BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Talks.cam//talks.cam.ac.uk//
X-WR-CALNAME:Talks.cam
BEGIN:VEVENT
SUMMARY:Telomere to mitochondria signaling prevents age-associated cancer 
 initiation - Jan Karlseder\, Salk Institute for Biological Studies
DTSTART:20250123T130000Z
DTEND:20250123T140000Z
UID:TALK225232@talks.cam.ac.uk
CONTACT:Kate Davenport
DESCRIPTION:Telomere to mitochondria signaling prevents age-associated can
 cer initiation\n\nTobias Schmidt1\, Marco R. Cosenza2\, Joe Nassour3\, Car
 ly Tyer4\, Scott Hickey4\, Jan Korbel2\, Jan Karlseder1\n\n1Salk Institute
  for Biological Studies\, La Jolla\, CA\, USA.\n2Genome Biology\, European
  Molecular Biology Laboratory\, Heidelberg\, Germany.\n3Department of Bioc
 hemistry and Molecular Genetics\, University of Colorado\, Anschutz Medica
 l Campus\, Denver\, CO\, USA.\n4Oxford Nanopore Technologies\, Inc.\, New 
 York\, NY\, USA.\n\nCancers arise through accumulation of genetic and epig
 enetic alterations allowing cells to evade telomere-based proliferative ba
 rriers and achieve immortality. One such barrier is replicative crisis\, a
 n autophagy-dependent program eliminating checkpoint-deficient cells with 
 unstable telomeres. Cells that escape crisis exhibit cancer-relevant chrom
 osomal aberrations\, yet little is known about the molecular events regula
 ting the onset of this tumor suppressive barrier. We discovered that crisi
 s is executed through an intricate interplay between innate DNA and RNA se
 nsing machineries\, activated by critically short telomeres. We found that
  three hallmarks of aging\, telomeres\, mitochondria and inflammation\, sy
 nergize in molecular pathways to prevent age associated cancer initiation.
  Furthermore\, analysis of single cells during crisis and cells that escap
 ed crisis revealed a role for genome instability in executing the crisis p
 rogram. Our discoveries establish novel mechanisms for telomere-mediated t
 umor suppression\, whereby dysfunctional telomeres activate lethal innate 
 immune signaling to eliminate cells at risk for neoplastic transformation.
 \n\n
LOCATION:CRUK CI Lecture Theatre
END:VEVENT
END:VCALENDAR