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URL:https://murmitoyen.com/events/vanille/udem/detail/750191-an-epigenetic-
 program-protects-tumor-cells-from-the-senescence-tumor-suppressor-mechanis
 m
LOCATION:CHU Sainte-Justine\, 3175\, Chemin de la Côte-Sainte-Catherine\, 
 Montréal\, QC\, Canada\, H3T 1C5
SUMMARY:An epigenetic program protects tumor cells from the senescence tumo
 r suppressor mechanism
DESCRIPTION:CONFÉRENCE SCIENTIFIQUE de l'Unité collaboratrive en épigén
 étique moléculaire (UCEM) 
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\nInvitation des Drs Noël Raynal et Ser
 ge McGraw
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\n 
\n 
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\n 
\nGerardo Ferbeyre\, MD\, PhD Professeu
 r\, Département de biochimie\, Université de Montréal 
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\
 nAn epigenetic program protects tumor cells from the senescence tumor supp
 ressor mechanism 
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\nCancer is traditionally understood as a genetic d
 isease caused by mutations that activate oncogenes or inactivate tumor sup
 pressor genes. Of interest\, gene expression can be also controlled by sta
 ble but ultimately reversible changes in the chromatin that also contribut
 e to tumor progression. Senescence is a stable cell cycle arrest that effi
 ciently prevents tumor formation. However\, sometimes senescence fails as 
 an anti-cancer mechanism and cancer progress. Under the genetic model\, it
  was thought that this failure was due to mutations in genes required for 
 senescence and therefore little could be done to restore this form of tumo
 r suppression. Here\, I will propose that epigenetic changes protect prost
 ate cancer cells from senescence. We discovered that a drug currently in c
 linical trials for the treatment of breast cancer and known as palbociclib
  is actually a “safe” epigenetic modulator. In studies conducted with 
 cells in culture and in a mouse model\, we found that senescence was defec
 tive in prostate cancer cells and that palbociclib could restore the senes
 cence response to these cells. The mechanism explaining this result involv
 es a novel interaction between the cyclin dependent kinase CDK4\, the targ
 et for palbociclib\, and the epigenetic enzyme DNMT1.
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