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Anciens séminaires 2010-2016

Liste complète des anciens séminaires 2010-2014 :  angry     2015 :  pdf     2016 :  pdf     

Mercredi 14 juin 2017, 11h00

 

Erwan Corcuff, Directeur de la société Axenis

Jean-Jacques Mention, PhD en immunologie à la société Axenis (Institut Pasteur)

 

"Des souris humanisées pour une médecine innovante / Humanized mice for innovative  medicine"

 

Contact :  emmanuelle.liaudet-coopman@inserm.fr

 

AXENIS, a spin-off of the Institut Pasteur, is a French contract research organization (CRO) generating, exploiting and developing mouse models humanized for molecular and cellular components of the immune system. The model portfolio of AXENIS is based on the proprietary immuno-deficient BRGS (BALB/c Rag2tm1Fwa IL-2Rγctm1Cgn SIRPαNOD) mouse model, which is particularly permissive to the long-term establishment of a variety of human xenografts, including human tumor cells.

When BRGS mice are transplanted with human hematopoietic stem and progenitor cells, such as umbilical cord blood CD34+ cells, the resulting ‘Human Immune System’ (HIS) mice support the development and maintenance of a large diversity of human hematopoietic cell subsets, such as B cells, T cells (including CD4+ Treg cells), NK cells, and myeloid cells such as conventional dendritic cells (cDCs), plasmacytoid dendritic cells (pDCs) and monocytes/macrophages. This myeloid compartment can be boosted with a simple exogenous Flt3-ligand treatment in BRGS mice lacking the corresponding mouse receptor (Flk2/Flt3). The boost of human dendritic cells accumulation and maturation in this novel BRGSF (BALB/c Rag2tm1Fwa IL-2Rγctm1Cgn SIRPαNOD Flk2tm1Irl) HIS mouse model strongly potentiates human B and T cell functionality, resulting in unprecedented levels of human, antigen-specific immune responses.

 

These optimized humanized mouse models introduce a variety of new solutions for academia, biotech companies and bio-pharmaceutical industries that are looking for innovative in vivo models for immuno-oncology, inflammation, host-pathogen interactions and preclinical validation of biotherapeutics, e.g. vaccines, monoclonal antibodies, cellular products or small molecules targeting hematopoietic cells. Furthermore, HIS mice represent an attractive preclinical platform for the evaluation of therapeutics requiring the simultaneous presence of both human tumor and human effector cells, such as immune checkpoint inhibitors, bispecific antibodies or CAR-T cells. As such, HIS mice can therefore be used both as a standardized model or in personalized medicine approaches.

 

Vendredi 9 juin 2017, 11h00

Conférence de "IRCM-SIRIC Montpellier-Cancer seminar series"

 

Prof. Erwin Wagner, CNIO, Madrid.

 

"Stress signaling in Inflammation and Cancer"

 

Contact : piona.dariavach@icm.unicancer.fr

 

résumé :

Our studies aim to analyze gene function in healthy and pathological conditions, e.g. in tumour development, using the mouse as a model organism, but also employing patient-derived samples. Specifically, the functions of the AP-1 (Fos/Jun) transcription factor complex regulating cell proliferation, differentiation and oncogenesis, as well as the cross-talk between organs are being investigated. The goal is to define molecular pathways leading to disease/cancer development and to identify novel therapeutic targets. We focus on elucidating a causal link between inflammation, cancer and AP-1 (Fos/Jun) expression using cell type-specific, switchable genetically engineered mouse models. We are also developing and characterizing new GEMMs for cancer and human diseases, such as for bone loss, fibrosis and psoriasis, and applying these to preclinical studies.

 

I will focus in my talk on recent studies towards understanding liver and skin pathologies at the cross-road between inflammation, metabolism and cancer, and will discuss the adverse effects of cancer cachexia, a deadly wasting syndrome and metabolic impairment with systemic manifestations frequently observed in cancer patients.

Vendredi 2 juin 2017, 11h00

Pierre-Antoine Defossez, CNRS UMR7216, Université Paris 7

 

“Functions of methyl-DNA binding proteins in normal cells and in cancer"

 

Contact : claude.sardet@inserm.fr

 

Vendredi 12 mai 2017, 14h00

Arnaud Vigneron, CRCM, Centre Léon Bérard, Université Lyon 1

 

"Metabolic hormones link the stemness features of mammary cancer cells to their neoplastic transformation"

 

Contact : laurent.lecam@inserm.fr

 

Vendredi 28 avril 2017, 14h00

Charles Geminard, institut de Biologie Valrose (iBV), CNRS/INSERM, Nice

 

“Left-Right asymmetry in Drosophila”

 

Contact : alexandre.djiane@inserm.fr

Vendredi 31 mars 2017, 11h00

David Santamaria, IECB, Université de Bordeaux

 

"Novel oncogenic mechanisms in lung adenocarcinoma"

 

Pour plus d'infos :  David Santamaria

 

Résumé :

We have recently utilized mouse models to study the very early stages of lung adenocarcinoma. This approach bypassed the difficulties imposed by tumour heterogeneity in full-blown tumours and also facilitated the identification of novel therapeutic targets with low toxicity and potential clinical applicability. Our study also revealed that cancer cell fate and tumour malignancy are established at an unanticipated early step. We plan to continue using mouse models and tissue organoids to identify and investigate novel signalling pathways and oncogenic functions that govern the onset of lung adenocarcinoma. Our approach will have special emphasis on the identification of novel factors implicated in the negative feedback of the MAPK pathway given the essential role of this signalling route in tumour progression and the emergence of resistance to targeted therapies. Furthermore, our recent observations indicate that the signal intensity of the MAPK pathway is a critical determinant of tumor development, influences the nature of the cancer initiating cell and ultimately dictates the resulting tumor phenotype. Finally, we also intend to pay particular attention to the significant percentage (up to 40 %) of lung adenocarcinoma patients without identified oncogenic driver to potentially translate this knowledge into novel therapeutic treatments.

 

Vendredi 3 mars 2017, 14h00

Dmitry Bulavin, IRCAN, Nice

 

"p38 MAPK builds a hyaluronan cancer niche to drive lung tumorigenesis"

 

Résumé :

Expansion of neoplastic lesions generates the initial signal that instigates the creation of a tumor niche. Nontransformed cell types within the microenvironment continuously coevolve with tumor cells to promote tumorigenesis. Here, we identify p38MAPK as a key component of human lung cancer, and specifically stromal interactomes, which provides an early, protumorigenic signal in the tissue microenvironment. We found that lung cancer growth depends on short-distance cues produced by the cancer niche in a p38-dependent manner. We identified fibroblast-specific hyaluronan synthesis at the center of p38-driven tumorigenesis, which regulates early stromal fibroblast activation, the conversion to carcinoma-associated fibroblasts (CAFs), and cancer cell proliferation. Systemic down-regulation of p38MAPK signaling in a knock-in model with substitution of activating Tyr182 to phenylalanine or conditional ablation of p38 in fibroblasts has a significant tumor-suppressive effect on K-ras lung tumorigenesis. Furthermore, both Kras-driven mouse lung tumors and orthotopically grown primary human lung cancers show a significant sensitivity to both a chemical p38 inhibitor and an over-the-counter inhibitor of hyaluronan synthesis. We propose that p38MAPK-hyaluronan-dependent reprogramming of the tumor microenvironment plays a critical role in driving lung tumorigenesis, while blocking this process could have far-reaching therapeutic implications.

 

Contact : jacques.colinge@inserm.fr

 

Mercredi 15 février 2017, 11h00

 

Bruno Ségui

 

"Tumor Necrosis Factor a blockade overcomes resistance to anti-Programmed-cell Death-1 in experimental melanoma"

 

Enseignant à l'Université Paul Sabatier de Toulouse et chercheur à l'INSERM UMR1037

 

Anti-Programmed Cell Death-1 (PD-1) antibodies have considerably changed the treatment for melanoma. However, many patients do not display therapeutic response or eventually relapse. Moreover, patients treated with anti-PD-1 develop immune-related adverse events that can be cured with anti-Tumor Necrosis Factor α (TNF) antibodies. Whether anti-TNF antibodies affect the anti-cancer immune response remains unknown. Our recent work has highlighted that TNFR1-dependent TNFa signaling impairs the accumulation of CD8+ tumor-infiltrating T lymphocytes (CD8+ TIL) in mouse melanoma (Bertrand et al., Cancer Res. 2015). Our unpublished data indicate that in mice TNF or TNFR1 blockade synergizes with anti-PD-1 on anti-cancer immune response towards solid cancers. Mechanistically, TNF blockade prevented anti-PD-1-induced TIL cell death as well as PD-L1/2 and TIM-3 expression. TNF expression positively correlated with expression of PD-L1/2 and TIM-3 in human melanoma specimens. This study provides a strong rationale to develop a combination therapy based on the use of anti-PD-1 and anti-TNF in cancer patients.

 

Lundi 30 janvier 2017, 11h00

Wilhem Leconet,  Department of Urology, Weill Cornell Medical College, New York.

 

"Controlled delivery of a small bispecific antibody in prostate cancer using the BEPO™ technology"

 

Contact : bruno.robert@inserm.fr

Vendredi 27 janvier 2017, 14h00

Olivier Peyruchaud, INSERM U1033 Equipe Lysbone, Faculté de Médecine-est, Lyon

 

"Rôle de l'acide lysophosphatidique dans la dissémination métastatique des cancers du sein induite par les plaquettes sanguines"

 

Contact : vincent.cavailles@inserm.fr

Jeudi 19 janvier 2017, 14h00

Conférence de "IRCM-SIRIC Montpellier-Cancer seminar series"
 
Emmanuelle Charafe-Jauffret/Christophe Ginestier,  CRCM/Institut Paoli Calmettes, Marseille
 
"Targeting Breast Cancer stem cells"
 

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