Anciens séminaires 2010-2016

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

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"

© Institut de Recherche en Cancérologie de Montpellier - 2011 - Tous droits réservés - Mentions légales - Conception : ID Alizés