. Biography: Jesús Gil was born in Zara goza\, Spain. He obtained his PhD studying how the dsRNA- dependent prot ein kinase induces apoptosis and activates NF-B\, in 2000 at the Univer sidad Autónoma in Madrid. From 2000 to 2003 he worked with David Beach a t the Wolfson Institute for Biomedical Research\, University College Lon don\, where he screened for genes bypassing senescence\, identifying CBX 7. In January 2004\, he joined Gordon Peters' group at the CRUK London R esearch Institute\, investigating how CBX7 regulates the INK4/ARF locus. During 2005 he visited Scott Lowe's laboratory at Cold Spring Harbor\, New York\, developing models to study CBX7 function in vivo. Since Nov. 2005 he leads the Cell Proliferation Group at the MRC London Institute o f Medical Sciences (MRC LMS) were his main interest is to understands ho w senescence is regulated. His laboratory studies the molecular pathways regulating senescence and the senescence-associated secretory phenotype (SASP) and their pathophysiological implications. To this end they use different mammalian systems of senescence and a variety of strategies to perform functional screens. The ultimate end is to understand the molec ular mechanisms controlling senescence and exploit them for therapeutic benefit. In 2008\, Jesús was named an EMBO Young Investigator. He got te nured in 2010 and in 2011 obtained the EACR Cancer researcher Award ’hig hly commended’. Since 2013 he is a Professor at Imperial College where i t heads the Department of Molecular Sciences at the Institute of Clinica l Sciences. LOCATION:via MS Teams CATEGORIES:BiomedicalSciences,DivisionalSeminars,CSRL LAST-MODIFIED:20210416T143633Z ORGANIZER;CN=Jas Bains: END:VEVENT END:VCALENDAR