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SUMMARY:Caspase-2 as a tumour suppressor. - Professor Sharad Kumar\, Senio
 r Principal Research Fellow of the NHMRC Australia\, a Co-Founder and Co-D
 irector of the Centre for Cancer Biology\, a Professor of Cell Biology and
  the Chair of Cancer Biology at the University of South Australia
DTSTART:20190703T113000Z
DTEND:20190703T123000Z
UID:TALK126949@talks.cam.ac.uk
CONTACT:Emma Copley
DESCRIPTION:Caspase-2\, the most evolutionarily conserved member of the ca
 spase family\, has redundant function in cell death during development. Ou
 r recent work suggests that caspase-2 is a tumour suppressor as caspase-2 
 deficiency enhances tumourigenesis in several mouse models. Interestingly 
 caspase-2-deficient tumours always show enhanced chromosomal instability (
 CIN) and aneuploidy. Increased CIN and aneuploidy are also characteristics
  of caspase-2-deficient mouse embryonic fibroblasts in culture as well as 
 human tumour cells with CASP2 gene knockout. We further found that caspase
 -2 is required for apoptotic deletion of cells carrying mitotic defects. T
 hus apoptotic activity of caspase-2 is necessary for deleting cells with C
 IN to limit aneuploidy and we propose that this is linked to the tumour su
 ppressor function of caspase-2. Other recent studies have suggested that i
 n response of cytokinesis failure caspase-2-mediates cleavage of Mdm2 that
  results in p53 stabilization and cell cycle arrest\, thus preventing poly
 ploidy. It is therefore possible that caspase-2 is involved in two checkpo
 ints\, one leading to apoptosis of cells with CIN and the other\, cell cyc
 le arrest following cytokinesis failure. We are now investigating how casp
 ase-2 senses mitotic errors and becomes activated and how is such activati
 on regulated.  
LOCATION:Dixon Greaves Room\, Department of Pathology\, Tennis Court Road
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