Mercredi 15 mai 2019, 11h00, Séminaire MabImprove

Peter Lenting


INSERM U1176, Hémostase, Inflammation et Thrombose


"Application of classic antibodies and nanobodies in hemorrhagic disorders"


Contact: jerome.rollin@univ-tours.fr


In Brief

The treatment of hemorrhagic disorders like hemophilia and von Willebrand disease is largely dependent on replacement therapy using the missing protein. Such therapies are expensive, require frequent intravenous injections and are (in case of FVIII-replacement therapy) associated with the development of inhibitory antibodies in up to 30% of the patients. Over the last decades, alternative approaches have been or are being developed, some of which are based on the therapeutic use of antibodies or antibody-based proteins. Also in our laboratory, we have developed antibody-based therapies, some of which being advanced candidates for clinical development.

One example regards antibody LTX-508, a monoclonal antibody that binds to von Willebrand factor (VWF). VWF is a multimeric protein responsible for the recruitment of platelets. In patients that receive mechanical circulatory support (as in LVAD or ECMO), VWF is excessively degraded. Up to 50% of these patients manifest bleeding complications, which are associated with prolonged hospitalization and increased mortality. Antibody LTX-508 aims to reduce degradation of VWF under these conditions. Another example relates to a FVIII-nanobody fusion protein, designated FVIII-KB013bv. In this protein, FVIII is fused with a nanobody directed against its carrier protein VWF. The presence of the nanobody increases its affinity for VWF 25-fold, and this increased affinity is associated with a two-fold prolonged half-life and, more importantly, a 7-fold reduction in the number of mice that develop inhibitory antibodies against FVIII. Finally, we have also developed nanobodies against antithrombin, a main inhibitor of the coagulation cascade. The nanobodies interfere with antithrombin activity, and can be used to restore the hemostatic balance in hemophilia A and B. In vitro and in vivo data confirm that such nanobodies can correct for the absence of FVIII or FIX. The advantage of such nanobody-based therapy is that these antibodies can be given both subcutaneously and intravenously, while their stability may allow storage at room temperature rather than 4?C.

Vendredi 17 mai 2019, 14h, séminaire SIRIC/IRCM

Majid Khatib


Préprotéine converstases, invasion tumorale et métastases, U1029 INSERM, Bordeaux


"Protein maturation in colorectal cancer and immunotherapy"


contact: vanessa.guillaumon@icm.unicancer.fr

Lundi 20 mai 2019, 14h, séminaire IRCM

Ygal Haupt


MacCallum Cancer Center, Melbourne, Australia


"Novel Strategies for Restoring Tumour Suppression to Treat Cancer"


contact: laurent.lecam@inserm.fr

Vendredi 24 mai, séminaire IRCM

Henri-Alexandre Michaud (HALEX)


Immunité et Cancer, IRCM, Montpellier


"In bed with cells: how mass cytometry and imaging may reveal the intimate in-situ cell-cell interactions"


contact: charles.theillet@inserm.fr

Vendredi 7 juin 2019, 14h, séminaire IRCM

Bruno Quesnel


Institut pour la Recherche sur le Cancer de Lille, Université de Lille, U900 INSERM 


"Tumor dormancy: quiescence or equilibrium?"


Contact: Julie.Pannequin@igf.cnrs.fr


In brief:

Tumor dormancy occurs when cancer cells are present but the tumor does not grow. Following treatment, patients may enter complete remission in which persistent cells represent the minimal residual disease (MRD). Experimental models and clinical data suggest that the absolute quantity of this MRD is extremely low. Very few cancer cells can persist for years or decades, and induce late relapse, sometimes decades after diagnosis. A key question is whether these long-term persisting cells remain in a truly quiescent state or if a stable equilibrium establish between residual cancer cells and factors of destruction, including treatments or immune response. Although several experimental and clinical data indicate that dormant tumor cells may remain in G0 in specific tumor micro-environments, other results show clonal evolutions, epigenetic modifications, and active suppression of immune response, suggesting that dormancy may be also an active process.

Vendredi 14 Juin 2019, 14h, Séminaire IRCM

Julien Sage


Professor of Pediatrics and Genetics, Stanford University, Ca., USA


"Intra- and Inter-tumoral heterogeneity in small cell lung cancer"


Contact: laurent.lecam@inserm.fr

Jeudi 20 juin 2019, 14h, séminaire IRCM

Sébastien Carréno


Institut de Recherche en Immunologie and Cancérologie (IRIC), Université de Montréal, Canada


"Signalization controlling cell morphogenesis: From fly mitosis to human cell motility"


contact: marie-alix.poul@inserm.fr

Vendredi 5 juillet 2019, 14h, séminaire IRCM

Scott Dixon


Department of Biology, Stanford University, Ca., USA


"A Novel Protein Acyltransferase Complex Involved in Cancer Cell Signaling and Death"


Contact: laurent.lecam@inserm.fr

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