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1. The TLR3 L412F polymorphism prevents TLR3-mediated tumor cell death induction in pediatric sarcomas

Author

Bisaccia, Joseph, Meyer, Swann, Bertrand-Chapel, Adrien, Hecquet, Quentin, Barbet, Virginie, Kaniewski, Bastien, Léon, Sophie, Gadot, Nicolas, Rochet, Isabelle, Fajnorova, Iveta, Leblond, Pierre, Cordier-Bussat, Martine, Corradini, Nadège, Vasiljevic, Alexandre, Billaud, Marc, Picard, Cécile, Broutier, Laura, Gallerne, Cindy, Dutour, Aurélie, Blay, Jean-Yves, and Castets, Marie

Published
2023
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2. BMP2 and BMP7 cooperate with H3.3K27M to promote quiescence and invasiveness in pediatric diffuse midline gliomas

Author

Huchedé, Paul, primary, Meyer, Swann, additional, Berthelot, Clément, additional, Hamadou, Maud, additional, Bertrand-Chapel, Adrien, additional, Rakotomalala, Andria, additional, Manceau, Line, additional, Tomine, Julia, additional, Lespinasse, Nicolas, additional, Lewandowski, Paul, additional, Cordier-Bussat, Martine, additional, Broutier, Laura, additional, Dutour, Aurélie, additional, Rochet, Isabelle, additional, Blay, Jean-Yves, additional, Degletagne, Cyril, additional, Attignon, Valéry, additional, Montero-Carcaboso, Angel, additional, Grand, Marion Le, additional, Pasquier, Eddy, additional, Vasiljevic, Alexandre, additional, Gilardi-Hebenstreit, Pascale, additional, Meignan, Samuel, additional, Leblond, Pierre, additional, Ribes, Vanessa, additional, Cosset, Erika, additional, and Castets, Marie, additional

Published
2023
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3. Correction: Schwann cells support oncogenic potential of pancreatic cancer cells through TGFβ signaling

Author

Roger, Elodie, Martel, Sylvie, Bertrand-Chapel, Adrien, Depollier, Arnaud, Chuvin, Nicolas, Pommier, Roxane M., Yacoub, Karam, Caligaris, Cassandre, Cardot-Ruffino, Victoire, Chauvet, Véronique, Aires, Sophie, Mohkam, Kayvan, Mabrut, Jean-Yves, Adham, Mustapha, Fenouil, Tanguy, Hervieu, Valérie, Broutier, Laura, Castets, Marie, Neuzillet, Cindy, Cassier, Philippe A., Tomasini, Richard, Sentis, Stéphanie, and Bartholin, Laurent

Published
2020
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4. Schwann cells support oncogenic potential of pancreatic cancer cells through TGFβ signaling

Author

Roger, Elodie, Martel, Sylvie, Bertrand-Chapel, Adrien, Depollier, Arnaud, Chuvin, Nicolas, Pommier, Roxane M., Yacoub, Karam, Caligaris, Cassandre, Cardot-Ruffino, Victoire, Chauvet, Véronique, Aires, Sophie, Mohkam, Kayvan, Mabrut, Jean-Yves, Adham, Mustapha, Fenouil, Tanguy, Hervieu, Valérie, Broutier, Laura, Castets, Marie, Neuzillet, Cindy, Cassier, Philippe A., Tomasini, Richard, Sentis, Stéphanie, and Bartholin, Laurent

Published
2019
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5. Human primary liver cancer-derived organoid cultures for disease modeling and drug screening

Author

Broutier, Laura, Mastrogiovanni, Gianmarco, Verstegen, Monique MA, Francies, Hayley E, Gavarró, Lena Morrill, Bradshaw, Charles R, Allen, George E, Arnes-Benito, Robert, Sidorova, Olga, Gaspersz, Marcia P, Georgakopoulos, Nikitas, Koo, Bon-Kyoung, Dietmann, Sabine, Davies, Susan E, Praseedom, Raaj K, Lieshout, Ruby, IJzermans, Jan N M, Wigmore, Stephen J, Saeb-Parsy, Kourosh, Garnett, Mathew J, van der Laan, Luc JW, and Huch, Meritxell

Subjects
Liver cancer -- Development and progression -- Models -- Research, Cell culture -- Usage -- Research, Biological sciences, Health
Abstract

Human liver cancer research currently lacks in vitro models that can faithfully recapitulate the pathophysiology of the original tumor. We recently described a novel, near-physiological organoid culture system, wherein primary human healthy liver cells form long-term expanding organoids that retain liver tissue function and genetic stability. Here we extend this culture system to the propagation of primary liver cancer (PLC) organoids from three of the most common PLC subtypes: hepatocellular carcinoma (HCC), cholangiocarcinoma (CC) and combined HCC/CC (CHC) tumors. PLC-derived organoid cultures preserve the histological architecture, gene expression and genomic landscape of the original tumor, allowing for discrimination between different tumor tissues and subtypes, even after long-term expansion in culture in the same medium conditions. Xenograft studies demonstrate that the tumorogenic potential, histological features and metastatic properties of PLC-derived organoids are preserved in vivo. PLC-derived organoids are amenable for biomarker identification and drug-screening testing and led to the identification of the ERK inhibitor SCH772984 as a potential therapeutic agent for primary liver cancer. We thus demonstrate the wide-ranging biomedical utilities of PLC-derived organoid models in furthering the understanding of liver cancer biology and in developing personalized-medicine approaches for the disease., Author(s): Laura Broutier [1]; Gianmarco Mastrogiovanni [1, 2]; Monique MA Verstegen [3]; Hayley E Francies [4]; Lena Morrill Gavarró [2]; Charles R Bradshaw [1]; George E Allen [1]; Robert Arnes-Benito [...]

Published
2017
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6. Alterations of the TGFb-sequestration complex member ADAMTSL1 levels are associated with muscular defects and rhabdomyosarcoma aggressiveness

Author

Juban, Gaëtan, primary, Bertrand-Chapel, Adrien, additional, Meyer, Swann, additional, Kneppers, Anita, additional, Huchedé, Paul, additional, Gallerne, Cindy, additional, Benayoun, Ruth, additional, Cohen, Enzo, additional, Lopez-Gonzales, Alejandro, additional, Larbi, Sabrina Ben, additional, Creveaux, Marion, additional, Vaille, Lucile, additional, Bouvier, Amélie, additional, Théodore, Marine, additional, Broutier, Laura, additional, Dutour, Aurélie, additional, Cordier-Bussat, Martine, additional, Blay, Jean-Yves, additional, Streichenberger, Nathalie, additional, Picard, Cécile, additional, Corradini, Nadège, additional, Allamand, Valérie, additional, Castets, Perrine, additional, Mounier, Rémi, additional, and Castets, Marie, additional

Published
2023
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7. Criteria for preclinical models of cholangiocarcinoma:scientific and medical relevance

Author

Calvisi, Diego, Boulter, Luke, Vaquero, Javier, Saborowski, Anna, Fabris, Luca, Rodrigues, Pedro, Coulouarn, Cédric, Castro, Rui, Segatto, Oreste, Raggi, Chiara, van der Laan, Luc, Carpino, Guido, Goeppert, Benjamin, Roessler, Stephanie, Kendall, Timothy, Evert, Matthias, Gonzalez-Sanchez, Ester, Valle, Juan, Vogel, Arndt, Bridgewater, John, Borad, Mitesh, Gores, Gregory, Roberts, Lewis, Marin, Jose, Andersen, Jesper, Alvaro, Domenico, Forner, Alejandro, Banales, Jesus, Cardinale, Vincenzo, Macias, Rocio, Vicent, Silve, Chen, Xin, Braconi, Chiara, Verstegen, Monique, Fouassier, Laura, Scheiter, Alexander, Selaru, Florin, Evert, Katja, Utpatel, Kirsten, Broutier, Laura, Cadamuro, Massimiliano, Huch, Meritxell, Goldin, Robert, Gradilone, Sergio, Saito, Yoshimasa, University of Regensburg, University of Edinburgh, Instituto de Salud Carlos III [Madrid] (ISC), Hannover Medical School [Hannover] (MHH), Yale School of Medicine [New Haven, Connecticut] (YSM), University of the Basque Country/Euskal Herriko Unibertsitatea (UPV/EHU), Oncogenesis, Stress, Signaling (OSS), Université de Rennes (UR)-CRLCC Eugène Marquis (CRLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CRLCC Eugène Marquis (CRLCC), Universidade de Lisboa, Università degli Studi di Firenze = University of Florence (UniFI), Erasmus University Medical Center [Rotterdam] (Erasmus MC), Università degli Studi di Roma 'Foro Italico', Heidelberg University Hospital [Heidelberg], University of Barcelona, Centro de Investigación Biomédica en Red en el Área temática de Enfermedades Hepáticas y Digestivas (CIBERehd), Liver Unit, Clínica Universitaria, CIBER-EHD, Institut d'Investigació Biomèdica de Bellvitge [Barcelone] (IDIBELL), The Christie NHS Foundation Trust [Manchester, Royaume-Uni], University of Manchester [Manchester], University College of London [London] (UCL), Mayo Clinic, Mayo Clinic [Rochester], Universidad de Salamanca, University of Copenhagen = Københavns Universitet (UCPH), Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome] (UNIROMA), Universidad Pública de Navarra [Espagne] = Public University of Navarra (UPNA), University of California [San Francisco] (UC San Francisco), University of California (UC), University of Glasgow, Centre de Recherche Saint-Antoine (CRSA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), The authors thank the European Network for the Study of Cholangiocarcinoma (ENS-CCA) and the European H2020 COST Action CA18122. The authors also acknowledge the valuable contributions of the external advisory panel. C.C. is supported by Inserm, Université de Rennes 1 and by a grant from the French Ministry of Health and the French National Cancer Institute (PRT-K20-136), CHU Rennes, CLCC Eugène Marquis, Rennes. M.M.A.V. and L.J.W.v.d.L. are supported by Medical Delta Regenerative Medicine 4D (Generating complex tissues with stem cells and printing technology) and TKI-LSH grant EMC-LSH19002. S.R. is supported by the German Research Foundation (DFG, project no. 314905040 and no. 493697503) and by German Cancer Aid (Deutsche Krebshilfe, project no. 70113922). S.V. is supported by Ministerio de Ciencia, Innovación y Universidades, Convocatoria 2019 para incentivar la Incorporación Estable de Doctores (IED2019-001007-I), by FEDER/Ministerio de Ciencia, Innovación y Universidades – Agencia Estatal de Investigación (PID2020‐116344‐RB‐100) and by the Government of Navarra-Health Research Department (58, and 2018). J.V. is funded by Ministerio de Ciencia e Innovación, part of Agencia Estatal de Investigación (AEI), through the Retos Investigación grant number PID2019-108651RJ-I00/DOI 10.13039/501100011033. The authors thank CERCA Programme/Generalitat de Catalunya for institutional support. R.I.R.M. and J.J.G.M. are supported by Instituto de Salud Carlos III, Spain (PI20/00189, PI19/00819) co-funded by the European Union. L. Fouassier belongs to a team supported by the Fondation pour la Recherche Médicale (Equipe FRM 2020 no. EQU202003010517) and is supported by Inserm and Sorbonne Université, INCa and ITMO Cancer of Aviesan within the framework of the 2021–2030 Cancer Control Strategy, on funds administered by Inserm.

Subjects
Hepatology, [SDV]Life Sciences [q-bio], Gastroenterology, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology
Abstract

International audience; Cholangiocarcinoma (CCA) is a rare malignancy that develops at any point along the biliary tree. CCA has a poor prognosis, its clinical management remains challenging, and effective treatments are lacking. Therefore, preclinical research is of pivotal importance and necessary to acquire a deeper understanding of CCA and improve therapeutic outcomes. Preclinical research involves developing and managing complementary experimental models, from in vitro assays using primary cells or cell lines cultured in 2D or 3D to in vivo models with engrafted material, chemically induced CCA or genetically engineered models. All are valuable tools with well-defined advantages and limitations. The choice of a preclinical model is guided by the question(s) to be addressed; ideally, results should be recapitulated in independent approaches. In this Consensus Statement, a task force of 45 experts in CCA molecular and cellular biology and clinicians, including pathologists, from ten countries provides recommendations on the minimal criteria for preclinical models to provide a uniform approach. These recommendations are based on two rounds of questionnaires completed by 35 (first round) and 45 (second round) experts to reach a consensus with 13 statements. An agreement was defined when at least 90% of the participants voting anonymously agreed with a statement. The ultimate goal was to transfer basic laboratory research to the clinics through increased disease understanding and to develop clinical biomarkers and innovative therapies for patients with CCA.

Published
2023

8. Fusion-negative Rhabdomyosarcoma 3D-organoids as an innovative model to predict resistance to cell death inducers

Author

Savary, Clara, primary, Huchedé, Paul, additional, Luciana, Léa, additional, Tourbez, Arthur, additional, Deligne, Clémence, additional, Picard, Cécile, additional, Diot, Thomas, additional, Coquet, Claire, additional, Meynard, Nina, additional, Grand, Marion Le, additional, Tonon, Laurie, additional, Gadot, Nicolas, additional, Degletagne, Cyril, additional, Léon, Sophie, additional, Attignon, Valéry, additional, Bomane, Alexandra, additional, Rochet, Isabelle, additional, Müller, Kevin, additional, Mournetas, Virginie, additional, Bergeron, Christophe, additional, Rinaudo, Paul, additional, Dutour, Aurélie, additional, Cordier-Bussat, Martine, additional, Dijoud, Frédérique, additional, Corradini, Nadège, additional, Maucort-Boulch, Delphine, additional, Pasquier, Eddy, additional, Blay, Jean-Yves, additional, Castets, Marie, additional, and Broutier, Laura, additional

Published
2022
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11. Targeting netrin-1/DCC interaction in diffuse large B-cell and mantle cell lymphomas

Author

Broutier, Laura, Creveaux, Marion, Vial, Jonathan, Tortereau, Antonin, Delcros, Jean-Guy, Chazot, Guillaume, McCarron, Mark J, Léon, Sophie, Pangault, Céline, Gadot, Nicolas, Colombe, Amélie, Boulland, Marie-Laure, Blachier, Jonathan, Marie, Julien C, Traverse-Glehen, Alexandra, Donzé, Olivier, Chassagne-Clément, Catherine, Salles, Gilles, Tarte, Karin, Mehlen, Patrick, and Castets, Marie

Published
2016
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13. Building consensus on definition and nomenclature of hepatic, pancreatic, and biliary organoids

Author

Marsee, Ary, primary, Roos, Floris J.M., additional, Verstegen, Monique M.A., additional, Gehart, Helmuth, additional, de Koning, Eelco, additional, Lemaigre, Frédéric, additional, Forbes, Stuart J., additional, Peng, Weng Chuan, additional, Huch, Meritxell, additional, Takebe, Takanori, additional, Vallier, Ludovic, additional, Clevers, Hans, additional, van der Laan, Luc J.W., additional, Spee, Bart, additional, Marsee, Ary, additional, Roos, Floris, additional, Verstegen, Monique, additional, Forbes, Stuart, additional, van der Laan, Luc, additional, Boj, Sylvia, additional, Baptista, Pedro, additional, Schneeberger, Kerstin, additional, Soroka, Carol, additional, Heim, Markus, additional, Nuciforo, Sandro, additional, Zaret, Kenneth, additional, Saito, Yoshimasa, additional, Lutolf, Matthias, additional, Cardinale, Vincenzo, additional, Simons, Ben, additional, van IJzendoorn, Sven, additional, Kamiya, Akihide, additional, Chikada, Hiromi, additional, Wang, Shuyong, additional, Mun, Seon Ju, additional, Son, Myung Jin, additional, Onder, Tamer Tevfik, additional, Boyer, James, additional, Sato, Toshiro, additional, Georgakopoulos, Nikitas, additional, Meneses, Andre, additional, Broutier, Laura, additional, Boulter, Luke, additional, Grün, Dominic, additional, IJzermans, Jan, additional, Artegiani, Benedetta, additional, van Boxtel, Ruben, additional, Kuijk, Ewart, additional, Carpino, Guido, additional, Peltz, Gary, additional, Banales, Jesus, additional, Man, Nancy, additional, Aloia, Luigi, additional, LaRusso, Nicholas, additional, George, Gregory, additional, Rimland, Casey, additional, Yeoh, George, additional, Grappin-Botton, Anne, additional, Stange, Daniel, additional, Prior, Nicole, additional, Tirnitz-Parker, Janina E.E., additional, Andersson, Emma, additional, Braconi, Chiara, additional, Hannan, Nicholas, additional, Lu, Wei-Yu, additional, Strom, Stephen, additional, Sancho-Bru, Pau, additional, Ogawa, Shinichiro, additional, Corbo, Vincenzo, additional, Lancaster, Madeline, additional, Hu, Huili, additional, Fuchs, Sabine, additional, and Hendriks, Delilah, additional

Published
2021
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14. DCC constrains tumour progression via its dependence receptor activity

Author

Castets, Marie, Broutier, Laura, Molin, Yann, Brevet, Marie, Chazot, Guillaume, Gadot, Nicolas, Paquet, Armelle, Mazelin, Laetitia, Jarrosson-Wuilleme, Loraine, Scoazec, Jean-Yves, Bernet, Agnes, and Mehlen, Patrick

Subjects
Gene expression -- Research, Colorectal cancer -- Genetic aspects -- Development and progression -- Research, Tumor suppressor genes -- Physiological aspects -- Research, Apoptosis -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The role of deleted in colorectal carcinoma (DCC) as a tumour suppressor has been a matter of debate for the past 15 years. DCC gene expression is lost or markedly reduced in the majority of advanced colorectal cancers (1) and, by functioning as a dependence receptor, DCC has been shown to induce apoptosis unless engaged by its ligand, netrin-1 (ref. 2). However, so far no animal model has supported the view that the DCC loss-of-function is causally implicated as predisposing to aggressive cancer development (3). To investigate the role of DCC-induced apoptosis in the control of tumour progression, here we created a mouse model in which the pro-apoptotic activity of DCC is genetically silenced. Although the loss of DCC-induced apoptosis in this mouse model is not associated with a major disorganization of the intestines, it leads to spontaneous intestinal neoplasia at a relatively low frequency. Loss of DCC-induced apoptosis is also associated with an increase in the number and aggressiveness of intestinal tumours in a predisposing APC mutant context, resulting in the development of highly invasive adenocarcinomas. These results demonstrate that DCC functions as a tumour suppressor via its ability to trigger tumour cell apoptosis., The development of colonic carcinoma from normal colonic epithelium has been shown to be associated with the mutation of a specific set of genes (4). Loss of heterozygosity on chromosome [...]

Published
2012
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16. Ephrin-B3 supports glioblastoma growth by inhibiting apoptosis induced by the dependence receptor EphA4

Author

Royet, Amélie, primary, Broutier, Laura, additional, Coissieux, Marie-May, additional, Malleval, Céline, additional, Gadot, Nicolas, additional, Maillet, Denis, additional, Gratadou-Hupon, Lise, additional, Bernet, Agnès, additional, Nony, Pascale, additional, Treilleux, Isabelle, additional, Honnorat, Jérôme, additional, Liebl, Daniel, additional, Pelletier, Laurent, additional, Berger, François, additional, Meyronet, David, additional, Castets, Marie, additional, and Mehlen, Patrick, additional

Published
2017
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17. Fusion-negative rhabdomyosarcoma 3D organoids to predict effective drug combinations: A proof-of-concept on cell death inducers

Author

Savary, Clara, Luciana, Léa, Huchedé, Paul, Tourbez, Arthur, Coquet, Claire, Broustal, Maëlle, Lopez Gonzalez, Alejandro, Deligne, Clémence, Diot, Thomas, Naret, Olivier, Costa, Mariana, Meynard, Nina, Barbet, Virginie, Müller, Kevin, Tonon, Laurie, Gadot, Nicolas, Degletagne, Cyril, Attignon, Valéry, Léon, Sophie, Vanbelle, Christophe, Bomane, Alexandra, Rochet, Isabelle, Mournetas, Virginie, Oliveira, Luciana, Rinaudo, Paul, Bergeron, Christophe, Dutour, Aurélie, Cordier-Bussat, Martine, Roch, Aline, Brandenberg, Nathalie, El Zein, Sophie, Watson, Sarah, Orbach, Daniel, Delattre, Olivier, Dijoud, Frédérique, Corradini, Nadège, Picard, Cécile, Maucort-Boulch, Delphine, Le Grand, Marion, Pasquier, Eddy, Blay, Jean-Yves, Castets, Marie, and Broutier, Laura

Abstract

Rhabdomyosarcoma (RMS) is the main form of pediatric soft-tissue sarcoma. Its cure rate has not notably improved in the last 20 years following relapse, and the lack of reliable preclinical models has hampered the design of new therapies. This is particularly true for highly heterogeneous fusion-negative RMS (FNRMS). Although methods have been proposed to establish FNRMS organoids, their efficiency remains limited to date, both in terms of derivation rate and ability to accurately mimic the original tumor. Here, we present the development of a next-generation 3D organoid model derived from relapsed adult and pediatric FNRMS. This model preserves the molecular features of the patients’ tumors and is expandable for several months in 3D, reinforcing its interest to drug combination screening with longitudinal efficacy monitoring. As a proof-of-concept, we demonstrate its preclinical relevance by reevaluating the therapeutic opportunities of targeting apoptosis in FNRMS from a streamlined approach based on transcriptomic data exploitation.

Published
2023
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18. Targeting netrin-1/ DCC interaction in diffuse large B-cell and mantle cell lymphomas.

Author

Broutier, Laura, Creveaux, Marion, Vial, Jonathan, Tortereau, Antonin, Delcros, Jean‐Guy, Chazot, Guillaume, McCarron, Mark J, Léon, Sophie, Pangault, Céline, Gadot, Nicolas, Colombe, Amélie, Boulland, Marie‐Laure, Blachier, Jonathan, Marie, Julien C, Traverse‐Glehen, Alexandra, Donzé, Olivier, Chassagne‐Clément, Catherine, Salles, Gilles, Tarte, Karin, and Mehlen, Patrick

Abstract

DCC ( Deleted in Colorectal Carcinoma) has been demonstrated to constrain tumor progression by inducing apoptosis unless engaged by its ligand netrin-1. This has been shown in breast and colorectal cancers; however, this tumor suppressive function in other cancers is not established. Using a transgenic mouse model, we report here that inhibition of DCC-induced apoptosis is associated with lymphomagenesis. In human diffuse large B-cell lymphoma ( DLBCL), an imbalance of the netrin-1/ DCC ratio suggests a loss of DCC-induced apoptosis, either via a decrease in DCC expression in germinal center subtype or by up-regulation of netrin-1 in activated B-cell ( ABC) one. Such imbalance is also observed in mantle cell lymphoma ( MCL). Using a netrin-1 interfering antibody, we demonstrate both in vitro and in vivo that netrin-1 acts as a survival factor for ABC- DLBCL and MCL tumor cells. Together, these data suggest that interference with the netrin-1/ DCC interaction could represent a promising therapeutic strategy in netrin-1-positive DLBCL and MCL. [ABSTRACT FROM AUTHOR]

Published
2016
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20. DCC constrains tumour progression via its dependence receptor activity

Author

Castets, Marie, primary, Broutier, Laura, additional, Molin, Yann, additional, Brevet, Marie, additional, Chazot, Guillaume, additional, Gadot, Nicolas, additional, Paquet, Armelle, additional, Mazelin, Laetitia, additional, Jarrosson-Wuilleme, Loraine, additional, Scoazec, Jean-Yves, additional, Bernet, Agnès, additional, and Mehlen, Patrick, additional

Published
2011
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22. [DCC, come back of a suppressor gene in colorectal cancer].

Author

Broutier L and Castets M

Subjects
Adenocarcinoma pathology, Animals, Apoptosis genetics, Colorectal Neoplasms pathology, Disease Progression, Genes, Suppressor physiology, Humans, Mice, Mice, Transgenic, Models, Biological, Adenocarcinoma genetics, Colorectal Neoplasms genetics, Genes, DCC physiology
Published
2012
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