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SUMMARY:Cancer and ageing: Rival demons?   - Judith Campisi\, Buck Institu
 te for Research on Ageing and Lawrence Berkeley National Laboratory
DTSTART:20191121T130000Z
DTEND:20191121T140000Z
UID:TALK114007@talks.cam.ac.uk
CONTACT:Kate Davenport
DESCRIPTION:	Cancer is primarily a disease of ageing\, similar to many oth
 er age-related pathologies ranging from sarcopenia to neurodegeneration.  
 In contrast to many age-related diseases\, which are loss-of-function in n
 ature\, cancer can be considered a gain-of-function disease because cancer
  cells must acquire new properties\, generally by somatic mutation\, in or
 der to develop into a lethal tumor.  Given that potentially oncogenic muta
 tions occur throughout life\, why do most cancers take decades to develop?
   One answer is there are powerful tumor suppressive mechanisms\, selected
  throughout evolution\, that keep cancer at bay for approximately half the
  mammalian life span.  One of these tumor suppressive mechanisms is a cell
  fate decision termed cellular senescence.  Cells undergo senescence in re
 sponse to many types of stress or damage\, including potentially oncogenic
  mutations.  Senescent cells arrest proliferation\, essentially irreversib
 ly\, and develop a complex senescence-associated secretory phenotype (SASP
 ) that includes many inflammatory cytokines and chemokines\, growth factor
 s\, proteases and bioactive metabolites\, including lipids.  Senescent cel
 ls increase with age in most\, if not all\, mammalian tissues\, and are pr
 esent at higher numbers in many diseased\, compared to age-matched non-dis
 eased\, tissues.  There is now mounting evidence that senescent cells\, an
 d particularly their SASPs\, are prime drivers of many age-related patholo
 gies\, including\, ironically\, late-life cancer.  Further\, many genotoxi
 c and cytotoxic anti-cancer drugs induce senescence in both tumor and norm
 al cells\, suggesting that senescent cells might be responsible for the pr
 emature aging phenotypes that commonly develop in cancer patients treated 
 with certain anti-cancer therapies.  Mouse models\, and a new class of dru
 gs that selectively kill senescent cells\, give hope that the balance betw
 een tumor suppression and aging can be tipped to reduce the incidence of a
 ge-related cancer and extend health span.  \n
LOCATION:CRUK CI Lecture Theatre
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