Anciens séminaires 2010-2018

Liste complète des anciens séminaires 2010-2014 :  angry     2015 :  pdf     2016 :  pdf     2017 :  pdf

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

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 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

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 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

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 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

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 26 avril 2019, 14h, Séminaire IRCM

Akeila Bellahcène


GIGA-CANCER, Université de Liège, Belgique


"Targeting glycolysis-derived oncometabolites as a promising anti-cancer strategy”


Contact: andrei.turtoi@inserm.fr


In brief

Metabolic adaptation of cancer cells is recognized as a main hallmark of cancer. Tumour cells are notably characterized by an increased glucose uptake and a high glycolytic flux also known as the “Warburg effect”. One underestimated consequence of this glycolytic switch is the production of methylglyoxal (MG). MG is a highly reactive dicarbonyl that reacts with nucleic acids and proteins to form advanced glycation end products (AGEs), thus creating a dicarbonyl stress. The non toxic accumulation of MG and AGEs adducts are implicated in many pathological situations including diabetes, heart disease, neurodegenerative disease, ageing and cancer. Dr. Bellahcène’s team got interested since 2013 in the study of dicarbonyl stress in the development and progression of cancer. Upon MG stress, breast cancer cells show enhanced growth and metastatic potential in vivo that is efficiently reversed using carnosine, a natural MG scavenger. Given the explosion of interest and information on cancer metabolism, exploring the mechanisms regulating the levels of MG oncometabolite will be determinant for understanding tumor biology and improving cancer therapy.

Mardi 23 Avril 2019, 11h, séminaire MabImprove

Friedrich Koch-Nolte


Center of Immunology, Medical University of Hamburg-Eppendorf, Allemagne


"Nanobodies from transgenic mice"


Contact: velge@univ-tours.fr


In brief:

Llamas and other camelids produce unusual antibodies composed only of heavy chains. The variable domains of these antibodies (designated VHHs or nanobodies) have been shaped by evolution for high solubility and stability, independent of a partner VL domain. Nanobodies have emerged as promising therapeutics in various disease areas including heamtology, oncology, inflammation and infection. With their long CDR3s, nanobodies can reach hidden epitopes that are not accessible for conventional antibodies. In order to facilitate the generation of nanobodies for biomedical applications, we have generated nanobody-transgenic mice. Immunization of these mice induces antigen-specific heavy chain antibody responses with efficient somatic hypermutation and class switch. These mice thus provide a flexible new platform for generating innovative nanobody-based biologics. They also provide a basis for genetic modification of nanobodies and the generation of designer nanobodies.

Mercredi 27 Mars 2019, 11h00 : Séminaire MAbImprove

Annie Marc, Emmanuel Guedon et Isabelle Chevalot


Laboratoire Réactions et Génie des Procédés (LRGP), UMR CNRS 7274, Université de Lorraine


"Intensification et maîtrise des procédés de production de biomédicaments" 

Contact: nathalie.vourch@univ-tours.fr



La demande en forte croissance des biomédicaments produits par cellules animales impose d'intensifier les capacités de production. Ces produits incluent de nombreuses biomolécules, dont en particulier les anticorps recombinants, ainsi que des cellules utilisées elle-mêmes pour leur intérêt thérapeutique. Cependant, l'extrapolation de l'échelle de la boîte de culture à celle du bioréacteur reste loin d'être une évidence. Le défi consiste à comprendre, maîtriser et contrôler ces bioprocédés par une approche pluridisciplinaire, en vue d'obtenir des performances optimales, et ce, en dépit de l'environnement contraignant auquel sont soumises les cellules. Une vue d'ensemble des spécificités de ces procédés et des recherches en cours sera proposée et illustrée par des exemples.


Plus d’informations sur http://lrgp-nancy.cnrs.fr/spip.php?rubrique74

Mercredi 20 mars 2019, 11h. Séminaire MAbImprove

Christophe Blanchetot 




"Antibody Functional Diversity as the Key to Unlocking Novel Target Biology" 


Contact: nathalie.vourch@univ-tours.fr


In brief: 

Argenx is a clinical-stage biotechnology company using its suite of differentiated technologies to engage with academic centers of excellence to access exciting, novel targets where proof of concept in disease models is yet to be shown. Through its so-called Innovative Access Program, argenx brings its proprietary antibody technologies and know-how to collaborations with target biology specialists, enabling rapid progress into translational studies and creation of novel antibody candidates with therapeutic product potential.
Plus d'informations sur www.argenx.com/en-GB/content/argenx-in-short/2/


Vendredi 22 février 2019, 14h

Valerio Iebba


INSERM U1015 Gustave Roussy, Villejuif/Université de Rome La Sapienza, Rome


"Intestinal microbiota and Escherichia coli involvement in inflammation and cancer"

Contact: claude.sardet@inserm.fr

Vendredi 15 février, 14h

Eva Gonzalez Suarez


IDIBELL Bellvitge Biomedical Research Institute, Barcelone


"Novel therapeutic opportunities for breast cancer treatment"


contact: charles.theillet@inserm.fr

Mercredi 13 Février 2019, 14h; SIRIC Cancer Highlight Seminar

Sophie Lelièvre


Purdue University Center for Cancer Research, West Lafayette, In. USA


“Cancer-on-a-chip to study progression mechanisms and anticancer drug sensitivity”


Contact: charles.theillet@inserm.fr


In brief:
The design of tissue-chips is gaining momentum because these engineered cell culture platforms provide highly controlled microenvironments for the study of normal and diseased tissues. I will discuss how tissue-chips can be used to recreate the organ geometry necessary for the full recapitulation of cell behavior, using the example of carcinomas that develop within ducts. Indeed, the curved environment of hemichannels confers mechanical constraints that influence drug sensitivity. So far, this system is surpassing other cell culture models for the assessment of drug efficacy at the cancer cell level, as shown with the example of triple negative breast cancer. Another use of tissue-chips is to create gradients of molecules in the microenvironment that are conducive to tissue heterogeneity responsible for cancer progression and drug resistance. We have designed a gradient-on-a-chip with which we demonstrated that increased matrix stiffness associated with breast cancer progression lowers the concentration at which progression promoting oxidizing molecules worsen cancer phenotypes. Throughout the seminar basic principles of tissue-chip design will be presented and the applications of cancers-on-a-chip for precision medicine will be highlighted.

Vendredi 8 Février 2019, 14h

Laetitia Marzi


NCI/NIH, Bethesda, Md., USA


"Non-camptothecin TOP1 inhibitors 1st and 2nd generation development"


contact: celine.gongora@inserm.fr


In brief:

Contrary to other anticancer targets, topoisomerase I (TOP1) is targeted by only one chemical class of FDA approved drugs: topotecan and irinotecan, the derivatives of camptothecin. The indenoisoquinolines LMP400, LMP744, and LMP776 are novel non-camptothecin TOP1 inhibitors in clinical trial (phase 1). They overcome camptothecin limitation such as chemical instability, resistance by drug efflux, short plasma half-life or severe diarrheas. To further improve their metabolic stability, their methoxy groups have been replaced by fluorine, as in the fluoroindenoisoquinolines LMP517, LMP135, and LMP134.

In order to build the rationale for phase 2 clinical trials for the indenoisoquinolines, we have taken two approaches. First, CellMinerCDB (http://discover.nci.nih.gov/cellminercdb) was used to mine the cancer cell lines genomic databases. And second, because TOP1-mediated replication DNA damage is repaired by homologous recombination (HR), we tested “synthetic lethality” in HR-deficient (HRD) cells. We also tested the induction and stability of TOP1 cleavage complexes (TOP1cc) by the new fluorinated compounds and the induction and persistence of DNA damage they generate compared to their parent compound.

Genomic database mining revealed that a dominant drug response determinant is Schlafen 11 (SLFN11), a putative nuclear helicase/nuclease that kills cells undergoing replication stress. We also found that BRCA1-, BRCA2- and PALB2-deficient cells are 3 to 5 times hypersensitive to the indenoisoquinolines 1st generation. The fluoroindenoisoquinolines induced TOP1cc and DNA damage at nanomolar concentrations, and at higher levels than the parent indenoisoquinolines. LMP135 showed greater antitumor activity than topotecan in small-cell lung cancer cell H82 xenografts. Genomic database also showed that the activity of the fluoroindenoisoquinolines was mostly correlated with camptothecin derivatives and the parent indenoisoquinolines, consistent with TOP1 targeting.

Our results provide a rationale for Phase 2 indenoisoquinolines clinical trials with the indenoisoquinolines in HR-deficient cancers and for measuring Schlafen 11 (SLFN11) as a clinical response determinant. And it also shows the potential value of the fluoroindenoisoquinolines for further development as novel anticancer agents targeting TOP1.

Mercredi 6 février 2019, 10h00. Séminaire MabImprove

Mary Poupot 


Centre de Recherche en Cancérologie de Toulouse, Toulouse


"Development of an anti-tumor associated macrophage antibody for cancer immunotherapies”


Contact: valerie.gouilleux@univ-tours.fr


In brief:

Among cellular components of the Tumor microenvironment (TEM), tumor associated macrophages (TAM) are modified macrophages educated by the tumor to favor its development. Being able to eliminate or deactivate these cells is a challenge today in anticancer therapies. We recently produced a new antibody specifically directed against human TAM. We chose the chronic lymphoblastic leukaemia (CLL) as model which is a malignant hemopathy with only 50% of complete remission and a deleterious effect of the treatment on the immune system of the patients. The resistance of the residual disease is due to the intrinsic properties of cancer cells but also to their close contact in lymph nodes with nurse like cells (NLC). We defined these cells as CLL’s TAM, infiltrating the lymph nodes and associated with the aggressiveness of the disease in a contact dependant manner. Target these cells would be a new therapeutic insight in cancer. NLC are easily produced in vitro by the culture of PBMC from CLL patients by the differentiation of monocytes in contact with CLL cells. After a mouse immunization with these NLC, we selected one antibody specifically targeting NLC (patent Inserm). This antibody called 6-25 does not bind to leukemic cells or healthy B and T lymphocytes and monocytes. Moreover, immunohistochemistry and immunofluorescence analyses of different human tumors proved that our antibody can target different TAM. In parallel, we found that the target of the 6-25 mAb is the sideroflexin 3 (patent Inserm). The advantage of our anti-SFXN3 antibody is the specificity of TAM targeting with a promising future in anticancer therapies.

Jeudi 17 Janvier 2019, 14h

Cyril Esnault

IGMM, CNRS Montpellier


"How do environmental cues control cell behaviour or fate decision programs? Learning from Rho and Ras transcriptional effectors."


contact: claude.sardet@inserm.fr


Short presentation


Environmental cues such as growth factor, hormone, nutrient and cytokine concentrations are essential in regulating cell behaviour and differentiation processes. Cells integrate these external stimuli through signalling pathways to mediate their response. Aberrant signalling processes are a common feature of diseases such as cancer, so understanding them is critical for the development of therapeutic interventions. In our previous work, we have focussed on the Ras and Rho pathways, whose activity is disrupted in a large proportion of human cancers. The Ras pathway is instrumental in control of cancer cell proliferation, while the Rho pathway is a critical player in metastasis. The model we have used is the fibroblast serum response, a classical model for cell cycle re-entry and wound healing. The transcriptional response to serum is in its large part controlled by the Serum Response Factor (SRF). SRF functions in partnership with members of two families of signal-regulated cofactors: the MRTFs (myocardin-related transcription factors; MRTF-A, MRTF-B, and myocardin itself) and the TCF (ternary complex factor) family of Ets domain proteins (SAP-1, Elk-1, and Net). The MRTFs, which bind G-actin, respond to fluctuations in G-actin concentration induced by Rho GTPase, while TCF activity is controlled by Ras–ERK signaling. Investigating at the genomic scale the serum response, we have described how transcription and epigenetic rearrangement are regulated. We have defined the regulatory elements and genes that are regulated by Rho and Ras signalling pathways and explored how SRF and its coactivators modulate the circadian rhythm, the response to mechanical signals and control the balance between cell proliferation and invasion. In addition to soluble biochemical messengers, cells also need to respond to physical constraints i.e. external forces or mechanical cues such as stretch, compression and changes in the stiffness of the extracellular matrix (ECM). Although they are of critical patho-physiological importance, the molecular events elicited in response to mechanical cues have remained elusive. Indeed, during oncogenesis progression, the extracellular matrix (ECM) surrounding the tumour is stiffening due to matrix remodelling. It can arise from fibrosis or in response to tumour compression and cytoskeletal tension. Mechanosensation and tumour progression are paired: ECM stiffening supports the metastatic program and promotes cytoskeletal rearrangements required during cell invasion. Moreover, normal cellular differentiation has also been shown to be critically dependent on integration of mechanical cues. Mesenchymal Stem Cells (MSCs) are multipotent cells, which are able to differentiate into a variety of connective tissues. In this process, mechanical cues are determinant drivers of the lineage choice: the bone marrow is composed of discrete regions of variable matrix compositional properties, exposing MSCs to low tension conditions favour adipogenesis, while higher tensions favour myogenesis and the highest tensions drive differentiation to osteogenesis. Similarly, physical cues from the microenvironment regulate epidermal stem cell fate decisions. In that case, actin cytoskeleton rearrangement induces keratinocyte differentiation. However, while Rho and Ras signalling pathways have been identified in the response to matrix stiffness, how mechanosensation signals are transduced, integrated by the cell, how they impact on the transcriptional or epigenetic programs, what are the transcription factor networks involved apart from SRF/MRTF and YAP/TAZ and how such cues regulate cell behaviour are still open questions that I further aim to address.



Mercredi 16 janvier 2019, 11h00 : Séminaire MAbImprove

Nicolas Boissel 


Departement d'Hématologie, Hopital Saint-Louis et Université Paris Diderot, Paris, France


“Development of immunotherapy for the treatment of acute myeloid leukaemia”


Contact: watier@med.univ-tours.fr


Vendredi 14 décembre 2018, 14H

Sylvain Méloche


IRIC, Université de Montréal, Qc, Canada


"Identification and preclinical validation of new therapeutic targets in liver cancer."


Contact: marie-alix.poul@inserm.fr


Séminaire dans le cadre des enseignements du M2 Cancer Biology ?

Lundi 19 novembre 2018, 14h

Sylvie Mader


IRIC, Université de Montréal, Qc, Canada


"Targeting estrogen receptor signaling in breast cancer treatment: lessons from omics approaches and live cell biosensors"


Contact: marie-Alix.poul@inserm.fr


Séminaire dans le cadre des enseignements du M2 Cancer Biology 

Vendredi 26 octobre 2018, 4h

Chann Lagadec

INSERM U908, Cell Plasticity and Cancer, Université de Lille


“Reborn from fire, or how non-cancer stem cells reprogram as CSC under radiation-induced inflammatory chemokines stimulation”



Cancer stem cell (CSC) identification in solid and hematologic tumors has paved the way to many fundamental and translational studies. However, recent studies have depicted the presence of cancer stem cell plasticity. Indeed, differentiated breast cancer cells (non-CSCs) can generate iCSCs (induced CSCs) in response to various stimuli. Nevertheless, reprogramming mechanisms remain unknown, and strategies to reduce the reprogramming of non-CSCs into iCSCs might prevent treatment-resilient cancer cells driving recurrences. We demonstrated, for the first time, that chemokines are involved in reprogramming and can be used to target radiation-induced CSC enrichment. In combination with radiation treatment, inhibition of these chemokines allows increased survival of mice in xenograft model. We also demonstrated that the expression of chemokines and their receptors is associated with CSC profiles in tumor patients. More interestingly, expression of specific chemokines or their receptors could be useful as prediction markers. We are actually investigating intracellular mechanisms driving anti-cancer treatments-induced reprogramming. Also, we are developing the first animal transgenic model to track and distinguish CSCs from iCSCs, and so to study in vivo reprogramming.


Mercredi 10 Octobre 2018, 14h

Somadri Ghosh 


Université Libre de Bruxelles


"A role of SHIP2 in metastasis of breast cancer“


Contact: andrei.turtoi@inserm.fr

Vendredi 21 septembre 2018, 14h

Eric Soler


IGMM, CNRS, Université de Montpellier


"Chromatin looping as a regulator of normal and pathological erythropoiesis"


contact: eric.julien@inserm.fr

Vendredi 7 septembre 2018, 14h

Joffrey Pelletier


IDIBELL, Barcelone


“Targeting GMP synthesis reveals a hierarchy of p53-cell cycle checkpoints in CRCs”


contact: laurent.lecam@inserm.fr

Vendredi 13 Juillet 2018, 14H

Franck Vandemoere, 


IGF, CNRS UMR5203, INSERM U1191, Montpellier


"Regulation by phosphorylation of two GPCRs targeted by antipsychotics"


Contact: pierre.martineau@inserm.fr

Vendredi 6 Juillet 2018, 14h00

Fanny Jaulin, 


INSERM-U981 Institut Gustave Roussy, Villejuif.


"Collective epithelial-based metastases in colorectal carcinoma patients"


As a critical step in cancer progression and a challenge to patient treatment, tumour cell dissemination has been the subject of intense investigation across a range of model systems, in vitro and in animals. These studies have led to the assumption that the fatal progression of carcinoma is associated with a loss of epithelial architecture and polarity1-3 as single tumour cells escape from the primary tumour to reach secondary sites4,5. However, these studies have been performed using experimental model systems and the mechanisms driving metastatic spread in cancer patients remain under-investigated. Here, we collected and monitored over 50 patient specimens ex vivo to investigate the cell biology of colorectal cancer (CRC) metastasis as it spreads to the peritoneum. This reveals a new mode of cancer dissemination. Large clusters of cancer epithelial cells displaying an inverted apico-basolateral polarity, which we term Tumour Spheres with Inverted Polarity (TSIPs), were observed throughout the process of tumour dissemination. We show that TSIPs form and propagate through the collective apical budding of hyper-methylated neoplastic tissues. Despite their inverted topology, TSIPs collectively invade extracellular matrices, paired patients¹ peritoneum explants and initiate metastases in mice xenograft models. Further, the presence of TSIPs in peritoneal effusions correlates with metastases burden and adverse patient prognosis. Thus, despite their having a robust epithelial architecture, TSIPs appear to drive the peritoneal dissemination of CRC, as well as other primary cancers, such as breast carcinoma.  By applying cell biological methods to live primary cancer specimens, we provide an alternative conception of cancer dissemination that goes against the prevailing consensus and could not be anticipated from experimental model systems.


Contact: charles.theillet@inserm.fr

Vendredi 29 Juin 2018, 14h00

Daniel Fisher


IGMM, CNRS Montpellier


"Not just a proliferation marker: Ki-67 promotes carcinogenesis by organising the nucleus to promote cellular plasticity"


Contact: charles.theillet@inserm.fr

Vendredi 22 Juin 2018, 14h00

Jérôme Déjardin


IGH, CNRS, Montpellier 


"Atypical heterochromatin stimulates alternative lengthening of telomeres"


Contact: claude.sardet@inserm.fr

Mercredi 20 Juin 2018, 14h00

Giulio Preta


Life Science Center, Vilnius University, Lithuania


'Targeting lipid rafts as a strategy against infection and cancer"


Short summary of the work: 

Lipid rafts are membrane micro-domains that are enriched in cholesterol, sphingomyelin, sphingolipids and phospholipids. Their importance for living cells is underlined by their involvement in many processes including bacterial and viral entry, cardiovascular and prion diseases as well as cancer. Targeting lipid rafts is emerging as an innovative strategy to limit bacterial or viral infection and to increase the sensitivity to apoptosis of different types of tumours. Behind well-known cholesterol depleting agents (cyclodextrin) new compounds involved in cholesterol homeostasis were recently discovered. These potential drug candidates are capable to modify the lipid rafts composition and to alter the signalling platform associated with them.  Multiple technologies including confocal microscopy to visualize lipid rafts, viability assays to determine the toxic effect of compounds on the cells, offer the opportunity to study in details the changes induced by this new class of cholesterol-targeting agents.

Mardi 12 Juin 2018, 14h00

Julien Faget


ISREC/EPFL, Lausanne, Suisse


"Learning from models of immunotherapy resistant lung cancer"



Vendredi 8 Juin 2018, 14h00

Roberto Ronca


Department of Molecular and Translational Medicine, University of Brescia

"Stromal delivery of long Pentraxin-3 impairs FGF/FGFR-dependent tumor growth and metastasis"


Summary of the work: 

The fibroblast growth factor (FGF)/FGF receptor (FGFR) system plays a crucial role in cancer by affecting tumor growth, angiogenesis, drug resistance and escape from anti-angiogenic anti-vascular endothelial growth factor therapy. The soluble pattern recognition receptor long-pentraxin 3 (PTX3) acts as a multi-FGF antagonist. In a recent study we demonstrated that local and systemic delivery of human PTX3 in transgenic mice driven by the endothelial specific Tie2 promoter inhibits tumor growth, angiogenesis and metastasis in heterotopic, orthotopic and autochthonous FGF-dependent tumor models. Moreover, NMR data and pharmacophore modeling of the interaction of a minimal PTX3-derived FGF-binding pentapeptide with FGF2 were used for the identification of the first small molecule chemical (NSC12) which acts as an orally active extracellular FGF trap with significant implications in cancer therapy. We are currently characterizing the role of PTX3 expression in different types of solid and hematological tumors.



Vendredi 18 Mai 2018, 14h00

Han Li


Cellular Plasticity and Disease Modelling Group, Institut Pasteur, Paris


"Cellular plasticity in cancer and ageing"


Webmore information


Contact: antonio.maraver@inserm.fr

Vendredi 27 Avril 2018, 14h00

William Ritchie


Head of Artificial Intelligence and Gene Regulation, IGH, Montpellier


“Artificial Intelligence empowers transcriptomics but will ultimately cause its demise"


The seminar in short:

In my talk, I will show how simple information theory concepts such as entropy and information content allow scientists to better understand gene regulation in numerous types of disease. I will then demonstrate that recent advances in artificial intelligence approaches such as genetic programming and neural nets may be so powerful that they abrogate our need to understand these functions at all. Recent research in my team will show how AI allows us to explore sequencing data from cancer samples with no a priori and is more powerful than current approaches for classifying and predicting outcomes.


Contact: charles.theillet@inserm.fr

Vendredi 20 Avril 2018, 14h00

Mickael Ploquin,


10x Genomics


"Single cell transcriptomics and proteomics"




Résumé de la présentation :  High-throughput, single-cell expression measurements enable discovery of gene expression dynamics for profiling individual cell types. The Chromium Single Cell Controller which is a dedicated instrument for single cell applications and features a simple and comprehensive workflow, enabling users to quickly and easily prepare single cell sequencing libraries in less than one workday.


With the unique ability to interrogate hundreds to millions of cells, the Single Cell Chromium Controller supports a variety of applications, including the existing Chromium™ Single Cell 3’ Solution, as well as a future product featuring to perform full-length sequencing of V(D)J segments from single B or T cells. The system is accompanied by Chromium Single Cell 3’ Reagent Kits with advanced chemistry and microfluidics consumables based on GemCode™ Technology and features full compatibility with the Illumina® HiSeq® 4000 and other HiSeq®, NovaSeq®, NextSeq® and MiSeq® sequencers.

Jeudi 29 Mars 2018, 14h00

Max Chaffanet


Département d’Oncologie Moléculaire Institut Paoli Calmettes, Marseille


“Profilage oncogénomique des cancers avancés dans les essais PANDORA et PERMED à l’IPC"


Contact: charles.theillet@inserm.fr

Vendredi 9 Février 2018, 14h00

Sylvain Lehmann et Brigitte Couette


Projet IBDLR (Initiative Biomarqueurs et Diagnostic en Languedoc-Roussillon), BioCampus, Montpellier


"Présentation de l’ (IBDLR) : Actions et Appel à candidature "Labellisation de projets Biomarqueurs" 


Contact: charles.theillet@inserm.fr


Bref résuméL’objet de cette présentation, qui s’inscrit dans une démarche systématique auprès des différents Instituts/laboratoires, est de faire connaître notre initiative qui a pour vocation de faciliter l’émergence et la validation de nouveaux Biomarqueurs en accompagnant les chercheurs sur le chemin de la valorisation économique de leurs activités de recherche.

IBDLR sert d’interface entre les laboratoires de recherche et les structures de valorisation : https://www.polebiosante-rabelais.fr/polerabelais/projets-structurants/ibdlr

Ses missions :
  • Faciliter l’émergence et la validation de nouveaux Biomarqueurs
  • Apporter son expertise pour accompagner les projets vers un niveau de maturité technologique pour une prise en charge par les acteurs régionaux de la valorisation
  • Décerner un label pour les projets ayant des perspectives pouvant intéresser des industriels
  • Financer des équipements performants pour la validation des Biomarqueurs (CPER-IBDLR)
  • Organiser des évènements autour des Biomarqueurs

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