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SUMMARY:The Role of Oncostatin M Receptor Overexpression in the Tumour Mic
 roenvironment of Cervical Squamous Cell Carcinoma  - Valtteri Tulkki – P
 hD Candidate\, Pathology\, Wolfson College\, University of Cambridge 
DTSTART:20170224T171000Z
DTEND:20170224T172000Z
UID:TALK71150@talks.cam.ac.uk
CONTACT:Wolfson College Cambridge
DESCRIPTION:The main cause of cervical squamous cell carcinoma (SCC) is th
 e viral integration of human papillomavirus (HPV) to the epithelial cells 
 that leads to genomic instability. This instability leads to gain and over
 -expression of Oncostatin M receptor (OSMR) in advanced SCC which is assoc
 iated with significantly worse clinical outcome (1). Cervical SCC cells th
 at over-express OSMR show enhanced responsiveness to its major ligand Onco
 statin-M (OSM)\, which in turn\, mediates multiple pro-malignant effects\,
  including a pro-angiogenic phenotype\, increased cell migration\, invasio
 n\, epithelial to mesenchymal transition\, metastasis and immune cell recr
 uitment (2\, 3). OSMR overexpressing cells are able to trigger OSM secreti
 on from monocytes and macrophages in vitro\, to create a niche that promot
 es the angiogenic switch through hypoxia signalling pathways. OSMR overexp
 ression is linked with the expression of several genes associated with tum
 our associated macrophages and an immunosuppressive tumour microenvironmen
 t (TME) in SCCs. In order to study the role of OSMR in SCCs and the TME\, 
 we have examined the effect of syngeneic mouse SCC cell lines with either 
 overexpression or loss of OSMR in wild-type and OSMR knock-out mice by usi
 ng 18 marker immune cell fluorescence-activated cell sorting (FACS) panel 
 to characterize multiple populations of lymphocytes and myeloid cells. The
 se studies will underpin our assessment of OSMR as a potential therapeutic
  target in SCCs.\n
LOCATION:Lee Hall\, Wolfson College Cambridge
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