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7 results on '"Laurie Tonon"'

1. The NF-κB RelA transcription factor is not required for CD8+ T-cell function in acute viral infection and cancer

Author

Allison Voisin, Maud Plaschka, Marlène Perrin-Niquet, Julie Twardowski, Insaf Boutemine, Baptiste Eluard, Guilhem Lalle, Pierre Stéphan, Khaled Bouherrou, Laurie Tonon, Roxane Pommier, Anthony Ferrari, Ulf Klein, Mélanie Wencker, Véronique Baud, Philippe A. Cassier, and Yenkel Grinberg-Bleyer

Subjects
CD8 + T cells, NF-KappaB, cancer, immunotherapy, LCMV, Immunologic diseases. Allergy, RC581-607
Abstract

CD8+ T cells are critical mediators of pathogen clearance and anti-tumor immunity. Although signaling pathways leading to the activation of NF-κB transcription factors have crucial functions in the regulation of immune responses, the CD8+ T cell-autonomous roles of the different NF-κB subunits, are still unresolved. Here, we investigated the function of the ubiquitously expressed transcription factor RelA in CD8+ T-cell biology using a novel mouse model and gene-edited human cells. We found that CD8+ T cell-specific ablation of RelA markedly altered the transcriptome of ex vivo stimulated cells, but maintained the proliferative capacity of both mouse and human cells. In contrast, in vivo experiments showed that RelA deficiency did not affect the CD8+ T-cell response to acute viral infection or transplanted tumors. Our data suggest that in CD8+ T cells, RelA is dispensable for their protective activity in pathological contexts.

Published
2024
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2. CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity

Author

Maha Siouda, Audrey D. Dujardin, Laetitia Barbollat-Boutrand, Marco A. Mendoza-Parra, Benjamin Gibert, Maria Ouzounova, Jebrane Bouaoud, Laurie Tonon, Marie Robert, Jean-Philippe Foy, Vincent Lavergne, Serge N. Manie, Alain Viari, Alain Puisieux, Gabriel Ichim, Hinrich Gronemeyer, Pierre Saintigny, and Peter Mulligan

Subjects
Molecular Mechanism of Gene Regulation, Stem Cells Research, Functional Aspects of Cell Biology, Cancer, Science
Abstract

Summary: Epigenetic deregulation of gene transcription is central to cancer cell plasticity and malignant progression but remains poorly understood. We found that the uncharacterized epigenetic factor chromodomain on Y-like 2 (CDYL2) is commonly over-expressed in breast cancer, and that high CDYL2 levels correlate with poor prognosis. Supporting a functional role for CDYL2 in malignancy, it positively regulated breast cancer cell migration, invasion, stem-like phenotypes, and epithelial-to-mesenchymal transition. CDYL2 regulation of these plasticity-associated processes depended on signaling via p65/NF-κB and STAT3. This, in turn, was downstream of CDYL2 regulation of MIR124 gene transcription. CDYL2 co-immunoprecipitated with G9a/EHMT2 and GLP/EHMT1 and regulated the chromatin enrichment of G9a and EZH2 at MIR124 genes. We propose that CDYL2 contributes to poor prognosis in breast cancer by recruiting G9a and EZH2 to epigenetically repress MIR124 genes, thereby promoting NF-κB and STAT3 signaling, as well as downstream cancer cell plasticity and malignant progression.

Published
2020
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3. A high-risk retinoblastoma subtype with stemness features, dedifferentiated cone states and neuronal/ganglion cell gene expression

Author

André Nicolas, Céline Desbrousses, Mariona Suñol, Sylvain Baulande, Fabiana Lubieniecki, Sandrine Arrufat, David Gentien, Nanor Sirab, Eric Letouzé, Clément Hua, Simon Saule, Elodie Chapeaublanc, Paul Fréneaux, Fariba Nemati, Laurie Tonon, Claude Houdayer, Odette Mariani, Alain Viari, Magalie Larcher, Xavier Sastre-Garau, Sacha Reichman, Daniela Ottaviani, Nathalie Cassoux, Marion Gauthier-Villars, Isabelle Aerts, Céline Vallot, Guillermo Chantada, Aurélien de Reyniès, Genoveva Correa Llano, Liliana Mirabal-Ortega, Livia Lumbroso-Le Rouic, Angel M. Carcaboso, Jérôme Couturier, Dominique Stoppa-Lyonnet, Hervé Brisse, Jaume Català-Mora, Florent Dufour, Isabelle Bernard-Pierrot, François Doz, Meriem Sefta, Paula Schaiquevich, Emmanuel Barillot, Laurence Desjardins, Rosario Aschero, Nabila Elarouci, Celio Pouponnot, Tatiana Popova, F. Radvanyi, Catherine Dehainault, Jing Liu, Gabriela Lamas, Narjesse Karboul, Didier Decaudin, Alexandre Matet, Lisa Golmard, Céline Brulard, Sylvain Guibert, Guillem Pascual-Pasto, Olivier Goureau, Anne Biton, Institut Curie, CNRS, UMR144, Equipe Labellisée Ligue contre le Cancer, PSL Research University, 75005, Paris, France, Sorbonne Université (SU), Programme Cartes d'Identité des Tumeurs, Ligue Nationale Contre le Cancer, 75013, Paris, France, Equipe de recherche européenne en algorithmique et biologie formelle et expérimentale (ERABLE), Inria Grenoble - Rhône-Alpes, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria), Synergie Lyon Cancer-Platform of Bioinformatics-Gilles Thomas, Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Biologie Cellulaire et Cancer, Institut Curie [Paris]-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), (le programme) Cartes d'identité des tumeurs (CIT), Ligue Nationales Contre le Cancer (LNCC), Hospital Nacional de Pediatría J.P. Garrahan, Centre Léon Bérard [Lyon], Département de Biologie des Tumeurs, Institut Curie [Paris], Institut de la Vision, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Cancer et génome: Bioinformatique, biostatistiques et épidémiologie d'un système complexe, Mines Paris - PSL (École nationale supérieure des mines de Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Hub Bioinformatique et Biostatistique - Bioinformatics and Biostatistics HUB, Institut Pasteur [Paris] (IP)-Université Paris Cité (UPCité), Centre de Bioinformatique, Biostatistique et Biologie Intégrative (C3BI), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Signalisation, radiobiologie et cancer, Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Imagerie et cerveau (iBrain - Inserm U1253 - UNIV Tours ), Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Bretonneau, Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Unité de génétique et biologie des cancers (U830), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Département de Recherche Translationnelle, Centre de recherche de l'Institut Curie [Paris], Genomics Consulting (GeCo), Institut de Recerca Pediàtrica Hospital Sant Joan de Déu [Barcelona, Spain], Hospital Sant Joan de Déu [Barcelona], Consejo Nacional de Investigaciones Científicas y Técnicas [Buenos Aires] (CONICET), CHU Rouen, Normandie Université (NU), Département d'Imagerie Médicale [Institut Curie], Génomique fonctionnelle des tumeurs solides = Functional Genomics of Solid Tumors [CRC] (FunGeST), 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)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), CHI Créteil, École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité)-École pratique des hautes études (EPHE), and Pouponnot, Celio

Subjects
Male, Retinal Ganglion Cells, genetic structures, Cell, Gene Expression, General Physics and Astronomy, Stem cell marker, Metastasis, Transcriptome, 0302 clinical medicine, Neoplasm Metastasis, Cancer genetics, N-Myc Proto-Oncogene Protein, 0303 health sciences, Multidisciplinary, Retinoblastoma, 3. Good health, medicine.anatomical_structure, Child, Preschool, 030220 oncology & carcinogenesis, Retinal Cone Photoreceptor Cells, Female, Science, Retinal Neoplasms, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, Malignancy, Article, General Biochemistry, Genetics and Molecular Biology, Eye cancer, Paediatric cancer, Genetic Heterogeneity, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, Biomarkers, Tumor, medicine, Humans, Transcriptomics, Data mining, 030304 developmental biology, Retina, Infant, Cancer, General Chemistry, Cell Dedifferentiation, DNA Methylation, medicine.disease, eye diseases, Mutation, Cancer research, sense organs
Abstract

Retinoblastoma is the most frequent intraocular malignancy in children, originating from a maturing cone precursor in the developing retina. Little is known on the molecular basis underlying the biological and clinical behavior of this cancer. Here, using multi-omics data, we demonstrate the existence of two retinoblastoma subtypes. Subtype 1, of earlier onset, includes most of the heritable forms. It harbors few genetic alterations other than the initiating RB1 inactivation and corresponds to differentiated tumors expressing mature cone markers. By contrast, subtype 2 tumors harbor frequent recurrent genetic alterations including MYCN-amplification. They express markers of less differentiated cone together with neuronal/ganglion cell markers with marked inter- and intra-tumor heterogeneity. The cone dedifferentiation in subtype 2 is associated with stemness features including low immune and interferon response, E2F and MYC/MYCN activation and a higher propensity for metastasis. The recognition of these two subtypes, one maintaining a cone-differentiated state, and the other, more aggressive, associated with cone dedifferentiation and expression of neuronal markers, opens up important biological and clinical perspectives for retinoblastomas., Retinoblastoma is the most frequent intraocular paediatric malignancy whose molecular basis remains poorly understood. Here, the authors perform multi-omic analysis and identify two subtypes; one in a cone differentiated state and one more aggressive showing cone dedifferentiation and expressing neuronal markers.

Published
2021
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4. Neoepitopes-based vaccines: challenges and perspectives

Author

Sandrine Wittmann, Stéphane Depil, Paola Bonaventura, Laurie Tonon, Vincent Alcazer, Christophe Caux, Université Claude Bernard Lyon 1 (UCBL), Université de Lyon, Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), and Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
0301 basic medicine, CD4-Positive T-Lymphocytes, Cancer Research, medicine.medical_treatment, [SDV]Life Sciences [q-bio], T-Lymphocytes, Programmed Cell Death 1 Receptor, Context (language use), Human leukocyte antigen, Cancer Vaccines, Epitope, B7-H1 Antigen, 03 medical and health sciences, Epitopes, 0302 clinical medicine, Antigen, Antigens, Neoplasm, HLA Antigens, Neoplasms, Medicine, Humans, Precision Medicine, business.industry, Histocompatibility Antigens Class I, Cancer, medicine.disease, Acquired immune system, 3. Good health, Vaccination, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, Immunology, Mutation, business, Adjuvant
Abstract

First generations of cancer vaccines using shared tumour antigens have been associated with disappointing clinical results. However, the paradigm shift introduced by immune checkpoint inhibitors has led to a renewed interest on anti-tumoural vaccination based on mutation-associated neoantigens. First clinical results are encouraging with some signs of clinical activity associated with induction of a specific immune response. In advanced or metastatic diseases, vaccination may either enhance the response to Programmed cell death 1 (PD-1/-L1) antagonists by increasing the number of effectors within the tumour or induce an anti-tumoural T-cell response in immunologically 'cold' tumours. There is also a strong rationale to use cancer vaccines in an adjuvant setting to induce a long-term control of the residual disease. Prediction of neoepitopes efficiently presented by Human Leukocyte Antigen (HLA) molecules remains a challenge, as well as identification of clonal neoantigens. Some mechanisms of resistance are already identified, such as tumour loss of neoepitopes-presenting HLA class I molecules. In this context, the role of CD4+ T cells induced by different cancer vaccines should be clarified. Finally, although studies have focused on mutated epitopes corresponding to single nucleotide variants, other neoantigens could be of strong interest such as those linked to tumour specific RNA-splicing abnormalities or associated with insertions-deletions.

Published
2018
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5. Abstract P6-07-13: New insights on HER2 amplification from the constitutional and somatic standpoints: Results from the ICGC and SIGNAL/Phare studies

Author

Pierre Saintigny, Gaëtan MacGrogan, D Birbaum, Xavier Pivot, V Letexier, G Romieux, Laurent Arnould, Alain Viari, Anne Vincent-Salomon, Iris Pauporté, S Boyault, A Ferrari, A-S Sertier, David Cox, Isabelle Treilleux, Janice Kielbassa, Emilie Thomas, and Laurie Tonon

Subjects
Genetics, Whole genome sequencing, Cancer Research, Genetic heterogeneity, Cancer, Genome-wide association study, Amplicon, Biology, medicine.disease_cause, medicine.disease, Genome, Breast cancer, Oncology, medicine, skin and connective tissue diseases, Carcinogenesis
Abstract

Background: HER2-positive (HER2+) breast cancers are defined by the amplification and/or overexpression of the human epidermal growth factor receptor (HER2/ERBB2) gene on chromosome region 17q12. Although anti-HER2 targeted therapies have greatly improved treatment of HER2+ breast cancer, the magnitude of benefit varies widely between patients. Deciphering the genomic and genetic heterogeneity of HER2+ breast cancer may provide a basis to better understand their natural history, opening new avenues of treatment. Methods: As part of the ICGC Breast Cancer Working Group effort, we combined whole genome sequencing and transcriptomic analyses of 64 HER2+ primary invasive carcinomas, and a genome wide association study (GWAS) of over 9.836 breast cancer patients in the prospective SIGNAL/PHARE cohort (NCT00381901 – RECF1098). Results: Using WGS data we precisely delineate the ERBB2 amplicon as a 106 kb region involving six genes and show that the amplification mechanism was consistent with breakage-fusion-bridge (BFB) cycles. Four RNA expression-based groups were identified, displaying specific genomic alterations in terms of amplification, rearrangements and mutations. On other hand, GWAS analyses failed to identify any constitutional variants associated with HER2 amplification. Discussion: By combining whole genome sequencing and expression analysis, we provide evidence showing that HER2+ tumours display considerably more molecular heterogeneity than previously reported. These results are reinforced with the lack of association between any genetic variants and HER2 amplification from GWAS analyses. Taken as a whole, these results suggest that HER2+ breast cancers do not represent per se a homogeneous subtype, but are distributed along the whole breast cancer spectrum, from ER-positive luminal to ER-negative basal phenotype. Genome alterations present in HER2+ tumors are in accordance with these phenotypes, and it is likely that the HER2 amplification is a secondary event in the course of tumorigenesis, not favored by any particular constitutional or somatic genetic variants. Citation Format: Vincent-Salomon A, Ferrari A, Pivot X, Macgrogan G, Arnould L, Treilleux I, Romieux G, Sertier A-S, Thomas E, Tonon L, Boyault S, Kielbassa J, Letexier V, Pauporte I, Birbaum D, Saintigny P, Cox D, Viari A. New insights on HER2 amplification from the constitutional and somatic standpoints: Results from the ICGC and SIGNAL/Phare studies. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P6-07-13.

Published
2016
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6. A Comprehensive Assessment of Somatic Mutation Calling in Cancer Genomes

Author

Marc Dabad, John Douglas Mcpherson, Xose S. Puente, Liu Xi, Ivo Gut, Anne-Marie Patch, Semin Lee, Cyriac Kandoth, Ruben M. Drews, Charlotte Anderson, Eivind Hovig, Paul C. Boutros, Peter J. Campbell, Louis Letourneau, Paolo Ribeca, Hidewaki Nakagawa, Natalie Jäger, Daniel Vodak, Thomas J. Hudson, Anne Sophie Sertier, Pablo H. Hennings-Yeomans, John Zhang, Philip Ginsbach, Laurie Tonon, Emanuele Raineri, Sahil Seth, Sophia Derdak, Benedikt Brors, David T. W. Jones, Minghui He, Sergi Beltran, Rafael Valdés-Mas, David Torrents, Singer Ma, Myron Peto, Nagarajan Paramasivam, Matthew D. Eldridge, Robert E. Denroche, Paul T. Spellman, Francesc Castro Giner, Roland Eils, Timothy Beck, Sigve Nakken, Daniela S. Gerhard, Lawrence E. Heisler, Jared T. Simpson, Víctor Quesada, Rolf Kabbe, Andy G. Lynch, Patrick S. Tarpey, Lawrence Bower, Akihiro Fujimoto, Barbara Hutter, Matthias Schlesner, Marta Gut, Ivo Buchhalter, David A. Wheeler, Takafumi N. Yamaguchi, Simon Heath, Nicholas J. Harding, and Tyler Alioto

Subjects
Genetics, Whole genome sequencing, 0303 health sciences, Concordance, Cancer, Genomics, Computational biology, Biology, medicine.disease, Genome, DNA sequencing, 03 medical and health sciences, 0302 clinical medicine, Germline mutation, 030220 oncology & carcinogenesis, Mutation (genetic algorithm), medicine, 030304 developmental biology
Abstract

The emergence of next generation DNA sequencing technology is enabling high-resolution cancer genome analysis. Large-scale projects like the International Cancer Genome Consortium (ICGC) are systematically scanning cancer genomes to identify recurrent somatic mutations. Second generation DNA sequencing, however, is still an evolving technology and procedures, both experimental and analytical, are constantly changing. Thus the research community is still defining a set of best practices for cancer genome data analysis, with no single protocol emerging to fulfil this role. Here we describe an extensive benchmark exercise to identify and resolve issues of somatic mutation calling. Whole genome sequence datasets comprising tumor-normal pairs from two different types of cancer, chronic lymphocytic leukaemia and medulloblastoma, were shared within the ICGC and submissions of somatic mutation calls were compared to verified mutations and to each other. Varying strategies to call mutations, incomplete awareness of sources of artefacts, and even lack of agreement on what constitutes an artefact or real mutation manifested in widely varying mutation call rates and somewhat low concordance among submissions. We conclude that somatic mutation calling remains an unsolved problem. However, we have identified many issues that are easy to remedy that are presented here. Our study highlights critical issues that need to be addressed before this valuable technology can be routinely used to inform clinical decision-making.

Published
2014
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7. A comprehensive assessment of somatic mutation detection in cancer using whole-genome sequencing

Author

Matthew D. Eldridge, Sasithorn Chotewutmontri, Susanne Gröbner, Eivind Hovig, Ivo Gut, Minghui He, Hidewaki Nakagawa, Charlotte Anderson, Rafael Valdés-Mas, Lars Feuerbach, Sergi Beltran, Adam Butler, Nagarajan Paramasivam, John Douglas Mcpherson, Akihiro Fujimoto, Ann-Marie Patch, Ivo Buchhalter, Laurie Tonon, Stefan M. Pfister, Víctor Quesada, Jon W. Teague, Sabine Schmidt, David T. W. Jones, Sahil Seth, David Torrents, Singer Ma, Marta Gut, Semin Lee, Robert E. Denroche, Carlos López-Otín, Andy G. Lynch, David A. Wheeler, Takafumi N. Yamaguchi, Lucy Stebbings, Ruben M. Drews, Roland Eils, Marc Dabad, Tyler Alioto, Barbara Hutter, Rebecca Shepherd, Peter Lichter, Sigve Nakken, Daniel Vodak, Simon Heath, Rolf Kabbe, Christopher Previti, Paul T. Spellman, Nicola Waddell, Jared T. Simpson, John V. Pearson, Timothy Beck, Patrick S. Tarpey, Daniela S. Gerhard, Andrew Menzies, Francesc Castro Giner, Paolo Ribeca, Nicholas J. Harding, Liu Xi, Nicolle Diessl, Emanuele Raineri, Lawrence E. Heisler, Jonathan Hinton, Xose S. Puente, Cyriac Kandoth, Natalie Jäger, David T. Jones, Matthias Schlesner, Louis Letourneau, Sean M. Grimmond, Elias Campo, Peter J. Campbell, Keiran Raine, Lawrence Bower, Michael Heinold, Andrey Korshunov, Thomas J. Hudson, Anne Sophie Sertier, Benedikt Brors, Sophia Derdak, Paul C. Boutros, Myron Peto, John Zhang, Philip Ginsbach, Alioto, Tyler S [0000-0002-2960-5420], Buchhalter, Ivo [0000-0003-0764-5832], Hutter, Barbara [0000-0002-9034-0329], Hovig, Eivind [0000-0002-9103-1077], Patch, Ann-Marie [0000-0001-6121-4019], Drews, Ruben [0000-0001-7360-4970], Raine, Keiran [0000-0002-5634-1539], Ribeca, Paolo [0000-0001-5599-3933], Giner, Francesc Castro [0000-0001-6111-0754], Heath, Simon C [0000-0002-9550-0897], Denroche, Robert E [0000-0003-2197-7083], Yamaguchi, Takafumi N [0000-0003-1082-3871], Seth, Sahil [0000-0003-4579-3959], Boutros, Paul C [0000-0003-0553-7520], Hudson, Thomas J [0000-0002-1376-4849], Gut, Ivo G [0000-0001-7219-632X], Apollo - University of Cambridge Repository, Universitat de Barcelona, University of St Andrews. School of Medicine, and University of St Andrews. Statistics

Subjects
Cancer genome sequencing, General Physics and Astronomy, Genome informatics, Lymphoid, Genètica mèdica, Human genetics, 2.1 Biological and endogenous factors, DNA sequencing, Aetiology, Càncer, Cancer genetics, Exome, Cancer, Genetics, Multidisciplinary, Genome, Leukemia, Genètica humana, Medical genetics, High-Throughput Nucleotide Sequencing, 3. Good health, Mutation (genetic algorithm), Personal genomics, Human, Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC], Ciències de la salut::Medicina [Àrees temàtiques de la UPC], Bioinformatics, Context (language use), QH426 Genetics, Biology, Article, General Biochemistry, Genetics and Molecular Biology, Deep sequencing, RC0254, SDG 3 - Good Health and Well-being, Bioinformàtica, Humans, ddc:610, QH426, Whole genome sequencing, RC0254 Neoplasms. Tumors. Oncology (including Cancer), Genome, Human, Prevention, Human Genome, Mutació (Biologia), DAS, General Chemistry, Mutation (Biology), Leukemia, Lymphoid, Mutation, Medulloblastoma
Abstract

Financial support was provided by the consortium projects READNA under grant agreement FP7 Health-F4- 2008-201418, ESGI under grant agreement 262055, GEUVADIS under grant agreement 261123 of the European Commission Framework Programme 7, ICGC-CLL through the Spanish Ministry of Science and Innovation (MICINN), the Instituto de Salud Carlos III(ISCIII) and the Generalitat de Catalunya, Alioto, T.S., Buchhalter, I., Derdak, S., Hutter, B., Eldridge, M.D., Hovig, E., Heisler, L.E., Beck, T.A., Simpson, J.T., Tonon, L., Sertier, A.-S., Patch, A.-M., Jäger, N., Ginsbach, P., Drews, R., Paramasivam, N., Kabbe, R., Chotewutmontri, S., Diessl, N., Previti, C., Schmidt, S., Brors, B., Feuerbach, L., Heinold, M., Gröbner, S., Korshunov, A., Tarpey, P.S., Butler, A.P., Hinton, J., Jones, D., Menzies, A., Raine, K., Shepherd, R., Stebbings, L., Teague, J.W., Ribeca, P., Giner, F.C., Beltran, S., Raineri, E., Dabad, M., Heath, S.C., Gut, M., Denroche, R.E., Harding, N.J., Yamaguchi, T.N., Fujimoto, A., Nakagawa, H., Quesada, V., Valdés-Mas, R., Nakken, S., Vodák, D., Bower, L., Lynch, A.G., Anderson, C.L., Waddell, N., Pearson, J.V., Grimmond, S.M., Peto, M., Spellman, P., He, M., Kandoth, C., Lee, S., Zhang, J., Létourneau, L., Ma, S., Seth, S., Torrents, D., Xi, L., Wheeler, D.A., López-Otín, C., Campo, E., Campbell, P.J., Boutros, P.C., Puente, X.S., Gerhard, D.S., Pfister, S.M., McPherson, J.D., Hudson, T.J., Schlesner, M., Lichter, P., Eils, R., Jones, D.T.W., Gut, I.G.

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