Aurore TOULLEC

En résumé

Entreprises

• Fed Santé - Consultante

  2016 - maintenant Créé en 2016, le cabinet de recrutement et d'Interim Fed Santé, société du Groupe Fed, est spécialisé sur les métiers médicaux et paramédicaux.
  
  Nos clients et candidats nous sollicitent dans le cadre de :
  - recrutement direct en CDI,
  - recrutement direct en CDD,
  - Intérim à durée variable adaptée au contexte de l'entreprise.

• BiAur Consulting - Fondatrice BiAur Consulting

  2016 - 2016 Diffusion d'offres d'emploi/stage et conseil en recrutement spécialisé en Biologie et Biotechnologies.
  De la simple Multi-diffusion de vos offres d'emploi à un accompagnement personnalisé de vos recrutements. Découvrez mes services à la carte : http://biaur-consulting.fr

• BLOSSOM PARTNERS - Consultante en ressources humaines secteur sciences de la vie

  Villejust 2015 - 2016 Cliquez pour modifier la description du posteConsultante junior chez BLOSSOM PARTNERS, cabinet de recrutement spécialisé dans le domaine scientifique.
  
  Activité de recrutement :
  
  -Prospection et fidélisation de nouveaux clients
  - Audit de poste
  - Sourcing sur bases internes et externes, réseaux sociaux, approche directe,
  - Présélection de candidatures
  - Entretien en face à face
  - Test de personnalité
  - Présentation des candidats sélectionnés
  - Suivi de la relation clients
  - Suivi des candidats durant le processus de recrutement et d'intégration
  
  Communication :
  -Création et entretien du site web via Wordpress (www.blossom-partners.fr)
  -Création et entretien du profil de l'entreprise sur les réseaux sociaux (linkedin, viadéo, twitter ....)
  - participation a des congrès, séminaires et forums emploi.

• IRSN - Post doctorante

  Fontenay-aux-Roses 2012 - 2014 Cliquez pour modifier la description du posteChercheur Post-Doctorante, IRSN (Institut de Radioprotection et de Sureté Nucléaire), Laboratoire de Recherche en Radiobiologie et Radiopathologie, Dir. Dr Fabien Milliat
  
  Subject : Endothelium specific HIF-1α deletion protects from radiation-induced intestinal injury.
  
  We used a model of mice deficient for HIF-1α specifically in endothelial compartment (VeCadh-Cre/HIF-1αflox/flox) or control mice (HIF-1αflox/flox) which received a single irradiation dose (19 Gy) to an exteriorized localized ileal segment. At several times after irradiation (3 to 42 days) immunohistological analyses was performed. In control animals, we observed appearance of an hypoxic zone (after anti-pimonidazole staining) and increased expression of HIF-1α in the irradiated area at 7 days after irradiation. Three days after irradiation, tissue specific knockout of HIF-1α does not affect dramatically radiation-induced histological damages. At Day 7, we observed less histological radiation-induced damages in VeCadh-Cre/HIF-1αflox/flox mice compare with control HIF-1 flox/flox mice, which is associated with increased survival of these mice.
  Our results show a role for the endothelial HIF-1 pool in radiation-induced intestinal toxicity.

• Inserm - Post doctorante

  PARIS 13 2010 - 2012 Cliquez pour modifier la description du posteChercheur Post-Doctorante, hôpital Lariboisière, unité de « Recherche Translationnelle et Angiogenèse »- INSERM U965 Dir. Pr Marc Pocard
  
  Subject : VEGF189 overexpression in breast cancer cells delays lung colonization and tumor uptake.
  
  We used bioluminescence imaging and transcriptomic analysis to study the colonization capacity of human breast cancer cells (MDA-MB-231) overexpressing the VEGF165 or VEGF189 isoform (named V165-B, V189-B and cV-B respectively) in nude mice. Results: When injected into the circulation, V189-B cells induced less metastasis in lung and bone than V165-B and cV-B control cells, consistent with longer survival of these mice and delay in tumor uptake in mice injected with a V189-B clone. Moreover, we observed a smaller activated stromal compartment with the V189-B clone, as compared to V165-B and cV-B clones. In vitro V189-B cells showed both decreased cell invasion and survival. Using transcriptomic analysis, we identified a subset of 18 genes differentially expressed between V189 and V165 cell lines and in 120 human breast tumors. Our results showed a negative correlation between the expression pattern of VEGF189 and the levels of expression of seven genes that influenced metastasis. Conclusion: Our findings provide the first evidence that VEGF isoforms have different effects on breast cancer cell line colonization in vivo.

• Institut Curie - Doctorante

  PARIS 5 2005 - 2009 Cliquez pour modifier la description du posteDoctorat de Cancérologie spécialité biologie cellulaire et moléculaire des cancers, Institut Curie, sous la direction du Dr Fatima-Mechta Grigoriou. Unité « Génétique et biologie des cancers »- Inserm U 830, Dir. Olivier Delattre.
  
  Oxidative stress promotes myofibroblast differentiation and tumour spreading.
  EMBO Mol Med. 2010 Jun;2(6):211-30. doi: 10.1002/emmm.201000073.
  
  JunD regulates genes involved in antioxidant defence. We took advantage of the chronic oxidative stress resulting from junD deletion to examine the role of reactive oxygen species (ROS) in tumour development. In a model of mammary carcinogenesis, junD inactivation increased tumour incidence and revealed an associated reactive stroma. junD-inactivation in the stroma was sufficient to shorten tumour-free survival rate and enhance metastatic spread. ROS promoted conversion of fibroblasts into highly migrating myofibroblasts through accumulation of the hypoxia-inducible factor (HIF)-1alpha transcription factor and the CXCL12 chemokine. Accordingly, treatment with an antioxidant reduced the levels of HIF and CXCL12 and numerous myofibroblast features. CXCL12 accumulated in the stroma of HER2-human breast adenocarcinomas. Moreover, HER2 tumours exhibited a high proportion of myofibroblasts, which was significantly correlated to nodal metastases. Interestingly, this subset of tumours exhibited a significant nuclear exclusion of JunD and revealed an associated oxido-reduction signature, further demonstrating the relevance of our findings in human cancers. Collectively, our data uncover a new mechanism by which oxidative stress increases the migratory properties of stromal fibroblasts, which in turn potentiate tumour dissemination.

Formations

• Université Paris 11 Paris Sud DEA Cancérologie

  Kremlin Bicêtre 2005 - 2009 doctorat de cancerologie specialite biologie cellulaire et moleculaire

• Université Paris 11 Paris Sud DEA Cancérologie

  Kremlin Bicêtre 2004 - 2005 master 2 biologie cellulaire et moleculaire