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SUMMARY:Cancer-related inflammation - Dr Thorsten Hagemann\, Barts Cancer 
 Institute\, Queen Mary University of London
DTSTART:20120612T110000Z
DTEND:20120612T120000Z
UID:TALK35414@talks.cam.ac.uk
CONTACT:Mala Jayasundera
DESCRIPTION:Experimental and clinical evidence points to the fact that inf
 lammation\, particularly chronic inflammation\, affects all phases of carc
 inogenesis. Inflammation favours the initial genetic mutation or epigeneti
 c mechanisms that drive cell transformation and cancer initiation: It acts
  as a tumour promoter by establishing a tissue microenvironment that allow
 s the tumour to progress and metastasize and by establishing immunosuppres
 sive mechanisms that prevent an effective immune response against the tumo
 ur. \n\nThe tumour microenvironment has a fundamental impact on growth and
  spread of malignant disease and contributes at least partially. Resistanc
 e to cytotoxic and targeted therapies can no longer be viewed as simply th
 e failure of malignant cell kill. Inflammatory mediators and cells contrib
 ute to cancer-related inflammation. This systemic inflammation is in a fun
 ctional relationship with energy metabolism and genetic instability predis
 poses individuals to cancer and regulates the neoplastic disease in all it
 s aspects\, including the individual response of the organism to the disea
 se and overall morbidity and mortality.\n\nOur research concentrates in pa
 rticular on the role of myeloid cells within the tumour microenvironment. 
 The evidence that myeloid cells provide tropic support to tumours and the 
 genetic (and pharmacological) experiments that show that inhibition of thi
 s support leads to suppressed malignancy strongly argue that these cells o
 r their unique signalling pathways are therapeutic targets.\n\nKnowledge o
 f the cancer-related inflammatory and immune pathways should make it possi
 ble to identify molecular targets and to plan rational preventive and ther
 apeutic approaches.\n
LOCATION:CRI Lecture Theatre\, Cambridge Research Institute
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