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SUMMARY:The Senescence-Associated Innate Immune Sensors in Tumour Suppress
 ion - Dr Juan Carlos Acosta\; Cancer Research UK Edinburgh Centre\, MRC In
 stitute of Genetics &amp\; Molecular Medicine
DTSTART:20200703T140000Z
DTEND:20200703T150000Z
UID:TALK149812@talks.cam.ac.uk
CONTACT:Bobbie Claxton
DESCRIPTION:Cellular senescence is a tumour suppressor response that impai
 rs the propagation of mutated cells\, characterized by a robust cell cycle
  arrest and the senescence-associated secretory phenotype (SASP)\, a pro-i
 nflammatory secretome that reinforces senescence and promotes immune-clear
 ance of senescent cells. Cellular senescence is the outcome of most conven
 tional and pro-senescence anti-cancer treatments. However\, accumulation o
 f cancer-associated senescent cells during tumour initiation\, ageing\, or
  cancer treatments can facilitate cancer progression through the paracrine
  effects of the SASP or by senescent cell reprogramming to a cancer stem c
 ell-like state. Therefore\, novel strategies for controlling the adverse e
 ffects of cancer-associated senescent cells by SASP manipulation or by sen
 escent cell elimination (senolytics) are urgently needed. Previously\, we 
 discovered that the SASP depends on the activation of the inflammasome\, a
  molecular platform for Caspase-1 (CASP1) induction downstream of innate i
 mmune receptors. Inflammasomes are assembled by the activation of Pattern 
 Recognition Receptors (PRRs). PRRs are sensors of the innate immune system
  which recognize Pathogen Associated Molecular Patterns (PAMPs) abundant i
 n pathogens but absent in the host (i.g. LPS of Gram-negative bacteria)\, 
 and endogenous molecules from the host activated upon stress and damage or
  Damage Associated Molecular Patterns (DAMPs) (i.e. HMGB1 or alarmin).\nDu
 ring the seminar\, I will show our recent work identifying the essential r
 ole for the senescence-associated innate immune sensor Toll-Like Receptor 
 2 (TLR2) regulating the SASP in oncogene-induced senescence (OIS)\, and th
 e identification of the serum amyloids SAA1/2 as the specific DAMP for TLR
 2. Moreover\, I will show our efforts to demonstrate a tumour suppressor r
 ole of TLR2 in non-small cell lung carcinoma. Finally\, I will introduce o
 ur last results uncovering the new and specific mechanism of inflammasome 
 activation in OIS and discuss our efforts to exploit the inflammasome for 
 new treatments in cancer by stimulation the inflammatory cell death pyropt
 osis in cancer cells.\n\nJoin Zoom Meeting:\nhttps://zoom.us/j/91732190643
 ?pwd=YWkrTktGeW8zYzFKOEU5SVNaUE5wdz09\n\nMeeting ID:   917 3219 0643\nPass
 word:      733561
LOCATION:Zoom Seminar
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