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1. Full Text Hematopoietic Stem Cell Gene Therapy with a Lentiviral Vector in X-Linked Adrenoleukodystrophy
by Nathalie Cartier and Salima Hacein-Bey-Abina and Cynthia C. Bartholomae and Gabor Veres and Manfred Schmidt and Ina Kutschera and Michel Vidaud and Ulrich Abel and Liliane Dal-Cortivo and Laure Caccavelli and Nizar Mahlaoui and Véronique Kiermer and Denice Mittelstaedt and Céline Bellesme and Najiba Lahlou and François Lefrère and Stéphane Blanche and Muriel Audit and Emmanuel Payen and Philippe Leboulch and Bruno L'Homme and Pierre Bougnères and Christof Von Kalle and Alain Fischer and Marina Cavazzana-Calvo and Patrick Aubourg
Science, ISSN 0036-8075, 11/2009, Volume 326, Issue 5954, pp. 818 - 823
X-linked adrenoleukodystrophy (ALD) is a severe brain demyelinating disease in boys that is caused by a deficiency in ALD protein, an adenosine... 
Myeloid cells | Genetic vectors | Demyelinating diseases | B lymphocytes | Stem cells | Hematocrit | Cell lines | Gene therapy | Cells | Hematopoietic stem cells | Research Article | HIV VECTORS | SEVERE COMBINED IMMUNODEFICIENCY | INTEGRATION SITE SELECTION | MICROGLIA | BONE-MARROW-TRANSPLANTATION | HUMAN CD34(+) CELLS | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | NOD/SCID MICE | LONG-TERM ENGRAFTMENT | DIFFERENTIATE | Myeloablative Agonists - therapeutic use | Genetic Therapy | Leukocytes, Mononuclear - metabolism | Microglia - metabolism | Humans | Adrenoleukodystrophy - pathology | Male | Transplantation, Autologous | ATP-Binding Cassette Transporters - genetics | Hematopoiesis | Adrenoleukodystrophy - therapy | Hematopoietic Stem Cells - physiology | Female | Cell Differentiation | Fatty Acids - blood | Hematopoietic Stem Cells - virology | Child | Microglia - cytology | Gene Expression | Transduction, Genetic | Hematopoietic Stem Cell Transplantation | ATP Binding Cassette Transporter, Sub-Family D, Member 1 | HIV-1 - genetics | Virus Integration | Disease Progression | Cell Lineage | Animals | Brain - pathology | Mice | Adrenoleukodystrophy - genetics | Transplantation Conditioning | Genetic Vectors | Usage | Care and treatment | Adrenoleukodystrophy | Patient outcomes | Transplantation | Health aspects | Viruses | Genetic disorders | Neurological disorders | ABCD1 protein | Life Sciences | Cellular Biology
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2. Full Text Recurrent somatic alterations of FGFR1 and NTRK2 in pilocytic astrocytoma
by Jones, David T. W and Hutter, Barbara and Jäger, Natalie and Korshunov, Aney and Kool, Marcel and Warnatz, Hans-Jörg and Zichner, Thomas and Lambert, Sally R and Ryzhova, Marina and Quang, Dong Anh Khuong and Fontebasso, Adam M and Stütz, Aian M and Hutter, Sonja and Zuckermann, Marc and Sturm, Dominik and Gronych, Jan and Lasitschka, Bärbel and Schmidt, Sabine and Seker-Cin, Huriye and Witt, Henik and Sultan, Marc and Ralser, Meryem and Northcott, Paul A and Hovestadt, Volker and Bender, Sebastian and Pfaff, Elke and Stark, Sebastian and Faury, Damien and Schwartzentruber, Jeremy and Majewski, Jacek and Weber, Ursula D and Zapatka, Marc and Raeder, Benjamin and Schlesner, Matthias and Worth, Catherine L and Bartholomae, Cynthia C and von Kalle, Christof and Imbusch, Charles D and Radomski, Sylwester and Lawerenz, Chris and van Sluis, Peter and Koster, Jan and Volckmann, Richard and Versteeg, Rogier and Lehrach, Hans and Monoranu, Camelia and Winkler, Beate and Unterberg, Aneas and Herold-Mende, Christel and Milde, Till and Int Canc Genome Consortium and International Cancer Genome Consortium PedBrain Tumor Project and the International Cancer Genome Consortium PedBrain Tumor Project
Nature genetics, ISSN 1061-4036, 2013, Volume 45, Issue 8, pp. 927 - 932
Pilocytic astrocytoma, the most common childhood brain tumor, is typically associated with mitogen-activated protein kinase (MAPK) pathway alterations.... 
SIGNAL-TRANSDUCTION | MUTATIONAL PROCESSES | MAPK PATHWAY ACTIVATION | GROWTH | GENES | GENETICS & HEREDITY | DISTINCT SUBGROUPS | HISTONE H3.3 | PAIRED-END | CANCER | NOONAN-SYNDROME | Chromosome Breakpoints | Humans | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Receptor, trkB - genetics | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Brain Neoplasms - metabolism | MAP Kinase Signaling System | Fibroblast Growth Factors - metabolism | Oncogene Proteins, Fusion - chemistry | Cell Transformation, Neoplastic - genetics | Base Sequence | Proto-Oncogene Proteins B-raf - chemistry | Astrocytoma - genetics | Astrocytoma - metabolism | Cell Line | Brain Neoplasms - genetics | Models, Molecular | Chromosomes, Human, Pair 9 | Chromosomes, Human, Pair 6 | Cell Transformation, Neoplastic - metabolism | Animals | Oncogene Proteins, Fusion - genetics | Proto-Oncogene Proteins B-raf - genetics | Protein Conformation | Mice | Mutation | Receptor, trkB - metabolism | Nervous system cancer | Physiological aspects | Development and progression | Genetic aspects | Research | Protein kinases | Fibroblast growth factor receptors | Medical research | Pediatrics | Brain research | Brain cancer | Genomes | Kinases | Tumors | Cancer
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3. Full Text An unbiased genome-wide analysis of zinc-finger nuclease specificity
by Gabriel, Richard and Lombardo, Angelo and Arens, Anne and Miller, Jeffrey C and Genovese, Pietro and Kaeppel, Christine and Nowrouzi, Ali and Bartholomae, Cynthia C and Wang, Jianbin and Friedman, Geoffrey and Holmes, Michael C and Gregory, Philip D and Glimm, Hanno and Schmidt, Manfred and Naldini, Luigi and Von Kalle, Christof
Nature Biotechnology, ISSN 1087-0156, 09/2011, Volume 29, Issue 9, pp. 816 - 823
Zinc-finger nucleases (ZFNs) allow gene editing in live cells by inducing a targeted DNA double-strand break (DSB) at a specific genomic locus. However,... 
VECTOR INTEGRATION | DNA CLEAVAGE | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | GENE MODIFICATION | IN-VIVO | SITES | DOUBLE-STRAND BREAKS | RESTRICTION ENZYMES | KNOCKOUT | MAMMALIAN-CELLS | LENTIVIRAL VECTORS | Gene Targeting | Humans | Substrate Specificity | Genetic Loci | HIV Integrase - metabolism | DNA Breaks, Double-Stranded | Sequence Analysis, DNA | Genetic Vectors - genetics | Endodeoxyribonucleases - genetics | HIV Integrase - genetics | Endodeoxyribonucleases - metabolism | Cell Line, Tumor | Protein Binding | Lentivirus - genetics | Zinc Fingers - genetics | Binding Sites | Cluster Analysis | Physiological aspects | Nucleases | Zinc finger proteins | Research | DNA binding proteins | Analysis | Genomes | Zinc | Deoxyribonucleic acid--DNA
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4. Full Text Decoding the regulatory landscape of medulloblastoma using DNA methylation sequencing
by Hovestadt, Volker and Jones, David T. W and Picelli, Simone and Wang, Wei and Kool, Marcel and Northcott, Paul A and Sultan, Marc and Stachurski, Katharina and Ryzhova, Marina and Warnatz, Hans-Jörg and Ralser, Meryem and Brun, Sonja and Bunt, Jens and Jäger, Natalie and Kleinheinz, Kortine and Erkek, Serap and Weber, Ursula D and Bartholomae, Cynthia C and von Kalle, Christof and Lawerenz, Chris and Eils, Jürgen and Koster, Jan and Versteeg, Rogier and Milde, Till and Witt, Olaf and Schmidt, Sabine and Wolf, Stephan and Pietsch, Torsten and Rutkowski, Stefan and Scheurlen, Wolfram and Taylor, Michael D and Brors, Benedikt and Felsberg, Jörg and Reifenberger, Guido and Borkhardt, Arndt and Lehrach, Hans and Wechsler-Reya, Robert J and Eils, Roland and Yaspo, Marie-Laure and Landgraf, Pablo and Korshunov, Aney and Zapatka, Marc and Radlwimmer, Bernhard and Pfister, Stefan M and Lichter, Peter
Nature, ISSN 0028-0836, 2014, Volume 510, Issue 7506, pp. 537 - 541
Epigenetic alterations, that is, disruption of DNA methylation and chromatin architecture, are now acknowledged as a universal feature of tumorigenesis.... 
METHYLOME | SUPPRESSOR | HYPERMETHYLATION | GENE | CPG ISLAND SHORES | MULTIDISCIPLINARY SCIENCES | EMBRYONIC STEM-CELLS | CANCER GENOME | DIFFERENTIATION | IDENTIFICATION | EXPRESSION | Chromatin - metabolism | RNA-Binding Proteins - genetics | Humans | Gene Expression Regulation, Neoplastic | Gene Silencing | Genome - genetics | DNA Methylation - genetics | Promoter Regions, Genetic - genetics | Transcription Factors - metabolism | Animals | Chromatin Immunoprecipitation | Medulloblastoma - pathology | Cell Line, Tumor | Female | Transcription, Genetic | Mice | Histones - metabolism | Medulloblastoma - genetics | Binding Sites | Chromatin - genetics | Sequence Analysis, DNA - methods | Analysis | Medulloblastoma | Nucleotide sequencing | Research | Methylation | Health aspects | DNA sequencing | Transcription factors | DNA methylation | Cell division | Epigenetics | Genomes | Gene expression | Deoxyribonucleic acid--DNA | Methods | Tumors
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5. Full Text Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma
by Northcott, Paul A and Lee, Catherine and Zichner, Thomas and Stütz, Aian M and Erkek, Serap and Kawauchi, Daisuke and Shih, David J. H and Hovestadt, Volker and Zapatka, Marc and Sturm, Dominik and Jones, David T. W and Kool, Marcel and Remke, Marc and Cavalli, Florence M. G and Zuyderduyn, Scott and Bader, Gary D and VandenBerg, Scott and Esparza, Lourdes Aiana and Ryzhova, Marina and Wang, Wei and Wittmann, Anea and Stark, Sebastian and Sieber, Laura and Seker-Cin, Huriye and Linke, Linda and Kratochwil, Fabian and Jäger, Natalie and Buchhalter, Ivo and Imbusch, Charles D and Zipprich, Gideon and Raeder, Benjamin and Schmidt, Sabine and Diessl, Nicolle and Wolf, Stephan and Wiemann, Stefan and Brors, Benedikt and Lawerenz, Chris and Eils, Jürgen and Warnatz, Hans-Jörg and Risch, Thomas and Yaspo, Marie-Laure and Weber, Ursula D and Bartholomae, Cynthia C and von Kalle, Christof and Turányi, Eszter and Hauser, Peter and Sanden, Emma and Darabi, Anna and Siesjö, Peter and Sterba, Jaroslav and Zitterbart, Karel and Sumerauer, David and van Sluis, Peter and Versteeg, Rogier and Volckmann, Richard and Koster, Jan and Schuhmann, Martin U and Ebinger, Martin and Grimes, H. Leighton and Robinson, Giles W and Gajjar, Amar and Mynarek, Martin and von Hoff, Katja and Rutkowski, Stefan and Pietsch, Torsten and Scheurlen, Wolfram and Felsberg, Jörg and Reifenberger, Guido and Kulozik, Aneas E and von Deimling, Aneas and Witt, Olaf and Eils, Roland and Gilbertson, Richard J and Korshunov, Aney and Taylor, Michael D and Lichter, Peter and Korbel, Jan O and Wechsler-Reya, Robert J and Pfister, Stefan M and Neurosurgery and Neurokirurgi and Lund University and BioCARE: Biomarkers in Cancer Medicine improving Health Care, Education and Innovation and Lunds universitet
Nature, ISSN 0028-0836, 2014, Volume 511, Issue 7510, pp. 428 - 434
Medulloblastoma is a highly malignant paediatric brain tumour currently treated with a combination of surgery, radiation and chemotherapy, posing a... 
PIM-1 | SUPER-ENHANCERS | GENE | FINGER PROTEIN GFI-1 | MYC | MULTIDISCIPLINARY SCIENCES | CELL IDENTITY | MUTATIONS | MODEL | SUBGROUP | GENOME | Proto-Oncogene Proteins - metabolism | Oncogenes - genetics | Humans | Repressor Proteins - genetics | Proto-Oncogene Proteins - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | DNA-Binding Proteins - metabolism | Transcription Factors - metabolism | Chromosomes, Human, Pair 9 - genetics | Animals | Medulloblastoma - pathology | Genomic Structural Variation - genetics | Enhancer Elements, Genetic - genetics | Mice | Medulloblastoma - genetics | Child | Medulloblastoma - classification | Repressor Proteins - metabolism | Medulloblastoma | Analysis | Research | Nucleotide sequencing | Growth factor receptors | Health aspects | DNA sequencing | Medical research | DNA methylation | Epigenetics | Genomes | Gene expression | Deoxyribonucleic acid--DNA | Cancer | Index Medicus | Clinical Medicine | Neurologi | Neurology | Medical and Health Sciences | Medicin och hälsovetenskap | Surgery | Klinisk medicin | Kirurgi
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6. Full Text The genotoxic potential of retroviral vectors is strongly modulated by vector design and integration site selection in a mouse model of HSC gene therapy
by Montini, Eugenio and Cesana, Daniela and Schmidt, Manfred and Sanvito, Francesca and Bartholomae, Cynthia C and Ranzani, Marco and Benedicenti, Fabrizio and Sergi, Lucia Sergi and Ambrosi, Alessandro and Ponzoni, Maurilio and Doglioni, Claudio and Di Serio, Clelia and Von Kalle, Christof and Naldini, Luigi
Journal of Clinical Investigation, ISSN 0021-9738, 04/2009, Volume 119, Issue 4, pp. 964 - 975
gamma-Retroviral vectors (gamma RVs), which are commonly used in gene therapy, can trigger oncogenesis by insertional mutagenesis. Here, we have dissected the... 
MEDICINE, RESEARCH & EXPERIMENTAL | RELATIVE QUANTIFICATION | CANCER GENES | TUMOR SUPPRESSION | HEMATOPOIETIC STEM-CELLS | LENTIVIRAL VECTOR | IN-VIVO | INSERTIONAL MUTAGENESIS | ZINC-FINGER NUCLEASES | MURINE RETROVIRUS | VIRUS VECTORS | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Genetic Vectors - adverse effects | Mice, Transgenic | DNA Primers - genetics | Genes, p16 | Mice, Knockout | Animals | Gammaretrovirus - genetics | Base Sequence | Gammaretrovirus - pathogenicity | Hematopoietic Stem Cell Transplantation - adverse effects | Neoplasms, Experimental - genetics | Lentivirus - genetics | Lentivirus - pathogenicity | Mice | Mutation | Neoplasms, Experimental - etiology | Terminal Repeat Sequences | Genetic Therapy - adverse effects | Genetic Therapy - methods | Usage | Retroviruses | Animal models in research | Genetic vectors | Models | Genetic aspects | Research | Gene therapy | Health aspects | Index Medicus | Abridged Index Medicus
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7. Full Text Insertional mutagenesis combined with acquired somatic mutations causes leukemogenesis following gene therapy of SCID-X1 patients
by Howe, Steven J and Mansour, Marc R and Schwarzwaelder, Kerstin and Bartholomae, Cynthia and Hubank, Michael and Kempski, Helena and Brugman, Martijn H and Pike-Overzet, Karin and Chatters, Stephen J and De Ridder, Dick and Gilmour, Kimberly C and Adams, Stuart and Thornhill, Susannah I and Parsley, Kathryn L and Staal, Frank J. T and Gale, Rosemary E and Linch, David C and Bayford, Jinhua and Brown, Lucie and Quaye, Michelle and Kinnon, Christine and Ancliff, Philip and Webb, David K and Schmidt, Manfred and Von Kalle, Christof and Gaspar, H. Bobby and Thrasher, Adrian J
Journal of Clinical Investigation, ISSN 0021-9738, 09/2008, Volume 118, Issue 9, pp. 3143 - 3150
X-linked SCID (SCID-X1) is amenable to correction by gene therapy using conventional gammaretroviral vectors. Here, we describe the occurrence of clonal T cell... 
HEMATOPOIETIC-CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | SEVERE COMBINED IMMUNODEFICIENCY | VECTOR INTEGRATION | NOTCH1 | ACUTE LYMPHOBLASTIC-LEUKEMIA | T-CELL DEVELOPMENT | EXPRESSION | RECONSTITUTION | ADA | GAMMA-CHAIN | Follow-Up Studies | LIM Domain Proteins | Humans | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Severe Combined Immunodeficiency - therapy | Infant | Male | DNA-Binding Proteins - genetics | Chromosomes, Human, X | Receptors, Interleukin-2 - genetics | Severe Combined Immunodeficiency - complications | Adaptor Proteins, Signal Transducing | Mutagenesis | Models, Biological | Metalloproteins - genetics | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - etiology | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins | Mutation | Receptor, Notch1 - genetics | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - therapy | Genetic Therapy - adverse effects | Genetic Therapy - methods | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - complications | Complications and side effects | Care and treatment | Severe combined immunodeficiency | Genetic aspects | Research | Gene therapy | Methods | Risk factors | Index Medicus | Abridged Index Medicus
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8. Impact of raltegravir on HIV-1 RNA and DNA forms following initiation of antiretroviral therapy in treatment-naive patients
by Christoph Stephan and Hanna-Mari Baldauf and Joanne Barry and Frank A Giordano and Cynthia C Bartholomae and Annette Haberl and Markus Bickel and Manfred Schmidt and Stephanie Laufs and Lars Kaderali and Oliver T Keppler
The Journal of Antimicrobial Chemotherapy, ISSN 0305-7453, 10/2014, Volume 69, Issue 10, p. 2809
  The rapid early-phase decay of plasma HIV-1 RNA during integrase inhibitor-based therapy is not fully understood. The accumulation of biologically active... 
Antiretroviral drugs | Human immunodeficiency virus--HIV | Ribonucleic acid--RNA | Drug therapy | Deoxyribonucleic acid--DNA
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9. Full Text High-resolution insertion-site analysis by linear amplification-mediated PCR (LAM-PCR)
by Schmidt, Manfred and Schwarzwaelder, Kerstin and Bartholomae, Cynthia and Zaoui, Karim and Ball, Claudia and Pilz, Ingo and Braun, Sandra and Glimm, Hanno and von Kalle, Christof
Nature Methods, ISSN 1548-7091, 12/2007, Volume 4, Issue 12, pp. 1051 - 1057
Integrating vector systems used in clinical gene therapy have proven their therapeutic potential in the long-term correction of immunodeficiencies(1-4). The... 
SEVERE COMBINED IMMUNODEFICIENCY | GENE-THERAPY | VECTOR INTEGRATION | SCID-X1 | DISEASE | BIOCHEMICAL RESEARCH METHODS | Sequence Alignment - methods | Base Sequence | Chromosome Mapping - methods | Genetic Markers - genetics | DNA Transposable Elements - genetics | Molecular Sequence Data | Sequence Analysis, DNA - methods | Polymerase Chain Reaction - methods | Polymerase chain reaction | Physiological aspects | Usage | Research | Nucleotide sequence | Methods | Biomedical research | Gene therapy | Molecular biology | Research methodology | Genomics
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10. Full Text Hematopoietic stem cell gene transfer in a tumor-prone mouse model uncovers low genotoxicity of lentiviral vector integration
by Naldini, Luigi and Cesana, Daniela and Montini, Eugenio and Ambrosi, Alessandro and Ponzoni, Maurilio and Sanvito, Francesca and von Kalle, Christof and Bartholomae, Cynthia and Doglioni, Claudio and Schmidt, Manfred and Sergi, Lucia Sergi and Benedicenti, Fabrizio and Di Serio, Clelia
Nature Biotechnology, ISSN 1087-0156, 06/2006, Volume 24, Issue 6, pp. 687 - 696
Insertional mutagenesis represents a major hurdle to gene therapy and necessitates sensitive preclinical genotoxicity assays. Cdkn2a(-/-) mice are susceptible... 
ACTIVATION | HUMAN GENOME | THERAPY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | TRANSDUCTION | INSERTIONAL MUTAGENESIS | IDENTIFICATION | ACTIVE GENES | CANCER | EXPRESSION | TRANSPLANTATION | Gene Transfer Techniques | Hematopoietic Stem Cells - metabolism | Mutagenicity Tests - methods | Virus Integration | Genetic Vectors - genetics | Neoplasms - virology | Neoplasms - therapy | Animals | Transfection - methods | Neoplasms - genetics | Cell Line, Tumor | Female | Lentivirus - genetics | Mice | Disease Models, Animal | Genetic Therapy - methods | Models | Gene therapy | Toxicity | Rodents | Stem cells | Tumors
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11. Full Text Uncovering and Dissecting the Genotoxicity of Self-inactivating Lentiviral Vectors In Vivo
by Cesana, Daniela and Ranzani, Marco and Volpin, Monica and Bartholomae, Cynthia and Duros, Caroline and Artus, Alexandre and Merella, Stefania and Benedicenti, Fabrizio and Sergi Sergi, Lucia and Sanvito, Francesca and Brombin, Chiara and Nonis, Alessandro and Serio, Clelia Di and Doglioni, Claudio and von Kalle, Christof and Schmidt, Manfred and Cohen-Haguenauer, Odile and Naldini, Luigi and Montini, Eugenio
Molecular Therapy, ISSN 1525-0016, 04/2014, Volume 22, Issue 4, pp. 774 - 785
Self-inactivating (SIN) lentiviral vectors (LV) have an excellent therapeutic potential as demonstrated in preclinical studies and clinical trials. However,... 
RNA-POLYMERASE-II | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | MUTAGENESIS | PROTEIN-KINASE | PTEN | RETROVIRAL VECTORS | LIVER-CANCER | INTEGRATION | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | MOUSE MODEL | GENETICS & HEREDITY | GENE-THERAPY | Genetic Therapy | Promoter Regions, Genetic | Humans | Carcinogenesi