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Séminaires & conférences

 

POUR LES SÉMINAIRES EN VISIOCONFERENCE, SI VOUS SOUHAITEZ ASSISTER A L'UN D'EUX, MERCI DE CONTACTER BRIGITTE JARRIN QUI VOUS ENVERRA LE LIEN. secretariat@crc.jussieu.fr

    

                                Thursday, November 4, 13h30

SEMINAIRE EXTERIEUR

AMPHITHEATRE BILSKI-PASQUIER

Dynamics of repressive epigenomes in response

to cancer treatments

 

Céline VALLOT

(Institut Curie)

Invitée par Angélique Gougelot et Jessica Zucman-Rossi

Summary : The dynamic nature of chromatin and transcriptional features are expected to participate to tumor evolution, particularly in the context of response to cancer treatment and acquisition of resistance. Yet, the contribution of epigenetic plasticity to cancer cells remains unclear and means to target it are still rather non-specific and inefficient. We have recently achieved the mapping of histone marks at single-cell resolution in human breast tumors, enabling the investigation of the dynamics of chromatin marks, and its contribution to tumor evolution (Grosselin et al., Nat Genet 2019, Prompsy et al., Nat Comm 2020).  Using in vivo models of acquired resistance to cancer treatment, our data indicated that resistance to tamoxifen or chemotherapy may be associated with the emergence of an epigenetic subclone, characterized by a specific histone mark profile that could be stable along cell generations. More generally, the research projects of the group aim for a better understanding of the mechanisms of non-genetic selection, with the objective to design strategies to enhance or restore sensitivity to cancer treatments (Marsolier et al., biorxiv 2021).

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  Monday, November 8, 16h00

CYCLE ETHIQUE DU CRC

AMPHITHEATRE GUSTAVE ROUSSY

 

 Les rendez-vous Ethique du CRC

Science ouverte et intégrité scientifique

 

Hervé CHNEIWEISS

(Président du comité d'éthique de l'Inserm)

Invité par Isabelle Tratner, Marie-France Mamzer, Jessica Zucman-Rossi

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 Thursday, November 18, 13h30

SEMINAIRE TECHNIQUE

AMPHITHEATRE GUSTAVE ROUSSY

Accelerating the next generation of immune

médicine with cellular proteomics

 

Mourad FERHAT

(Société Isoplexis)

Invité par Chiara Maiuri et Lubka Roumenina

Summary :Join IsoPlexis’ talk to learn how functional phenotyping is addressing urgent challenges central to unlocking the next stage of personalized cancer immunotherapies and vaccines related to immunological mechanisms in infectious disease. With single-cell proteomics barcoding and detection of a full range of cytokines (30 ) per single-cell across thousands of single-cells, the IsoLight platform is showing the unique value of resolving the heterogeneity of a variety of immune cell types, elucidating key pre-clinical translational biomarkers to accelerate research and discovery.
In this talk we will show you how functional proteomics can help to :
• Identify functional pathways driving therapeutic resistance and develop combination therapies to combat resistant cell states and resolve tumor heterogeneity
• Understand the functional differences of tumor antigen potency in bi-specifics
• Pinpoint the unique polyfunctional monocyte cell types that drive tumor suppression
• Reveal choice of durable candidates for novel nanoparticle cancer vaccine

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 Thursday, November 25, 13h30

SEMINAIRE EXTERIEUR

Non-conventional roles for the complosome

in T cell physiology.

 EN VISIO

Claudia KEMPER

(NIH Bethesda, USA)

Invitée par Lubka Roumenina

Summary :The complement system is recognized since over a century as the prime protector of our vascular space. However recently an intracellularly active complement system – the complosome – has been identified. The complosome is heavily involved in regulating basic cell physiological precesses and particularly those of metabolic nature. Here I will give an overview of the role of the coplosome in the regulation of Th1 responses in health and disease.

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Thursday, December 2, 13h30

JEUNE CHERCHEUR

AMPHITHEATRE GUSTAVE ROUSSY

Role of immuno-metabolic regulator LECT2 in the

pathogenesis of metabolic-associated fatty liver

diseases (MAFLD)

 Céline POPHILLAT

(Equipe Chantal Desdouets)

Invitée par Guilhem Lignon et Angélique Gougelet

Summary : Metabolic-associated fatty liver diseases encompass a spectrum of hepatic disorders, notably non-alcoholic steatohepatitis (NASH) which is a favorable terrain for hepatocellular carcinoma (HCC) emergence. Therefore, there is an urgent need to better understand the mechanisms that trigger MAFLD progression to identify interesting molecular targets to propose innovative therapeutic strategies that remain until here very limited. We study the role of the hepatokine-like protein Leucocyte cell-derived chemotaxin 2 (LECT2) in the pathogenesis of NASH. We have previously shown that LECT2 exerts strong liver tumor-suppressive functions through its impact on macrophage polarization and function. Importantly, data also suggest that LECT2 is a key actor in metabolic disorders, as it positively correlates with BMI and waist circumference in humans. We have also demonstrated that LECT2 controls lipogenesis and cholesterol metabolism in hepatocytes in steady state. Accordingly, patients’ serum levels of LECT2 were positively correlated with steatosis. We find that LECT2 transcription is upregulated in different NAFL-inducing diet models such as High Fat High Sucrose or High Fat Diet, and NASH/HCC-inducing models such as choline-deficient high fat diet. In a LECT2-KO mouse model recreating a MAFLD phenotype using High Fat High Cholesterol diet, we show that the absence of LECT2 induces extended tissue damage, an altered inflammatory response and promotes tumor development, suggesting that LECT2 is an important factor in the microenvironment of the liver.

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Monday, December 6, 16h00

CYCLE ETHIQUE DU CRC

AMPHITHEATRE GUSTAVE ROUSSY

 Les rendez-vous Ethique du CRC

Déclarations Codecoh

 

Catherine PERRAULT

(Responsable de la cellule de bioéthique au MESRI)

Invitée par Marie-France Mamzer

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Thursday, December 9, 13h30

JEUNE CHERCHEUR

AMPHITHEATRE GUSTAVE ROUSSY

Muscle damage induced acute kidney injury

 Anne Grunenwald

(Equipe Isabelle Cremer)

Invitée par Angélique Gougelet et Guilhem Lignon

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 Monday, January 10, 16h00

CYCLE ETHIQUE DU CRC

 AMPHITHEATRE GUSTAVE ROUSSY

 Les rendez-vous Ethique du CRC

Les conflits d'intérêts

 

Didier DREYFUSS

(Médecin Hôpital Louis Mourier, Colombes)

Invité par Marie-France Mamzer

 

Summary : Comment conserver sa liberté en interagissant avec inductrie, Comment identifier les conflits d’intérêts ? Quand, comment et pourquoi faire une déclaration publique d’intérêt ?

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Thursday, January 13, 13h30

SEMINAIRE EXTERIEUR

EN VISIO UNIQUEMENT

Cytoprotective roles of cytosolic forms of C3

 Anna Blom

(Lund University, Suède)

Invitée par Lubka Roumenina

Summary : The complement system is one of the evolutionarily earliest developed immune systems with some components present as early as in sea cucumbers. It is so abundant and powerful in function that its discovery was awarded a Nobel Prize to Jules Bordet already in 1919. Complement is without a doubt a crucial blood component necessary for antimicrobial defence and has a long-described role in opsonizing extracellular pathogens for destruction by professional phagocytes. However, recent data show that the main complement factor C3 has so far unrecognized intracellular functions in cytoprotection by being able to interact with ATG16L1 and regulate autophagy in pancreatic beta cells. Further, intracellular C3 recognizes intracellular bacterial pathogens and protects cells from cytotoxic effects of cytokines. Despite the growing interest in intracellular C3 functions, the mechanism behind its generation is unclear. We propose that C3 can be present in the cytosol originating from an alternative translational start site, resulting in C3 lacking the signal peptide, which is therefore translated in the cytoplasm. In contrast to the secreted form, alternatively translated cytosolic C3 is not glycosylated and is present mainly in a reduced state. C3 can also be retrotranslocated from the endoplasmic reticulum into the cytosol, structurally resembling secreted C3. Future studies will elucidate specific functions for the various intracellular forms of C3 but it is already clear that C3 is involved in a complex network of interactions and functions within a cell, which are of relevance for diabetes, cancer and infections. It may even be so that intracellular functions of C3 preceded in evolution its egress into blood as component of the complement system

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Thursday, January 27, 13h30

SEMINAIRE TECHNIQUE

AMPHITHEATRE GUSTAVE ROUSSY

Titre en attente

 Oscar Castanon

(Société Argobio, Paris)

Invitée par ????

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Thursday, February 10, 13h30

SEMINAIRE EXTERIEUR

AMPHITHEATRE BILSKI-PASQUIER

Titre en attente

 Nicolas de Prost

(PUPH Henri Mondor, Créteil)

Invité par Guilhem Lignon

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Thursday, April 7, 13h30

SEMINAIRE EXTERIEUR

AMPHITHEATRE BILSKI-PASQUIER

Titre en attente

 Vincent Goffin

(Hôpital Necker, Paris)

Invité par Sylvie Babajko

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