BEGIN:VCALENDAR
VERSION:2.0
PRODID:https://murmitoyen.com/events/vanille/udem/
X-WR-TIMEZONE:America/Montreal
BEGIN:VEVENT
UID:69dafcc52c6bb
DTSTAMP:20260411T220037
DTSTART:20180130T150000
SEQUENCE:0
TRANSP:OPAQUE
DTEND:20180130T160000
URL:https://murmitoyen.com/events/vanille/udem/detail/805667-oncogenic-func
 tions-of-metabolic-defects-associated-to-brain-cancer-and-leukemia
LOCATION:CHU Sainte-Justine\, 3175\, Chemin de la Côte-Sainte-Catherine\, 
 Montréal\, QC\, Canada\, H3T 1C5
SUMMARY:Oncogenic Functions of Metabolic Defects Associated to Brain Cancer
  and Leukemia
DESCRIPTION:Conférence scientifique : Unité collaborative en épigénéti
 que moléculaire
\nOncogenic Functions of Metabolic Defects Associated to 
 Brain Cancer and Leukemia   Conférencier : Frédérick-Antoine Mallette\,
  PhD Professeur adjoint\, Département de médecine\, Université de Montr
 éal\, Centre de recherche de l'Hôpital Maisonneuve-Rosemont.
\nRésumé 
 :Gliomas and leukemias are devastating tumours that remain highly refracto
 ry to treatment\, thus highlighting the need for new and improved therapeu
 tic strategies. Mutations in the Krebs cycle enzymes isocitrate dehydrogen
 ase 1 and 2 (IDH1 and IDH2) are commonly observed in brain and blood cance
 rs. Although the precise molecular underpinnings for this remain elusive\,
  it has been shown IDH1/2 mutations confer altered metabolic function by i
 ncreasing production of the recently described oncometabolite R-2-hydroxyg
 lutarate (R-2HG) relative to the normal metabolite α-ketoglutarate (αKG)
 . Here we characterize the molecular basis of our recent unexpected observ
 ation of modulation of oncogenic cellular signaling pathways by R-2HG\, a 
 totally novel concept in molecular oncology. The notion of oncometabolite-
 mediated cancer stimulation has recently been described but the molecular 
 pathways regulated by R-2HG per se are largely unknown.
\nOur research aim
 s to probe a novel molecular link between R-2HG and modulation of cellular
  signaling\, offering completely fresh insight into the contribution of ID
 H1/2 mutations to glial transformation. Furthermore\, we demonstrate that 
 IDH1/2 mutations lead to telomere dysfunction such as telomere fragility\,
  which is caused by telomeric DNA replication defects. Cancer cells exploi
 t the metabolism differently than their normal counterparts. The proposed 
 research project will investigate previously unsuspected oncogenic activit
 ies of metabolic defects associated to cancer.
END:VEVENT
BEGIN:VTIMEZONE
TZID:America/Montreal
X-LIC-LOCATION:America/Montreal
END:VTIMEZONE
END:VCALENDAR