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SUMMARY:The p53 family in the cancer cell response to hypoxia - Dr Ivano A
 melio\, MRC Toxicology Unit\, Cambridge
DTSTART:20190212T123000Z
DTEND:20190212T133000Z
UID:TALK120001@talks.cam.ac.uk
CONTACT:Sue Griffin
DESCRIPTION:The p53 family of tumour suppressors (p53\, p73\, p63) has an 
 essential role in the response to cellular stress and somatic cells largel
 y rely on p53 and its siblings to overcome toxic insult and to maintain ho
 meostasis. Inactivation of p53 (i.e. TP53 gene mutations) and deregulation
  of p73 and p63 are frequently observed in cancer\, altering the response 
 to cellular stressors and consequent direct implications for disease patho
 genesis. Hypoxia (reduced O2) is a tumour microenvironmental factor common
 ly observed in advanced cancers. Hypoxia and its major regulator the Hypox
 ia-inducible Factor-1 (HIF-1) have long been associated with resistance to
  therapy\, metastasis\, and poor survival rates in cancer patients.\n \nOu
 r work demonstrated that the tumour suppressor TAp73 opposes HIF-1 activat
 ion in cancer cells\, resulting in reduced angiogenesis and tumor progress
 ion. This new mechanism of control of HIF-1 protein stability has clinical
  implications as TAp73/HIF-1 axis correlates with stage and prognosis of t
 he disease. The complexity of the interplay between the p53 family and the
  HIF-1 was further highlighted by our discovery of novel gain-of-function 
 effect of p53 mutants in hypoxic tumours. We demonstrated that p53 mutants
  impinge on the HIF-1 transcriptional capability regulating a selective hy
 poxic-gene expression reponse\, involved in pro-tumorigenic non-cell-auton
 omous functions. Overall our findings shed light on the complex interfamil
 y crosstalk p53 family/HIF indicating this as a molecular axis of major re
 levance in cancer pathogenesis.\n
LOCATION:Lecture Theatre\, Department of Pathology\, Tennis Court Road
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