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UID:1124@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20221018T130000

DTEND;TZID=Asia/Jerusalem:20221018T140000

DTSTAMP:20220929T102024Z

URL:https://biology.technion.ac.il/en/seminars/phd-graduate-seminar-of-mor
 -cohen-harel-meiri-lab/

SUMMARY:PhD Graduate Seminar of Mor Cohen-Harel (Meiri Lab) [No Categories]
DESCRIPTION:Location: hybrid- in the Faculty Auditorium/ZOOM: https://techn
 ion.zoom.us/j/98617011894  Mor Cohen-Harel (Meiri Lab)\n Affiliation: \n H
 ost:\n "The Antitumor Effects of Cannabinoids in Glioblastoma Multiforme"\
 nGlioblastoma multiforme is an aggressive brain tumor whose current treatm
 ents are insufficient due to its high invasiveness and heterogeneity\, rap
 id growth and acquired therapy resistance. There is a great need to develo
 p therapeutics that overcome this resistance and improve the treatment. So
 me studies have shown that the major cannabinoids from the Cannabis plant\
 , Δ9-tetrahydrocannabinol (Δ9-THC) and Cannabidiol (CBD)\, can improve g
 lioblastoma cell response to radiation and chemotherapy\, and moreover\, d
 irectly affect tumor growth and cell viability.\nAs our lab routinely char
 acterizes over 140 phytocannabinoids that exist in cannabis extracts in ad
 dition to THC and CBD\, this research focused on discovering phytocannabin
 oids with antitumor effects on glioblastoma and understanding their mechan
 ism of action. We studied each extract's properties\, recognized the minim
 al effective concentration that induces cell death in glioblastoma and def
 ined the most effective cannabis extract.\nWe examined the combination of 
 this extract with Bortezomib (BTZ)\, a proteasome inhibitor currently used
  as a second-line treatment in glioblastoma\, and demonstrated a stronger 
 and more rapid apoptotic response\, in an additive manner.\nFrom this effe
 ctive extract\, we isolated and identified Cannabigerol (CBG) as the essen
 tial cannabinoid for inducing glioblastoma programmed cell death. CBG show
 ed great potency also as a single treatment when used in a high dose. We f
 ound that CBG targets glioblastoma via the CB1 receptor of the endocannabi
 noid system. It's signaling pathway involves a significant upregulation of
  the transcription factor EGR1\, which leads to an increase in multiple do
 wnstream apoptotic markers and directs the cell to apoptosis. We were able
  to demonstrate that CBG works in a similar manner also in an in-vivo mice
  model. Therefore\, we believe that CBG is a promising therapeutic candida
 te that may be used\, alone or in a combination with BTZ\, in the treatmen
 t of glioblastoma patients. 
LOCATION:hybrid- in the Faculty Auditorium/ZOOM: https://technion.zoom.us/j
 /98617011894

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