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4 results on '"Fabien Petel"'

1. Molecular Classification of Malignant Pleural Mesothelioma: Identification of a Poor Prognosis Subgroup Linked to the Epithelial-to-Mesenchymal Transition

Author

Jessica Zucman-Rossi, Fabien Petel, Gabrielle Couchy, Paul Hofman, Pascal Andujar, Marie-Christine Copin, Aurélie Cazes, Aurélien de Reyniès, Marie-Claude Jaurand, Françoise Galateau-Sallé, Sandrine Imbeaud, Jean-Claude Pairon, Annie Renier, Didier Jean, Françoise Le Pimpec-Barthes, Nabila Elarouci, Ilir Hysi, Jean, Didier, Ligue Nationale Contre le Cancer - Paris, Ligue Nationale Contre le Cancer (LNCC), (le programme) Cartes d'identité des tumeurs (CIT), Ligue Nationales Contre le Cancer (LNCC), Génomique fonctionnelle des tumeurs solides (U674), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Laboratoire d'Anatomie Pathologique [CHU Caen], Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN), Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Angiogénèse embryonnaire et pathologique, Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Labex MemoLife, Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Ligue Nationnale Contre le Cancer, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7), Centre interdisciplinaire de recherche en biologie (CIRB), École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Labex MemoLife, and Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)

Subjects
Male, Mesothelioma, Cancer Research, Pathology, Lung Neoplasms, Microarray, Gene mutation, [SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, 0302 clinical medicine, CDKN2A, CDKN2B, Tumor Cells, Cultured, Cluster Analysis, MESH: Aged, 0303 health sciences, BAP1, MESH: Middle Aged, MESH: Neoplasm Staging, Middle Aged, Prognosis, 3. Good health, Oncology, 030220 oncology & carcinogenesis, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Female, MESH: Biomarkers, Tumor, Ubiquitin Thiolesterase, medicine.medical_specialty, Epithelial-Mesenchymal Transition, MESH: Mutation, Pleural Neoplasms, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, [SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics, MESH: Pleural Neoplasms, MESH: Prognosis, 03 medical and health sciences, MESH: Gene Expression Profiling, [SDV.CAN] Life Sciences [q-bio]/Cancer, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Biomarkers, Tumor, medicine, Humans, MESH: Tumor Suppressor Proteins, MESH: Tumor Cells, Cultured, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, Aged, Neoplasm Staging, 030304 developmental biology, MESH: Humans, MESH: Mesothelioma, Gene Expression Profiling, Tumor Suppressor Proteins, Mesothelioma, Malignant, Cancer, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, MESH: Ubiquitin Thiolesterase, medicine.disease, MESH: Cluster Analysis, MESH: Male, MESH: Lung Neoplasms, Gene expression profiling, MESH: Epithelial-Mesenchymal Transition, [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, Mutation, Cancer research, MESH: Female
Abstract

Purpose: Despite research efforts to develop more effective diagnostic and therapeutic approaches, malignant pleural mesothelioma (MPM) prognosis remains poor. The assessment of tumor response to therapy can be improved by a deeper phenotypical classification of the tumor, with emphasis on its clinico-biological heterogeneity. The identification of molecular profiles is a powerful approach to better define MPM subclasses and targeted therapies. Experimental Design: Molecular subclasses were defined by transcriptomic microarray on 38 primary MPM cultures. A three-gene predictor, identified by quantitative reverse transcription PCR, was used to classify an independent series of 108 frozen tumor samples. Gene mutations were determined in BAP1, CDKN2A, CDKN2B, NF2, and TP53. Epithelial-to-mesenchymal transition (EMT) markers were studied at the mRNA and protein levels. Results: Unsupervised hierarchical clustering on transcriptomic data defined two robust MPM subgroups (C1 and C2), closely related to prognosis and partly to histologic subtypes. All sarcomatoid/desmoplastic MPM were included in the C2 subgroup. Epithelioid MPM were found in both subgroups, with a worse survival prognosis in the C2 subgroup. This classification and its association with histologic subtypes and survival were validated in our independent series using the three-gene predictor. Similar subgroups were found after classification of other MPM series from transcriptomic public datasets. C1 subgroup exhibited more frequent BAP1 alterations. Pathway analysis revealed that EMT was differentially regulated between MPM subgroups. C2 subgroup is characterized by a mesenchymal phenotype. Conclusions: A robust classification of MPM that defines two subgroups of epithelioid MPM, characterized by different molecular profiles, gene alterations, and survival outcomes, was established. Clin Cancer Res; 20(5); 1323–34. ©2014 AACR.

Published
2014
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2. Comparison of the latest commercial short and long oligonucleotide microarray technologies

Author

Daniela Geromin, Jean-Michel Cayuela, Aurélien de Reyniès, David S. Rickman, Fabien Petel, François Sigaux, and Philippe Dessen

Subjects
Genetics, Reproducibility, lcsh:QH426-470, Microarray, lcsh:Biotechnology, Gene Expression Profiling, Reproducibility of Results, Context (language use), Computational biology, Biology, Polymerase Chain Reaction, Gene expression profiling, Gene Expression Regulation, Neoplastic, lcsh:Genetics, Oligonucleotide Microarray, lcsh:TP248.13-248.65, Cell Line, Tumor, Cluster Analysis, Humans, Relative precision, DNA microarray, Biotechnology, Oligonucleotide Array Sequence Analysis, Research Article
Abstract

BackgroundWe compared the relative precision and accuracy of expression measurements obtained from three different state-of-the-art commercial short and long-oligonucleotide microarray platforms (Affymetrix GeneChip™, GE Healthcare CodeLink™ and Agilent Technologies). The design of the comparison was chosen to judge each platform in the context of a multi-project program.ResultsAll wet-lab experiments and raw data acquisitions were performed independently by each commercial platform. Intra-platform reproducibility was assessed using measurements from all available targets. Inter-platform comparisons of relative signal intensities were based on a common and non-redundant set of roughly 3,400 targets chosen for their unique correspondence toward a single transcript. Despite many examples of strong similarities we found several areas of discrepancy between the different platforms.ConclusionWe found a higher level of reproducibility from one-color based microarrays (Affymetrix and CodeLink) compared to the two-color arrays from Agilent. Overall, Affymetrix data had a slightly higher level of concordance with sample-matched real-time quantitative reverse-transcriptase polymerase chain reaction (QRT-PCR) data particularly for detecting small changes in gene expression levels.

Published
2005

3. Transcriptome classification of HCC is related to gene alterations and to new therapeutic targets

Author

Boyault, Sandrine, Rickman, David, de Reyniès, Aurélien, Balabaud, Charles, Rebouissou, Sandra, Jeannot, Emmanuelle, Hérault, Aurélie, Saric, Jean, Belghiti, Jacques, Franco, Dominique, Bioulac-Sage, Paulette, Laurent-Puig, Pierre, Zucman-Rossi, Jessica, 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), Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7), Département de Bioinformatique, Ligue Nationale Contre le Cancer (LNCC), Fibrose hépatique et cancer du foie, Université Bordeaux Segalen - Bordeaux 2-IFR66-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'Hépato-Gastro-Entérologie, CHU Bordeaux [Bordeaux]-Hôpital Saint-André, Service de chirurgie digestive, Service de chirurgie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Beaujon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre de chirurgie ambulatoire [Béclère], Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Antoine Béclère [Clamart], Laboratoire d'anatomie pathologique, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Bases moléculaires de la réponse aux xénobiotiques (U775 (IFR95)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), We warmly thank Jacqueline Godet, François Sigaux and Philippe Dessen managers of the Carte d'Identité des Tumeurs (CIT) program founded by the Ligue Nationale contre le Cancer, Daniela Geromin, Christelle Thibault, Patricia Legoix, Damien Gerald, Olivier Bluteau, for their experimental help, Fabien Petel for his help in the submission of the data to EBI, Philippe Bois for critical reading of the manuscript. We thank the technicians from the CEPH, Fondation Jean Dausset for their help in sequencing and all the clinicians that referred the patients. This work was supported by the Ligue Nationale Contre le Cancer and the Fondation de France. SB, SR and EJ are supported by a Fondation de France, a Ligue Nationale Contre le Cancer and a Association pour la Recherche sur le Cancer grant fellowship, respectively., and Zucman-Rossi, Jessica

Subjects
MESH: Mutation, MESH: DNA, Neoplasm, [SDV.CAN]Life Sciences [q-bio]/Cancer, ß-catenin, MESH: Cell Cycle Proteins, [SDV.CAN] Life Sciences [q-bio]/Cancer, MESH: Liver Neoplasms, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], HBV, tumor suppressor gene, MESH: Carcinoma, Hepatocellular, neoplasms, MESH: Genes, Neoplasm, MESH: Adenoma, MESH: Middle Aged, MESH: Humans, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, MESH: 1-Phosphatidylinositol 3-Kinase, MESH: Gene Expression Regulation, Neoplastic, digestive system diseases, MESH: Male, [SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, AKT pathway, MESH: Multigene Family, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], microarray, MESH: Female, MESH: Nuclear Pore
Abstract

Hepatocellular carcinomas (HCCs) are a heterogeneous group of tumors that differ in risk factors and genetic alterations. We further investigated transcriptome-genotype-phenotype correlations in HCC. Global transcriptome analyses were performed on 57 HCCs and 3 hepatocellular adenomas and validated by quantitative RT-PCR using 63 additional HCCs. We determined loss of heterozygosity, gene mutations, promoter methylation of CDH1 and CDKN2A, and HBV DNA copy number for each tumor. Unsupervised transcriptome analysis identified 6 robust subgroups of HCC (G1-G6) associated with clinical and genetic characteristics. G1 tumors were associated with low copy number of HBV and overexpression of genes expressed in fetal liver and controlled by parental imprinting. G2 included HCCs infected with a high copy number of HBV and mutations in PIK3CA and TP53. In these first groups, we detected specific activation of the AKT pathway. G3 tumors were typified by mutation of TP53 and overexpression of genes controlling the cell cycle. G4 was a heterogeneous subgroup of tumors including TCF1-mutated hepatocellular adenomas and carcinomas. G5 and G6 were strongly related to beta-catenin mutations that lead to Wnt pathway activation; in particular, G6 tumors were characterized by satellite nodules, higher activation of the Wnt pathway, and E-cadherin underexpression. CONCLUSION: These results have furthered our understanding of the genetic diversity of human HCC and have provided specific identifiers for classifying tumors. In addition, our classification has potential therapeutic implications because 50% of the tumors were related to WNT or AKT pathway activation, which potentially could be targeted by specific inhibiting therapies.

Published
2007
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4. Transcriptome classification of HCC is related to gene alterations and to new therapeutic targets.: Transcriptome and HCC classification

Author

Boyault, Sandrine, Rickman, David, De Reyniès, Aurélien, Balabaud, Charles, Rebouissou, Sandra, Jeannot, Emmanuelle, Hérault, Aurélie, Saric, Jean, Belghiti, Jacques, Franco, Dominique, Bioulac-Sage, Paulette, Laurent-Puig, Pierre, Zucman-Rossi, Jessica, 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), Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7), Département de Bioinformatique, Ligue Nationale Contre le Cancer, Fibrose hépatique et cancer du foie, Université Bordeaux Segalen - Bordeaux 2-IFR66-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'Hépato-Gastro-Entérologie, CHU Bordeaux [Bordeaux]-Hôpital Saint-André, Service de chirurgie digestive, Service de chirurgie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Beaujon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre de chirurgie ambulatoire [Béclère], Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Antoine Béclère [Clamart], Laboratoire d'anatomie pathologique, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Bases moléculaires de la réponse aux xénobiotiques (U775 (IFR95)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), We warmly thank Jacqueline Godet, François Sigaux and Philippe Dessen managers of the Carte d'Identité des Tumeurs (CIT) program founded by the Ligue Nationale contre le Cancer, Daniela Geromin, Christelle Thibault, Patricia Legoix, Damien Gerald, Olivier Bluteau, for their experimental help, Fabien Petel for his help in the submission of the data to EBI, Philippe Bois for critical reading of the manuscript. We thank the technicians from the CEPH, Fondation Jean Dausset for their help in sequencing and all the clinicians that referred the patients. This work was supported by the Ligue Nationale Contre le Cancer and the Fondation de France. SB, SR and EJ are supported by a Fondation de France, a Ligue Nationale Contre le Cancer and a Association pour la Recherche sur le Cancer grant fellowship, respectively., Genomique Fonctionnelle des Tumeurs Solides, Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Paris Descartes - Paris 5 ( UPD5 ) -IFR105-Université Paris Diderot - Paris 7 ( UPD7 ), Institut Universitaire d'Hématologie ( IUH ), Université Paris Diderot - Paris 7 ( UPD7 ), Université Bordeaux Segalen - Bordeaux 2-IFR66-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Beaujon, Université Paris-Sud - Paris 11 ( UP11 ) -Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Antoine Béclère, Bases moléculaires de la réponse aux xénobiotiques ( U775 (IFR95) ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), AP-HP - Hôpital Antoine Béclère [Clamart], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)

Subjects
MESH : Carcinoma, Hepatocellular, MESH : Liver Neoplasms, MESH: Mutation, MESH : Gene Expression Regulation, Neoplastic, MESH : Male, MESH : Multigene Family, MESH: DNA, Neoplasm, MESH : Genes, Neoplasm, [SDV.CAN]Life Sciences [q-bio]/Cancer, ß-catenin, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, MESH : Cell Cycle Proteins, MESH: Cell Cycle Proteins, MESH: Liver Neoplasms, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], MESH : 1-Phosphatidylinositol 3-Kinase, HBV, MESH : Middle Aged, MESH : Female, tumor suppressor gene, MESH: Carcinoma, Hepatocellular, neoplasms, MESH: Genes, Neoplasm, MESH: Adenoma, MESH: Middle Aged, MESH: Humans, MESH : Humans, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, MESH: 1-Phosphatidylinositol 3-Kinase, MESH: Gene Expression Regulation, Neoplastic, digestive system diseases, MESH: Male, AKT pathway, MESH : Adenoma, MESH : Nuclear Pore, [ SDV.BBM.GTP ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], MESH: Multigene Family, [ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, MESH : DNA, Neoplasm, MESH : Mutation, microarray, MESH: Female, MESH: Nuclear Pore
Abstract

Hepatocellular carcinomas (HCCs) are a heterogeneous group of tumors that differ in risk factors and genetic alterations. We further investigated transcriptome-genotype-phenotype correlations in HCC. Global transcriptome analyses were performed on 57 HCCs and 3 hepatocellular adenomas and validated by quantitative RT-PCR using 63 additional HCCs. We determined loss of heterozygosity, gene mutations, promoter methylation of CDH1 and CDKN2A, and HBV DNA copy number for each tumor. Unsupervised transcriptome analysis identified 6 robust subgroups of HCC (G1-G6) associated with clinical and genetic characteristics. G1 tumors were associated with low copy number of HBV and overexpression of genes expressed in fetal liver and controlled by parental imprinting. G2 included HCCs infected with a high copy number of HBV and mutations in PIK3CA and TP53. In these first groups, we detected specific activation of the AKT pathway. G3 tumors were typified by mutation of TP53 and overexpression of genes controlling the cell cycle. G4 was a heterogeneous subgroup of tumors including TCF1-mutated hepatocellular adenomas and carcinomas. G5 and G6 were strongly related to beta-catenin mutations that lead to Wnt pathway activation; in particular, G6 tumors were characterized by satellite nodules, higher activation of the Wnt pathway, and E-cadherin underexpression. CONCLUSION: These results have furthered our understanding of the genetic diversity of human HCC and have provided specific identifiers for classifying tumors. In addition, our classification has potential therapeutic implications because 50% of the tumors were related to WNT or AKT pathway activation, which potentially could be targeted by specific inhibiting therapies.

Published
2007
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