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Your search keyword '"Anna-Line Calatayud"' showing total 3 results
Start Over Author "Anna-Line Calatayud" Topic [sdv.can]life sciences [q-bio]/cancer
3 results on '"Anna-Line Calatayud"'

1. Analysis of Liver Cancer Cell Lines Identifies Agents With Likely Efficacy Against Hepatocellular Carcinoma and Markers of Response

Author

Quentin Bayard, Eric Letouzé, Jill Pilet, Jean-Charles Nault, Léa Meunier, Bettina Grasl-Kraupp, Camille Péneau, Nataliya Rohr-Udilova, Tiziana La Bella, Gabrielle Couchy, J. Calderaro, Stefano Caruso, Leanne de Koning, Jessica Zucman-Rossi, Sandrine Imbeaud, Bérengère Ouine, Anna-Line Calatayud, Sandra Rebouissou, Samia Rekik, Paulette Bioulac-Sage, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université Sorbonne Paris Cité (USPC), Génomique Fonctionnelle des Tumeurs Solides (U1162), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Medizinische Universität Wien = Medical University of Vienna, Institut Curie [Paris], Université Paris sciences et lettres (PSL), Physiopathologie du cancer du foie, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Pellegrin, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Hôpital Henri Mondor, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Hôpital Jean Verdier [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), 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), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), and Gestionnaire, Hal Sorbonne Université

Subjects
0301 basic medicine, chemistry.chemical_compound, 0302 clinical medicine, MEK Inhibitor, Antineoplastic Combined Chemotherapy Protocols, Gene expression, Gene Regulatory Networks, Protein Interaction Maps, Precision Medicine, Response to Therapy, Hepatocyte differentiation, MEK inhibitor, Liver Neoplasms, Gastroenterology, 3. Good health, Gene Expression Regulation, Neoplastic, Phenotype, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Liver Tumor, 030211 gastroenterology & hepatology, Signal transduction, Signal Transduction, medicine.drug, Sorafenib, Carcinoma, Hepatocellular, Tumor suppressor gene, Cell Survival, Clinical Decision-Making, Antineoplastic Agents, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, Cell Line, Tumor, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], microRNA, Biomarkers, Tumor, medicine, Humans, Genetic Predisposition to Disease, Hepatology, Patient Selection, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, Biomarker, [SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, 030104 developmental biology, chemistry, Alisertib, Cancer research, Drug Screening Assays, Antitumor, Transcriptome
Abstract

International audience; BACKGROUND AND AIMS: Hepatocellular carcinomas (HCCs) are heterogeneous aggressive tumors with low rates of response to treatment at advanced stages. We screened a large panel of liver cancer cell lines (LCCLs) to identify agents that might be effective against HCC and markers of therapeutic response.METHODS: We performed whole-exome RNA and microRNA sequencing and quantification of 126 proteins in 34 LCCLs. We screened 31 anticancer agents for their ability to decrease cell viability. We compared genetic, RNA, and protein profiles of LCCLs with those of primary HCC samples and searched for markers of response.RESULTS: The protein, RNA and mutational signatures of the LCCLs were similar to those of the proliferation class of HCC, which is the most aggressive tumor type. Cell lines with alterations in genes encoding members of the Ras-MAPK signaling pathway and that required fibroblast growth factor (FGF)19 signaling via FGF receptor 4 for survival were more sensitive to trametinib than to FGF receptor 4 inhibitors. Amplification of FGF19 resulted in increased activity of FGF19 only in tumor cells that kept a gene expression pattern of hepatocyte differentiation. We identified single agents and combinations of agents that reduced viability of cells with features of the progenitor subclass of HCC. LCCLs with inactivating mutations in TSC1 and TSC2 were sensitive to the mammalian target of rapamycin inhibitor rapamycin, and cells with inactivating mutations in TP53 were sensitive to the Aurora kinase A inhibitor alisertib. Amplification of MET was associated with hypersensitivity to cabozantinib and the combination of sorafenib and inhibitors of MAP kinase 1 and MAP kinase2 had a synergistic antiproliferative effect.CONCLUSION: LCCLs can be screened for drugs and agents that might be effective for treatment of HCC. We identified genetic alterations and gene expression patterns associated with response to these agents. This information might be used to select patients for clinical trials.

Published
2019
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2. Proliferation markers are associated with MET expression in hepatocellular carcinoma and predict tivantinib sensitivity in vitro

Author

Sandrine Imbeaud, Leanne de Koning, Yoann Martin, Nathalie Ganne-Carrié, Bettina Grasl-Kraupp, Nataliya Rohr-Udilova, Samia Rekik, Anna-Line Calatayud, Gabrielle Couchy, Paulette Bioulac-Sage, Sandra Rebouissou, Jean-Charles Nault, Tiziana La Bella, Marianne Ziol, Jessica Zucman-Rossi, REBOUISSOU, Sandra, Génomique Fonctionnelle des Tumeurs Solides (U1162), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Medizinische Universität Wien = Medical University of Vienna, Hôpital Pellegrin, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Bordeaux Research In Translational Oncology [Bordeaux] (BaRITOn), Université de Bordeaux (UB)-CHU Bordeaux [Bordeaux]-Institut National de la Santé et de la Recherche Médicale (INSERM), Comprehensive Cancer Center [Vienna, Austria], Medizinische Universität Wien = Medical University of Vienna-Institute of Cancer Research [Vienna, Austria], Translational Research Department, RPPA Platform, Institut Curie Research Center, Service d'Hépato-gastroentérologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Jean Verdier [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Communautés d’universités et établissements Sorbonne Paris Cité (COMUE Sorbonne Paris Cité), Université Sorbonne Paris Cité (USPC)-Chimie ParisTech-Université Paris sciences et lettres (PSL), 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), This work was supported by Inserm, the Ligue Nationale Contre leCancer (‘‘Equipe labellisée’’ program), the Fondation Bettencourt-Schueller (Coup d’élanAward), Labex OncoImmunology (Investissement d’Avenir) and MUTHEC INCAtranslationnel. Samia Rekik was supported by a fellowship from ARC., and Institute of Cancer Research [Vienna, Austria]-Medizinische Universität Wien = Medical University of Vienna

Subjects
0301 basic medicine, Cancer Research, Mitotic index, Carcinoma, Hepatocellular, proliferation, [SDV]Life Sciences [q-bio], Cell, tivantinib, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, Bioinformatics, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, [SDV.CAN] Life Sciences [q-bio]/Cancer, Cell Line, Tumor, Exome Sequencing, medicine, Biomarkers, Tumor, Humans, antimitotic, Tivantinib, Protein Kinase Inhibitors, Cell Proliferation, Cell growth, Liver Neoplasms, Cancer, hepatocellular carcinoma, Proto-Oncogene Proteins c-met, medicine.disease, Pyrrolidinones, 3. Good health, Vinblastine, Gene Expression Regulation, Neoplastic, [SDV] Life Sciences [q-bio], 030104 developmental biology, medicine.anatomical_structure, Oncology, chemistry, Paclitaxel, Drug Resistance, Neoplasm, 030220 oncology & carcinogenesis, Cancer research, Quinolines, MET, Liver cancer, medicine.drug
Abstract

Purpose: Tivantinib was initially reported as a selective MET inhibitor and is under phase III evaluation in "MET-high" hepatocellular carcinoma (HCC) patients. However, it has been also proposed as an antimitotic agent. We aimed to evaluate the antitumor effect of tivantinib in HCC cells by combining pharmacologic and molecular profiling. Experimental Design: Sensitivity to tivantinib, JNJ-38877605, PHA-665752, vinblastine, and paclitaxel was tested in a panel of 35 liver cancer cell lines analyzed with exome sequencing, mRNA expression of 188 genes, and protein expression. Drug effect was investigated by Western blot analysis and mitotic index quantification. Expression of candidate biomarkers predicting drug response was analyzed in 310 HCCs. Results: Tivantinib sensitivity profiles in the 35 cell lines were similar to those obtained with antimitotic drugs. It induced blockage of cell mitosis, and high cell proliferation was associated with sensitivity to tivantinib, vinblastine, and paclitaxel. In contrast, tivantinib did not suppress MET signaling, and selective MET inhibitors demonstrated an antiproliferative effect only in MHCC97H, the unique cell line displaying MET gene amplification. HCC tumors with high expression of cell proliferation genes defined a group of patients with poor survival. Interestingly, highly proliferative tumors also demonstrated high MET expression, likely explaining better therapeutic response of MET-high HCC patients to tivantinib. Conclusions: Tivantinib acts as an antimitotic compound, and cell proliferation markers are the best predictors of its antitumor efficacy in cell lines. Ki67 expression should be tested in clinical trials to predict tivantinib response. Clin Cancer Res; 23(15); 4364–75. ©2017 AACR.

Published
2017
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3. Exome sequencing of hepatocellular carcinomas identifies new mutational signatures and potential therapeutic targets

Author

Josep M. Llovet, Vincenzo Mazzaferro, Clément Meiller, Augusto Villanueva, Ludmil B. Alexandrov, Alexis Laurent, Eric Letouzé, Frédéric Soysouvanh, Kornelius Schulze, Sandra Rebouissou, Sandrine Imbeaud, Laura Pelletier, Jean-Charles Nault, Jayendra Shinde, Anna Line Calatayud, Jessica Zucman-Rossi, Michael R. Stratton, Charles Balabaud, Julien Calderaro, Jean-Frédéric Blanc, Paulette Bioulac-Sage, Gabrielle Couchy, Fabien Calvo, Roser Pinyol, Génomique Fonctionnelle des Tumeurs Solides (U1162), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), The Wellcome Trust Sanger Institute [Cambridge], Theoretical Division [LANL], Los Alamos National Laboratory (LANL), Assistance Publique-Hôpitaux de Paris, Department of Pathology, Centre hospitalier universitaire Henri Mondor, F-94000 Créteil, France, Hepatocellular Carcinoma Translational Research Laboratory, Barcelona-Clínic Liver Cancer Group Barcelona, Catalonia, Spain, Inserm, UMR-1053, Université de Bordeaux, Bordeaux, F-33076, France, Assistance Publique-Hôpitaux de Paris, Department of Digestive and Hepatobiliary Surgery, Centre hospitalier universitaire Henri Mondor, F-94000 Créteil, France, Inserm, UMR-955, F-94000 Créteil, France, Centre hospitalier universitaire de Bordeaux, Department of Hepatology, Hôpital Saint-André, Bordeaux, F-33076, France, Department of Liver Surgery and Transplant, Fondazione Istituto Tumori, via Venezian 1, 20133 Milan, Italy, Icahn School of Medicine at Mount Sinai [New York] (MSSM), Assistance Publique Hôpitaux de Paris, Hôpitaux Universitaires Paris – Seine Saint-Denis, Site Jean Verdier, Pôle d’Activité Cancérologique Spécialisée, Service d’Hépatologie, F-93143 Bondy, France, Centre hospitalier universitaire de Bordeaux, Pellegrin Hospital, Department of Pathology, Bordeaux, F-33076, France, Institució Catalana de Recerca i Estudis Avançats (ICREA), Assistance Publique-Hôpitaux de Paris, Hopital Europeen Georges Pompidou, F-75015 Paris, France, Schulze, Kornelius, Université Paris 13 (UP13) - Université Paris Diderot - Paris 7 (UPD7) - Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM), Cancer Genome Project, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, United Kingdom, Mount Sinai Liver Cancer Program (Division of Liver Diseases), Mount Sinai School of Medicine, New York, USA, and Institució Catalana de Recerca i Estudis Avançats, Barcelona. Catalonia, Spain

Subjects
Male, Carcinoma, Hepatocellular, Lactams, Macrocyclic, medicine.medical_treatment, DNA Mutational Analysis, Antineoplastic Agents, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.GEN] Life Sciences [q-bio]/Genetics, Biology, medicine.disease_cause, Bioinformatics, Article, Targeted therapy, [SDV.CAN] Life Sciences [q-bio]/Cancer, Risk Factors, CDKN2A, Cell Line, Tumor, Benzoquinones, NAD(P)H Dehydrogenase (Quinone), Genetics, medicine, Humans, Exome, HSP90 Heat-Shock Proteins, Molecular Targeted Therapy, Genetic Association Studies, Exome sequencing, ComputingMilieux_MISCELLANEOUS, Aged, Sequence Deletion, Hepatitis B virus, [SDV.GEN]Life Sciences [q-bio]/Genetics, [SDV.BIBS] Life Sciences [q-bio]/Quantitative Methods [q-bio.QM], Liver Neoplasms, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, medicine.disease, [SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM], [SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, 3. Good health, Hepatocellular carcinoma, Cancer research, Female, Liver cancer
Abstract

Genomic analyses promise to improve tumor characterization to optimize personalized treatment for patients with hepatocellular carcinoma (HCC). Exome sequencing analysis of 243 liver tumors identified mutational signatures associated with specific risk factors, mainly combined alcohol and tobacco consumption and exposure to aflatoxin B1. We identified 161 putative driver genes associated with 11 recurrently altered pathways. Associations of mutations defined 3 groups of genes related to risk factors and centered on CTNNB1 (alcohol), TP53 (hepatitis B virus, HBV) and AXIN1. Analyses according to tumor stage progression identified TERT promoter mutation as an early event, whereas FGF3, FGF4, FGF19 or CCND1 amplification and TP53 and CDKN2A alterations appeared at more advanced stages in aggressive tumors. In 28% of the tumors, we identified genetic alterations potentially targetable by US Food and Drug Administration (FDA)-approved drugs. In conclusion, we identified risk factor-specific mutational signatures and defined the extensive landscape of altered genes and pathways in HCC, which will be useful to design clinical trials for targeted therapy.

Published
2015
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