BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//talks.cam.ac.uk//v3//EN
BEGIN:VTIMEZONE
TZID:Europe/London
BEGIN:DAYLIGHT
TZOFFSETFROM:+0000
TZOFFSETTO:+0100
TZNAME:BST
DTSTART:19700329T010000
RRULE:FREQ=YEARLY;BYMONTH=3;BYDAY=-1SU
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0100
TZOFFSETTO:+0000
TZNAME:GMT
DTSTART:19701025T020000
RRULE:FREQ=YEARLY;BYMONTH=10;BYDAY=-1SU
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
CATEGORIES:MRC LMB Seminar list
SUMMARY:Deconstructin oncogenesis and tumour suppression t
 o find the best cancer drug targets - Gerard Evan\
 , Department of Biochemistry\, Unversity of Cambri
 dge
DTSTART;TZID=Europe/London:20101118T161500
DTEND;TZID=Europe/London:20101118T180000
UID:TALK27471AThttp://talks.cam.ac.uk
URL:http://talks.cam.ac.uk/talk/index/27471
DESCRIPTION:Myc and p53 are pleiotropic transcription factors 
 that\, respectively\, drive and suppress cancer. M
 yc levels are elevated and deregulated in most can
 cers\, suggesting a pivotal role for Myc in oncoge
 nic signaling. De-activation of Myc function in tu
 mours driven by oncogenically activated Myc trigge
 rs their rapid regression through a variety of int
 racellular and extracellular mechanisms\, includin
 g differentiation\, apoptosis and vascular collaps
 e. However\, Myc mutations are relatively rare and
  the aberrant Myc in most tumours appears to be a 
 consequence of aberrant upstream signals. The exte
 nt to which such endogenous Myc\, acting as a clie
 nt of upstream oncogenes\, is a therapeutic target
  depends on the degree to which it coordinates fun
 ctions essential for tumour maintenance and what t
 hose functions are\, neither of which is known. To
  investigate the therapeutic potential of Myc inhi
 bition we have constructed switchable genetic mous
 e models in which endogenous Myc can be systemical
 ly and reversibly inhibited in normal and tumour t
 issues in vivo. Our data indicate that inhibiting 
 Myc has a remarkably efficacious and durable thera
 peutic impact on multiple cancer types\, triggerin
 g widespread tumour cell apoptosis while eliciting
  only mild\, reversible and non-cytotoxic side eff
 ects in normal tissues. The p53 tumor suppressor\,
  or its attendant pathway\, is functionally inacti
 vated in almost all human cancers. However\, the m
 echanism by which p53 suppresses tumorigenesis rem
 ains obscure. p53 mediates the cellular apoptotic 
 and senescence response to DNA damage\, and this i
 s thought to be critical for both tumour suppressi
 on and for the progressive erosion of somatic rege
 nerative capacity that characterizes aging. Howeve
 r\, using a unique mouse model in which the endoge
 nous p53 gene is replaced by one encoding a ligand
 -dependent\, reversibly switchable variant of p53\
 , we show that the p53-mediated DNA damage respons
 e is dispensable for tumour suppression. Hence\, b
 y selectively manipulating the DNA damage and tumo
 ur suppressor functions of p53 it may be possible 
 to potentiate tumour suppression and cancer therap
 y whilst simultaneously extending life-span. 
LOCATION:Max Perutz Lecture Theatre\, Medical Research Coun
 cil (MRC) (MRC Laboratory of Molecular Biol
CONTACT:Paula Murphy
END:VEVENT
END:VCALENDAR