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SUMMARY:When good cells go bad: Causes and consequences of genetic changes
  in human pluripotent stem cells - Professor Ivana Barbaric\, Centre for S
 tem Cell Biology School of Biological Sciences\, University of Sheffield
DTSTART:20260211T123000Z
DTEND:20260211T133000Z
UID:TALK235231@talks.cam.ac.uk
CONTACT:Rachel Fellows
DESCRIPTION:Human pluripotent stem cells (hPSCs) are powerful tools for mo
 deling early human embryogenesis and provide a crucial source of different
 iated cells for regenerative medicine. Maintaining their genetic stability
  is paramount for both basic research and clinical applications. However\,
  it is now well-documented that hPSCs acquire non-random genetic changes u
 pon culture. Some of the acquired genetic aberrations are associated with 
 a selective growth advantage in variant hPSCs and are also linked to oncog
 enesis in other contexts. This raises significant concerns about their pot
 ential to confer tumorigenic or malignant properties on transplanted diffe
 rentiated cells or any residual undifferentiated hPSCs. Furthermore\, such
  genetic changes can undermine basic research by leading to unpredictable 
 results in disease modeling and developmental studies due to aberrant prol
 iferation rates or altered differentiation abilities.\n\nIn this talk\, I 
 will present our ongoing work focused on elucidating the molecular mechani
 sms that underpin the maintenance of hPSC genome integrity. I will discuss
  how disruptions to these mechanisms can lead to undesired genetic changes
 . Moreover\, I will also share our findings demonstrating that the dominan
 ce of genetically variant hPSCs in mosaic cultures is significantly enhanc
 ed through competitive interactions\, leading to the elimination of wild-t
 ype cells. Ultimately\, our work is informing novel approaches to minimize
  the occurrence of genetic changes in hPSC cultures\, ensuring their relia
 bility for both clinical and research use.
LOCATION:Seminar Room\, Gleeson Building\, MRC Toxicology Unit\, Tennis Co
 urt Road
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