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SUMMARY:Macrophages within Tumor Microenvironment: Study of Molecular and 
 Cellular Mechanisms Involved in the Anti-Tumor Response
DTSTART:20200210T110000
DTEND:20200210T120000
DTSTAMP:20260407T102915Z
UID:edb97ea2d877a7bac1d3ec658456b588dbb8e9c8c7f0f0a3b60ad351
CATEGORIES:Conferences - Seminars
DESCRIPTION:Melissa Prat\, Ph.D.\, UMR-152 / IRD / PharmaDev\, Equipe MRN2
 i\, University Hospital (CHU)\, Rangueil\, Toulouse (F)\nSEMINAR of the LA
 USANNE INTEGRATIVE METABOLISM and NUTRITION ALLIANCE (LIMNA)\n\nAbstract:\
 nMacrophages are crucial effectors of innate immune response and exhibit a
  remarkable plasticity that allows them to adapt to different stimuli pres
 ent in their microenvironment. During tumor development\, mediators secret
 ed by transformed cells « educate » Tumor-Associated Macrophages (TAMs)\
 , which acquire properties favorable to tumor growth. It is now widely acc
 epted that TAMs\, initially exhibiting an anti-tumor M1 phenotype\, differ
 entiate towards an M2 phenotype and promote tumor cell proliferation\, ang
 iogenesis\, metastases\, chemoresistance and immunosuppresion. While this 
 functional M1/M2 dichotomy facilitates the description of TAMs phenotype a
 nd their associated functions\, it is\, however\, in many cases an oversim
 plification of macrophage biology\, which is often more complex.\n\nWe sho
 wed that interleukine-13\, a Th2 cytokine known to be involved in macropha
 ge M2 polarization\, promotes macrophage cytotoxic activity against severa
 l tumor cell lines. Furthermore\, we demonstrated in an experimental model
  of ovarian adenocarcinoma the anti-tumor activity of 15(S)-HETE\, a natur
 al ligand of the PPARγ nuclear receptor involved in macrophage M2 polariz
 ation. These findings illustrate the complexity of the M1/M2 paradigm in t
 he description of macrophage pro- and anti-tumor functions and support the
  importance of targeting macrophages in cancer therapy.\n 
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153
STATUS:CONFIRMED
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