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8. A novel anti-galectin-9 immunotherapy limits the early progression of pancreatic neoplastic lesions in transgenic mice.

Author

Quilbe, Alexandre, Mustapha, Rami, Duchêne, Belinda, Kumar, Abhishek, Werkmeister, Elisabeth, Leteurtre, Emmanuelle, Moralès, Olivier, Jonckheere, Nicolas, Van Seuningen, Isabelle, and Delhem, Nadira

Subjects
PANCREATIC intraepithelial neoplasia, PANCREATIC tumors, TRANSGENIC mice, REGULATORY T cells, IMMUNE checkpoint inhibitors, PRECANCEROUS conditions, T cells
Abstract

Background: Pancreatic adenocarcinoma (PDAC) is a devastating disease with an urgent need for therapeutic innovation. Immune checkpoint inhibition has shown promise in a variety of solid tumors, but most clinical trials have failed to demonstrate clinical efficacy in PDAC. This low efficacy is partly explained by a highly immunosuppressive microenvironment, which dampens anti-tumor immunity through the recruitment or induction of immunosuppressive cells, particularly regulatory T cells (Tregs). In this context, our laboratory has developed a novel immunotherapeutic strategy aimed at inhibiting the suppressive activity of Tregs, based on a patented (EP3152234B1) monoclonal antibody (mAb) targeting galectin-9 (LGALS9). Materials and methods: CD4+ conventional T cells (TCD4 or Tconv), Treg ratio, and LGALS9 expression were analyzed by immunohistochemistry (IHC) and cytometry in blood and pancreas of K-rasLSL.G12D/+;Pdx-1-Cre (KC) and KrasWildType (WT);Pdx1-Cre (WT) mice aged 4-13 months. Pancreatic intraepithelial neoplasm (PanIN) progression and grade were quantified using FIJI software and validated by pathologists. The anti-galectin-9 mAb was validated for its use in mice on isolated murine C57BL/6 Treg by immunofluorescence staining and cytometry. Its specificity and functionality were validated in proliferation assays on rLGALS9-immunosuppressed murine Tconv and in suppression assays between murine Treg and Tconv. Finally, 2-month-old KC mice were treated with anti-LGALS9 and compared to WT mice for peripheral and infiltrating TCD4, Treg, and PanIN progression. Results: IHC and cytometry revealed a significant increase in LGALS9 expression and Treg levels in the blood and pancreas of KC mice proportional to the stages of precancerous lesions. Although present in WT mice, LGALS9 is expressed at a basal level with low and restricted expression that increases slightly over time, while Treg cells are few in number in their circulation and even absent from the pancreas over time. Using our anti-LGALS9 mAb in mice, it is shown that (i) murine Treg express LGALS9, (ii) the mAb could target and inhibit recombinant murine LGALS9, and (iii) neutralize murine Treg suppressive activity. Finally, the anti-LGALS9 mAb in KC mice reduced (i) LGALS9 expression in pancreatic cancer cells, (ii) the Treg ratio, and (iii) the total surface area and grade of PanIN. Conclusion: We demonstrate for the first time that an anti-LGALS9 antibody, by specifically targeting endogenous LGALS9 tumor and exogenous LGALS9 produced by Treg, was able to limit the progression of pancreatic neoplastic lesions in mice, opening up new prospects for its use as an immunotherapeutic tool in PDAC. [ABSTRACT FROM AUTHOR]

Published
2023
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9. Supplementary Table 2 from Autocrine Induction of Invasive and Metastatic Phenotypes by the MIF-CXCR4 Axis in Drug-Resistant Human Colon Cancer Cells

Author

Dessein, Anne-Frédérique, primary, Stechly, Laurence, primary, Jonckheere, Nicolas, primary, Dumont, Patrick, primary, Monté, Didier, primary, Leteurtre, Emmanuelle, primary, Truant, Stéphanie, primary, Pruvot, François-René, primary, Figeac, Martin, primary, Hebbar, Mohamed, primary, Lecellier, Charles-Henri, primary, Lesuffleur, Thécla, primary, Dessein, Rodrigue, primary, Grard, Georges, primary, Dejonghe, Marie-José, primary, de Launoit, Yvan, primary, Furuichi, Yasuhiro, primary, Prévost, Grégoire, primary, Porchet, Nicole, primary, Gespach, Christian, primary, and Huet, Guillemette, primary

Published
2023
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10. Supplementary Table 1 from Autocrine Induction of Invasive and Metastatic Phenotypes by the MIF-CXCR4 Axis in Drug-Resistant Human Colon Cancer Cells

Author

Dessein, Anne-Frédérique, primary, Stechly, Laurence, primary, Jonckheere, Nicolas, primary, Dumont, Patrick, primary, Monté, Didier, primary, Leteurtre, Emmanuelle, primary, Truant, Stéphanie, primary, Pruvot, François-René, primary, Figeac, Martin, primary, Hebbar, Mohamed, primary, Lecellier, Charles-Henri, primary, Lesuffleur, Thécla, primary, Dessein, Rodrigue, primary, Grard, Georges, primary, Dejonghe, Marie-José, primary, de Launoit, Yvan, primary, Furuichi, Yasuhiro, primary, Prévost, Grégoire, primary, Porchet, Nicole, primary, Gespach, Christian, primary, and Huet, Guillemette, primary

Published
2023
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11. Supplementary Figure 1 from Autocrine Induction of Invasive and Metastatic Phenotypes by the MIF-CXCR4 Axis in Drug-Resistant Human Colon Cancer Cells

Author

Dessein, Anne-Frédérique, primary, Stechly, Laurence, primary, Jonckheere, Nicolas, primary, Dumont, Patrick, primary, Monté, Didier, primary, Leteurtre, Emmanuelle, primary, Truant, Stéphanie, primary, Pruvot, François-René, primary, Figeac, Martin, primary, Hebbar, Mohamed, primary, Lecellier, Charles-Henri, primary, Lesuffleur, Thécla, primary, Dessein, Rodrigue, primary, Grard, Georges, primary, Dejonghe, Marie-José, primary, de Launoit, Yvan, primary, Furuichi, Yasuhiro, primary, Prévost, Grégoire, primary, Porchet, Nicole, primary, Gespach, Christian, primary, and Huet, Guillemette, primary

Published
2023
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12. Data from Autocrine Induction of Invasive and Metastatic Phenotypes by the MIF-CXCR4 Axis in Drug-Resistant Human Colon Cancer Cells

Author

Dessein, Anne-Frédérique, primary, Stechly, Laurence, primary, Jonckheere, Nicolas, primary, Dumont, Patrick, primary, Monté, Didier, primary, Leteurtre, Emmanuelle, primary, Truant, Stéphanie, primary, Pruvot, François-René, primary, Figeac, Martin, primary, Hebbar, Mohamed, primary, Lecellier, Charles-Henri, primary, Lesuffleur, Thécla, primary, Dessein, Rodrigue, primary, Grard, Georges, primary, Dejonghe, Marie-José, primary, de Launoit, Yvan, primary, Furuichi, Yasuhiro, primary, Prévost, Grégoire, primary, Porchet, Nicole, primary, Gespach, Christian, primary, and Huet, Guillemette, primary

Published
2023
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13. Supplementary Methods, Figure Legends 1 from Autocrine Induction of Invasive and Metastatic Phenotypes by the MIF-CXCR4 Axis in Drug-Resistant Human Colon Cancer Cells

Author

Dessein, Anne-Frédérique, primary, Stechly, Laurence, primary, Jonckheere, Nicolas, primary, Dumont, Patrick, primary, Monté, Didier, primary, Leteurtre, Emmanuelle, primary, Truant, Stéphanie, primary, Pruvot, François-René, primary, Figeac, Martin, primary, Hebbar, Mohamed, primary, Lecellier, Charles-Henri, primary, Lesuffleur, Thécla, primary, Dessein, Rodrigue, primary, Grard, Georges, primary, Dejonghe, Marie-José, primary, de Launoit, Yvan, primary, Furuichi, Yasuhiro, primary, Prévost, Grégoire, primary, Porchet, Nicole, primary, Gespach, Christian, primary, and Huet, Guillemette, primary

Published
2023
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17. TRPM7 Modulates Human Pancreatic Stellate Cell Activation

Author

Auwercx, Julie, primary, Kischel, Philippe, additional, Lefebvre, Thibaut, additional, Jonckheere, Nicolas, additional, Vanlaeys, Alison, additional, Guénin, Stéphanie, additional, Radoslavova, Silviya, additional, Van Seuningen, Isabelle, additional, Ouadid-Ahidouch, Halima, additional, Kocher, Hemant M., additional, Dhennin-Duthille, Isabelle, additional, and Gautier, Mathieu, additional

Published
2022
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18. Abstract 2965: Epigenetic mechanisms involved in acquired resistance to combined chemotherapies in digestive cancer cells

Author

Bachir, Elsa Hadj, primary, Poiraud, Charles, additional, Claux, Hugo, additional, Moghrabi, Soumaya El, additional, Paget, Sonia, additional, Duchêne, Belinda, additional, Jonckheere, Nicolas, additional, Neve, Bernadette, additional, Leteurtre, Emmanuelle, additional, Van Seuningen, Isabelle, additional, and Vincent, Audrey, additional

Published
2022
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21. Antagonistic Roles of the Tumor Suppressor miR-210-3p and Oncomucin MUC4 Forming a Negative Feedback Loop in Pancreatic Adenocarcinoma

Author

Boukrout, Nihad, primary, Souidi, Mouloud, additional, Lahdaoui, Fatima, additional, Duchêne, Belinda, additional, Neve, Bernadette, additional, Coppin, Lucie, additional, Leteurtre, Emmanuelle, additional, Torrisani, Jérôme, additional, Van Seuningen, Isabelle, additional, and Jonckheere, Nicolas, additional

Published
2021
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22. The EGF Domains of MUC4 Oncomucin Mediate HER2 Binding Affinity and Promote Pancreatic Cancer Cell Tumorigenesis

Author

Stoup, Nicolas, primary, Liberelle, Maxime, additional, Schulz, Céline, additional, Cavdarli, Sumeyye, additional, Vasseur, Romain, additional, Magnez, Romain, additional, Lahdaoui, Fatima, additional, Skrypek, Nicolas, additional, Peretti, Fabien, additional, Frénois, Frédéric, additional, Thuru, Xavier, additional, Melnyk, Patricia, additional, Renault, Nicolas, additional, Jonckheere, Nicolas, additional, Lebègue, Nicolas, additional, and Van Seuningen, Isabelle, additional

Published
2021
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25. Abstract LB106: The EGF domains of MUC4 oncomucin interact with ErbB2 and mediate tumorigenic activity of cancer cells represent new potential therapeutic targets

Author

STOUP, Nicolas, primary, LIBERELLE, Maxime, additional, SCHULZ, Céline, additional, VASSEUR, Romain, additional, MAGNEZ, Romain, additional, THURU, Xavier, additional, MELNYK, Patricia, additional, RENAULT, Nicolas, additional, JONCKHEERE, Nicolas, additional, LEBEGUE, Nicolas, additional, and VAN SEUNINGEN, Isabelle, additional

Published
2021
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26. The EGF domains of MUC4 oncomucin interact with ErbB2 and mediate tumorigenic activity of cancer cells represent new potential therapeutic targets

Author

Stoup, Nicolas, primary, Liberelle, Maxime, additional, Schulz, Céline, additional, Vasseur, Romain, additional, Magnez, Romain, additional, Thuru, Xavier, additional, Melnyk, Patricia, additional, Renault, Nicolas, additional, Jonckheere, Nicolas, additional, Lebegue, Nicolas, additional, and Van Seuningen, Isabelle, additional

Published
2021
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27. Conséquences du bypass gastrique à une anastomose sur la muqueuse oeso-gastrique dans un modèle préclinique murin

Author

Siebert, Matthieu, Ribeiro-Parenti, Lara, Nguyen, Nicholas, Hourseau, Muriel, Duchêne, Belinda, Humbert, Lydie, Jonckheere, Nicolas, Nuel, Grégory, Chevallier, Jean-Marc, Duboc, Henri, Rainteau, Dominique, Msika, Simon, Kapel, Nathalie, Couvelard, Anne, Bado, André, Le Gall, Maude, Université Grenoble Alpes - UFR Médecine (UGA UFRM), Université Grenoble Alpes (UGA), Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), Service d'Anatomopathologie [Bichat - Claude Bernard], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Lille Neurosciences & Cognition - U 1172 (LilNCog (ex-JPARC)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Center for Computational Imaging and Simulation Technologies in Biomedicine (CISTIB), Universitat Pompeu Fabra [Barcelona] (UPF), Laboratoire de Probabilités, Statistiques et Modélisations (LPSM (UMR_8001)), Université Paris Diderot - Paris 7 (UPD7)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), CHU Louis Mourrier, Microorganismes, Molécules Bioactives et Physiopathologie Intestinale (LBM-E4), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Louis Mourier - AP-HP [Colombes], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Ecosystème intestinal, probiotiques, antibiotiques (EA 4065), Université Paris Descartes - Paris 5 (UPD5), Service d'Anatomo-Pathologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Hôpital Beaujon [AP-HP], Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Lille Neurosciences & Cognition - U 1172 (LilNCog), and Laboratoire de Probabilités, Statistique et Modélisation (LPSM (UMR_8001))

Subjects
[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], [SDV.MHEP.CHI]Life Sciences [q-bio]/Human health and pathology/Surgery, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2020

28. Analysis of mPygo2 mutant mice suggests a requirement for mesenchymal Wnt signaling in pancreatic growth and differentiation

Author

Jonckheere, Nicolas, Mayes, Erin, Shih, Hung-Ping, Li, Boan, Lioubinski, Oleg, Dai, Xing, and Sander, Maike

Subjects
Stem cells -- Growth, Company growth, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2008.03.014 Byline: Nicolas Jonckheere (a), Erin Mayes (a), Hung-Ping Shih (a), Boan Li (b), Oleg Lioubinski (a), Xing Dai (b), Maike Sander (a) Keywords: Pygopus; Wnt; Pancreas development; Mesenchyme; Islet; Endocrine; Proliferation; Differentiation; Mouse Abstract: Pygopus has recently been identified in Drosophila as an essential component of the nuclear complex required for canonical Wnt signaling. Here, we have investigated the role of the mammalian pygopus ortholog, mPygo2, in pancreas development. We show that a null mutation of mPygo2 in mice causes pancreas hypoplasia due to decreased progenitor cell proliferation after embryonic day (e) 12.5. During the same time window, mPygo2-deficient embryos begin to display a reduction in endocrine progenitors and consequently a decrease in islet endocrine cell mass. Consistent with its function after e12.5, late-developing endocrine cell types, such as beta, delta and PP cells, are specifically reduced, while the earlier-forming alpha cells develop normally. We find canonical Wnt signaling to be predominantly active in the mesenchyme at the time when mPygo2 is required and demonstrate the dependence of Wnt signal transduction on mPygo2. Furthermore, conditional deletion of mPygo2.sup.flox allele in the pancreatic epithelium does not phenocopy the defects in mPygo2-null mutants. Since mPygo2 is expressed in the pancreatic mesenchyme and the role of the mesenchyme in epithelial progenitor cell expansion is well documented, our findings suggest an indirect role for mPygo2 in epithelial growth and differentiation through regulation of mesenchymal signals. Together, our data suggest a previously unappreciated role for mesenchymal Wnt signaling in regulating pancreatic organ growth and cell differentiation. Author Affiliation: (a) Department of Developmental and Cell Biology, University of California Irvine, Irvine, CA 92697-2300, USA (b) Department of Biological Chemistry, University of California Irvine, Irvine, CA 92697-1700, USA Article History: Received 23 October 2007; Revised 10 February 2008; Accepted 3 March 2008

Published
2008

29. Epigenetic Regulation by lncRNAs: An Overview Focused on UCA1 in Colorectal Cancer

Author

Neve, Bernadette, Jonckheere, Nicolas, Vincent, Audrey, Van Seuningen, Isabelle, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, and Jonckheere, Nicolas

Subjects
[SDV.CAN] Life Sciences [q-bio]/Cancer, lncRNA Urothelial Cancer Associated 1 (UCA1), [SDV]Life Sciences [q-bio], competing endogenous RNAs (ceRNA), [SDV.CAN]Life Sciences [q-bio]/Cancer, Review, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282, colorectal cancer (CRC), long non-coding RNA (lncRNA), ComputingMilieux_MISCELLANEOUS
Abstract

International audience; Colorectal cancers have become the second leading cause of cancer-related deaths. In particular, acquired chemoresistance and metastatic lesions occurring in colorectal cancer are a major challenge for chemotherapy treatment. Accumulating evidence shows that long non-coding (lncRNAs) are involved in the initiation, progression, and metastasis of cancer. We here discuss the epigenetic mechanisms through which lncRNAs regulate gene expression in cancer cells. In the second part of this review, we focus on the role of lncRNA Urothelial Cancer Associated 1 (UCA1) to integrate research in different types of cancer in order to decipher its putative function and mechanism of regulation in colorectal cancer cells. UCA1 is highly expressed in cancer cells and mediates transcriptional regulation on an epigenetic level through the interaction with chromatin modifiers, by direct regulation via chromatin looping and/or by sponging the action of a diversity of miRNAs. Furthermore, we discuss the role of UCA1 in the regulation of cell cycle progression and its relation to chemoresistance in colorectal cancer cells.

Published
2018

30. Mg2+ Transporters in Digestive Cancers

Author

Auwercx, Julie, primary, Rybarczyk, Pierre, additional, Kischel, Philippe, additional, Dhennin-Duthille, Isabelle, additional, Chatelain, Denis, additional, Sevestre, Henri, additional, Van Seuningen, Isabelle, additional, Ouadid-Ahidouch, Halima, additional, Jonckheere, Nicolas, additional, and Gautier, Mathieu, additional

Published
2021
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32. Unsupervised Hierarchical Clustering of Pancreatic Adenocarcinoma Dataset from TCGA Defines a Mucin Expression Profile that Impacts Overall Survival

Author

Jonckheere, Nicolas, primary, Auwercx, Julie, additional, Hadj Bachir, Elsa, additional, Coppin, Lucie, additional, Boukrout, Nihad, additional, Vincent, Audrey, additional, Neve, Bernadette, additional, Gautier, Mathieu, additional, Treviño, Victor, additional, and Van Seuningen, Isabelle, additional

Published
2020
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36. A new pancreatic adenocarcinoma‐derived organoid model of acquired chemoresistance to FOLFIRINOX: First insight of the underlying mechanisms.

Author

Hadj Bachir, Elsa, Poiraud, Charles, Paget, Sonia, Stoup, Nicolas, El Moghrabi, Soumaya, Duchêne, Belinda, Jouy, Nathalie, Bongiovanni, Antonino, Tardivel, Meryem, Weiswald, Louis‐Bastien, Vandepeutte, Marie, Beugniez, César, Escande, Fabienne, Leteurtre, Emmanuelle, Poulain, Laurent, Lagadec, Chann, Pigny, Pascal, Jonckheere, Nicolas, Renaud, Florence, and Truant, Stephanie

Subjects
CANCER chemotherapy, DRUG resistance in cancer cells, PROGNOSIS, DRUG resistance, DRUG therapy, ANTIMETABOLITES
Abstract

Background Information: Although improvements have been made in the management of pancreatic adenocarcinoma (PDAC) during the past 20 years, the prognosis of this deadly disease remains poor with an overall 5‐year survival under 10%. Treatment with FOLFIRINOX, a combined regimen of 5‐fluorouracil, irinotecan (SN‐38) and oxaliplatin, is nonetheless associated with an excellent initial tumour response and its use has allowed numerous patients to go through surgery while their tumour was initially considered unresectable. These discrepancies between initial tumour response and very low long‐term survival are the consequences of rapidly acquired chemoresistance and represent a major therapeutic frontier. To our knowledge, a model of resistance to the combined three drugs has never been described due to the difficulty of modelling the FOLFIRINOX protocol both in vitro and in vivo. Patient‐derived tumour organoids (PDO) are the missing link that has long been lacking in the wide range of epithelial cancer models between 2D adherent cultures and in vivo xenografts. In this work we sought to set up a model of PDO with resistance to FOLFIRINOX regimen that we could compare to the paired naive PDO. Results: We first extrapolated physiological concentrations of the three drugs using previous pharmacodynamics studies and bi‐compartmental elimination models of oxaliplatin and SN‐38. We then treated PaTa‐1818x naive PDAC organoids with six cycles of 72 h‐FOLFIRINOX treatment followed by 96 h interruption. Thereafter, we systematically compared treated organoids to PaTa‐1818x naive organoids in terms of growth, proliferation, viability and expression of genes involved in cancer stemness and aggressiveness. Conclusions: We reproductively obtained resistant organoids FoxR that significantly showed less sensitivity to FOLFORINOX treatment than the PaTa‐1818x naive organoids from which they were derived. Our resistant model is representative of the sequential steps of chemoresistance observed in patients in terms of growth arrest (proliferation blockade), residual disease (cell quiescence/dormancy) and relapse. Significance: To our knowledge, this is the first genuine in vitro model of resistance to the three drugs in combined therapy. This new PDO model will be a great asset for the discovery of acquired chemoresistance mechanisms, knowledge that is mandatory before offering new therapeutic strategies for pancreatic cancer. [ABSTRACT FROM AUTHOR]

Published
2022
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38. MOESM5 of Integrative analysis of the cancer genome atlas and cancer cell lines encyclopedia large-scale genomic databases: MUC4/MUC16/MUC20 signature is associated with poor survival in human carcinomas

Author

Jonckheere, Nicolas and Seuningen, Isabelle Van

Subjects
sense organs
Abstract

Additional file 5: Figure S4. Correlation of MUC4 expression and copy numbers of genes correlated with MUC4. The top genes were defined as genes harboring Pearsonâ s correlation higher than 0.5 with MUC4 expression. MUC4 mRNA expression and log2 copy number of ADGRF1, LCN2, MUC20, C1ORF116, STEAP4, SCEL, MUC16 were extracted using ( https://portals.broadinstitute.org/ccle ).

Published
2018
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40. Analyse des divergences économiques au sein de la zone euro: conséquences pour le futur de la zone monétaire

Author

Jonckheere, Nicolas, UCL - Faculté des sciences économiques, sociales, politiques et de communication, and Pensieroso, Luca

Subjects
politique monétaire, zone euro, divergences
Abstract

Le but de ce mémoire est de répondre à la question suivante: les divergences économiques au sein de la zone euro sont-elles telles qu'une séparation de la zone euro est une meilleure issue que le maintien de l'euro? Afin d'y répondre, nous faisons le point sur les bénéfices procurés par la zone euro ainsi que l'évolution de la gouvernance au sein de celle-ci dans un premier temps. Ensuite nous analysons les divergences au sein de la zone à l'aide d'une forme générale de la théorie de la zone monétaire optimale. Dans la troisième partie nous vérifions l'incidence de ces divergences sur l'efficacité de la politique monétaire. Enfin nous formulons nos recommandations pour garantir le futur de la zone euro. Master [120] en sciences économiques, orientation générale, Université catholique de Louvain, 2017

Published
2017

41. The oncogenic receptor ErbB2 modulates gemcitabine and irinotecan/SN-38 chemoresistance of human pancreatic cancer cells via hCNT1 transporter and multidrug-resistance associated protein MRP-2

Author

Skrypek, Nicolas, Vasseur, Romain, Audrey Vincent, Duchene, Belinda, Seuningen, Isabelle, Jonckheere, Nicolas, Jonckheere, Nicolas, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille

Subjects
Male, Antimetabolites, Antineoplastic, endocrine system diseases, Receptor, ErbB-2, pancreatic cancer, [SDV.CAN]Life Sciences [q-bio]/Cancer, Mice, SCID, Irinotecan, Transfection, Deoxycytidine, ErbB2, [SDV.CAN] Life Sciences [q-bio]/Cancer, Cell Line, Tumor, Antineoplastic Combined Chemotherapy Protocols, Databases, Genetic, Animals, Humans, RNA, Messenger, neoplasms, Cell Death, gemcitabine, Membrane Transport Proteins, chemoresistance, Xenograft Model Antitumor Assays, Multidrug Resistance-Associated Protein 2, digestive system diseases, Gene Expression Regulation, Neoplastic, Pancreatic Neoplasms, FOLFIRINOX, Drug Resistance, Neoplasm, Gene Knockdown Techniques, Camptothecin, RNA Interference, Multidrug Resistance-Associated Proteins, Signal Transduction, Research Paper
Abstract

International audience; Pancreatic adenocarcinoma (PDAC) is one of the most deadly cancers because of a lack of early diagnostic markers and efficient therapeutics. The fluorinated analog of deoxycytidine, gemcitabine and emerging FOLFIRINOX protocol (5-fluorouracil (5-FU), irinotecan/SN-38, oxaliplatin and leucovorin) are the main chemotherapies to treat PDAC. The ErbB2/HER2 oncogenic receptor is commonly overexpressed in PDAC. In this context, we aimed to decipher the ErbB2-mediated mechanisms of chemoresistance to the two main chemotherapy protocols used to treat PDAC.ErbB2 knocking down (KD) in CAPAN-1 and CAPAN-2 cells led to an increased sensitivity to gemcitabine and an increased resistance to irinotecan/SN-38 both in vitro and in vivo (subcutaneous xenografts) This was correlated to an increase of hCNT1 and hCNT3 transporters and ABCG2, MRP1 and MRP2 ATP-binding cassette transporters expression and resistance to cell death. We also show that MRP2 is repressed following activation of JNK, Erk1/2 and NF-κB pathways by ErbB2. Finally, in datasets of human PDAC samples, ErbB2 and MRP2 expression was conversely correlated. Altogether, we propose that ErbB2 mediates several intracellular mechanisms linked to PDAC cell chemoresistance that may represent potential targets in order to ameliorate chemotherapy response and allow stratification of patients eligible for either gemcitabine or FOLFIRINOX treatment.

Published
2015

44. Depletion of MUC5B mucin in gastrointestinal cancer cells alters their tumorigenic properties: implication of the Wnt/β-catenin pathway

Author

Lahdaoui, Fatima, primary, Messager, Mathieu, additional, Vincent, Audrey, additional, Hec, Flora, additional, Gandon, Anne, additional, Warlaumont, Maxime, additional, Renaud, Florence, additional, Leteurtre, Emmanuelle, additional, Piessen, Guillaume, additional, Jonckheere, Nicolas, additional, Mariette, Christophe, additional, and Van Seuningen, Isabelle, additional

Published
2017
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45. Flagellin-mediated protection against intestinal Yersinia pseudotuberculosis infection does not require interleukin-22.

Author

UCL - SSS/DDUV - Institut de Duve, UCL - SSS/DDUV/MEXP - Médecine expérimentale, Porte, Rémi, Van Maele, Laurye, Muñoz-Wolf, Natalia, Foligné, Benoit, Dumoutier, Laure, Tabareau, Julien, Cayet, Delphine, Gosset, Pierre, Jonckheere, Nicolas, Van Seuningen, Isabelle, Chabalgoity, A José, Simonet, Michel, Lamkanfi, Mohamed, Renauld, Jean-Christophe, Sirard, Jean-Claude, Carnoy, Christophe, UCL - SSS/DDUV - Institut de Duve, UCL - SSS/DDUV/MEXP - Médecine expérimentale, Porte, Rémi, Van Maele, Laurye, Muñoz-Wolf, Natalia, Foligné, Benoit, Dumoutier, Laure, Tabareau, Julien, Cayet, Delphine, Gosset, Pierre, Jonckheere, Nicolas, Van Seuningen, Isabelle, Chabalgoity, A José, Simonet, Michel, Lamkanfi, Mohamed, Renauld, Jean-Christophe, Sirard, Jean-Claude, and Carnoy, Christophe

Abstract

Signaling through toll-like receptors (TLRs), the main receptors in innate immunity, is essential for the defense of mucosal surfaces. It was previously shown that systemic TLR5 stimulation by bacterial flagellin induces an immediate, transient interleukin-22 (IL-22)-dependent antimicrobial response to bacterial or viral infections of the mucosa. This process was dependent on the activation of type 3 innate lymphoid cells (ILCs). The objective of the present study was to analyze the effects of flagellin treatment in a murine model of oral infection with Yersinia pseudotuberculosis (an invasive, Gram-negative, enteropathogenic bacterium that targets the small intestine). We found that systemic administration of flagellin significantly increased the survival rate after intestinal infection (but not systemic infection) by Y. pseudotuberculosis This protection was associated with a low bacterial count in the gut and the spleen. In contrast, no protection was afforded by administration of the TLR4 agonist lipopolysaccharide - suggesting the presence of a flagellin-specific effect. Lastly, we found that TLR5- and MyD88-mediated signaling was required for the protective effects of flagellin, whereas neither lymphoid cells nor IL-22 were involved.

Published
2017

46. Flagellin-Mediated Protection against Intestinal Yersinia pseudotuberculosis Infection Does Not Require Interleukin-22

Author

Porte, Rémi, primary, Van Maele, Laurye, additional, Muñoz-Wolf, Natalia, additional, Foligné, Benoit, additional, Dumoutier, Laure, additional, Tabareau, Julien, additional, Cayet, Delphine, additional, Gosset, Pierre, additional, Jonckheere, Nicolas, additional, Van Seuningen, Isabelle, additional, Chabalgoity, José A., additional, Simonet, Michel, additional, Lamkanfi, Mohamed, additional, Renauld, Jean-Christophe, additional, Sirard, Jean-Claude, additional, and Carnoy, Christophe, additional

Published
2017
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49. GATA-4/-6 and HNF-1/-4 families of transcription factors control the transcriptional regulation of the murine Muc5ac mucin during stomach development and in epithelial cancer cells.: Regulation of Muc5ac by GATA-6 and HNF-4α

Author

Jonckheere, Nicolas, Vincent, Audrey, Franquet-Ansart, Hélène, Witte-Bouma, Janneke, Korteland-van Male, Anita, Leteurtre, Emmanuelle, Renes, Ingrid, van Seuningen, Isabelle, Inserm UMR837 Team 5, Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Laboratory of Pediatrics, Division of Neonatology, Erasmus University Medical Center [Rotterdam] (Erasmus MC), This work was supported by a grant from l'Association François Aupetit (IVS). N. J is the recipient of a Ligue Nationale contre le Cancer (LNCC) postdoctoral fellowship. I V S is the recipient of a 'Contrat Hospitalier de Recherche Translationnelle'/CHRT 2010, AVIESAN., and Jonckheere, Nicolas

Subjects
MESH: Cell Differentiation, MESH: Cell Line, Tumor, MESH: GATA6 Transcription Factor, MESH: Mice, Inbred BALB C, [SDV.CAN]Life Sciences [q-bio]/Cancer, digestive system, MESH: Stomach, mucin, [SDV.CAN] Life Sciences [q-bio]/Cancer, MESH: Promoter Regions, Genetic, MESH: Gene Expression Regulation, Developmental, MESH: Animals, MESH: Neoplasms, development, MESH: Mice, MESH: Organ Specificity, GATA, MESH: Mucin 5AC, respiratory system, HNF, MESH: Epithelial Cells, embryonic structures, MESH: Transcriptional Activation, MESH: Hepatocyte Nuclear Factor 4, transcription, Muc5ac, stomach
Abstract

International audience; During human embryonic and fetal development of the gastrointestinal tract, the gene encoding the MUC5AC mucin has a spatio-temporal pattern of expression restricted to the stomach. In order to better understand the molecular mechanisms responsible for this restricted pattern of expression, we have studied Muc5ac expression in the developing stomach of the mouse and correlated it to that of transcription factors known to be involved in cell differentiation programs during development. Our results indicate that GATA-6 and HNF-4α expression increased concomitantly with the induction of Muc5ac expression in embryonic stomach. We then studied Muc5ac transcriptional regulation by these transcription factors and showed that they all transactivate Muc5ac promoter. We also identified several active GATA-4/-5/-6 and HNF-1/-4 cis-elements using gel shift assays, chromatin immunoprecipitation and site-directed mutagenesis. Among all Muc5ac regulators, only GATA-6 and HNF-4a expression was concomitant to that of Muc5ac in the developing stomach. This is thus in favor of an important role for these two transcription factors as regulators of expression of the Muc5ac mucin during stomach development and in epithelial cancer cells.

Published
2012

50. The mucin MUC4 is a transcriptional and post-transcriptional target of K-ras oncogene in pancreatic cancer. Implication of MAPK/AP-1, NF-κB and RalB signaling pathways

Author

Vasseur, Romain, primary, Skrypek, Nicolas, additional, Duchêne, Belinda, additional, Renaud, Florence, additional, Martínez-Maqueda, Daniel, additional, Vincent, Audrey, additional, Porchet, Nicole, additional, Van Seuningen, Isabelle, additional, and Jonckheere, Nicolas, additional

Published
2015
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