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    Friday Séminaire 06/02/2015

    Friday Séminaire 06/02/2015

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    Séminaire de Olivier Coqueret

    Intervenant local

    Le 6 février 2015

    Un séminaire sera donné par Olivier Coqueret, Institut de Cancérologie de l'Ouest Paul Papin, CRCNA, Inserm UMR892 "Ciblage Thérapeutique et Echappement Tumoral dans le Cancer Colorectal".

    Les étudiants souhaitant assister à la conférence doivent s'inscrire au préalable avant le Jeudi 05 Février à 12h00 dans la limite des places disponibles (inscription) (secr-inserm-angers @ contact.univ-angers.fr) en communiquant leur numéro de carte étudiante.

    Pour que la participation au séminaire soit validante, il est impératif que les étudiants émargent la feuille de présence.


    Pour rappel, les étudiants non inscrits ne seront pas acceptés.

    12h00 - 13h00
    CHU Angers - Bâtiment IBS-IRIS - salle de conférence RDC

     secr-inserm-angers@contact.univ-angers.fr

    «Progression tumorale et échappement à la chimiothérapie»

    In response to various stresses such as telomere shortening, oncogenic insults or chemotherapy treatments, mammalian cells undergo either apoptosis or senescence. Senescence is a long term cell cycle exit where cancer cells remain viable but proliferation is definitely arrested. The choice between apoptosis and senescence depends on the cell type, on the intensity of the damage and on the integrity of the p53-p21 pathway. Initially characterized in primary cells, animal models and human biopsies have demonstrated that senescence limits tumor progression and is necessary for chemotherapy response.
    It is unclear if chemotherapy-induced senescence (CIS) is always irreversible and if some cells can preserve their proliferative potential. During the last years, we have described that the STAT3-Myc pathway plays an important role in CIS resistance through the deregulation of p21waf1 and DNA repair signaling. We have also shown that CIS is not a definitive arrest and that cells can escape senescence in response to chemotherapy or oncogenic stress. These subpopulations emerge as more agressive and invasive cells that grow in soft agar and induce tumor formation in vivo.
    To extend these observations, we used quantitative proteomic analysis on tumor samples to identify proteins involved in this progression. We assumed (but this remains to be shown) that senescence is inactivated during the cancer successive stages. To our knowledge, we have described and patented the first proteomic signatures of the different stages of colorectal cancer and of triple negative breast cancers. Through these analysis, we came to the conclusion that the ideal marker must be detectable in the blood of patients using a simple test. For this reason, we have focused our proteomic approaches on the secretome of tumor cells. We described and patented specific markers of the different stages of colorectal and breast cancers that can be detected in the blood. We are currently determining if these soluble proteins are involved in treatment failure and CIS escape.
    In sum, our research project is focused on the identification of soluble markers of tumor progression and on the way tumor cells use this secretome to escape chemotherapyinduced senescence.