BEGIN:VCALENDAR
PRODID:-//Columba Systems Ltd//NONSGML CPNG/SpringViewer/ICal Output/3.3-
 M3//EN
VERSION:2.0
CALSCALE:GREGORIAN
METHOD:PUBLISH
BEGIN:VEVENT
DTSTAMP:20160121T095341Z
DTSTART:20160126T130000Z
DTEND:20160126T140000Z
SUMMARY:ECM remodeling during cancer progression
UID:{http://www.columbasystems.com/customers/uom/gpp/eventid/}n10g-ijo2m4
 nr-72prvp
DESCRIPTION:The extracellular matrix (ECM) is one of the most important r
 egulators of cellular and tissue function in the body. The ECM is known 
 to play a critical role in driving cancer progression\, and yet we lack 
 knowledge of how ECM is altered during tumour progression to promote can
 cer metastasis. We have found that an enzyme secreted by tumour and stro
 mal cells called lysyl oxidase (LOX) is responsible for altering the ECM
  at primary and metastatic sites to greatly enhance metastasis. LOX is a
 n amine oxidase that catalyses the crosslinking of collagens and elastin
  in the ECM. LOX activity alters the structural and biochemical properti
 es of the ECM\, to drive cell proliferation\, invasion and angiogenesis.
  Importantly\, LOX modifies pre-metastatic tissue microenvironments prio
 r to tumour cell arrival\, enhancing metastatic colonisation and outgrow
 th. Recently\, we showed that hypoxia inactivates cancer-associated fibr
 oblasts to decrease tumour stiffness and metastasis. These effects could
  be mimicked through inhibition of prolyl hydroxylase domain protein 2 (
 PHD2)\, a master regulator of hypoxia-inducible factor 1 alpha (HIF1a). 
 These findings support use of PHD inhibitors in the clinic to prevent ca
 ncer progression. Our current research focused on further investigating 
 how the ECM is remodelled during cancer progression and how this impacts
  on cell behaviour to drive metastasis. 
STATUS:TENTATIVE
TRANSP:TRANSPARENT
CLASS:PUBLIC
LOCATION:Michael Smith Lecture Theatre\, Michael Smith Building\, Manches
 ter
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