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Science (American Association for the Advancement of Science), ISSN 1095-9203, 2013, Volume 343, Issue 6167, pp. 189 - 193
Tumor recurrence is a leading cause of cancer mortality. Therapies for recurrent disease may fail, at least in part, because the genomic alterations driving... 
Geography | Glioma | REPORTS | Medical genetics | Evolution | Evolutionary genetics | Genomes | Genetic mutation | Genetic heterogeneity | Cancer | Tumors | RETINOBLASTOMA | IDH1 MUTATIONS | MULTIDISCIPLINARY SCIENCES | INTRATUMOR HETEROGENEITY | GROWTH | CLONAL EVOLUTION | MSH6 MUTATIONS | IDENTIFICATION | HUMAN CANCER | HUMAN-MALIGNANT GLIOMAS | TEMOZOLOMIDE | Dacarbazine - adverse effects | Dacarbazine - therapeutic use | Humans | Brain Neoplasms - pathology | Neoplasm Recurrence, Local - drug therapy | X-linked Nuclear Protein | Mutagenesis - drug effects | Proto-Oncogene Proteins c-akt - genetics | Tumor Suppressor Protein p53 - genetics | Glioma - genetics | Neoplasm Grading | TOR Serine-Threonine Kinases - genetics | DNA Mutational Analysis | Glioma - pathology | Dacarbazine - analogs & derivatives | Nuclear Proteins - genetics | DNA Helicases - genetics | Brain Neoplasms - genetics | Transcription Factors - genetics | Brain Neoplasms - drug therapy | Antineoplastic Agents, Alkylating - therapeutic use | Brain - drug effects | Proto-Oncogene Proteins B-raf - genetics | Neoplasm Recurrence, Local - chemically induced | Brain - pathology | Neoplasm Recurrence, Local - genetics | Antineoplastic Agents, Alkylating - adverse effects | Glioma - drug therapy | Care and treatment | Gene mutations | Gliomas | Physiological aspects | Genetic aspects | Research | Methods | Studies | Brain surgery | Mutagenesis | Brain cancer | Clinical outcomes | Index Medicus
Journal Article
Nature (London), ISSN 1476-4687, 2015, Volume 529, Issue 7584, pp. 110 - 114
Gain-of-function IDH mutations are initiating events that define major clinical and prognostic classes of gliomas(1,2). Mutant IDH protein produces a new... 
MAINTENANCE | METHYLATION | LANDSCAPE | DEMETHYLATION | MULTIDISCIPLINARY SCIENCES | INTEGRATED GENOMIC ANALYSIS | ARCHITECTURE | PHENOTYPE | EXPRESSION | 2-HYDROXYGLUTARATE | PRINCIPLES | Chromatin - metabolism | Up-Regulation | Humans | Glioma - genetics | Base Sequence | Glioma - pathology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Binding Sites | Chromatin - drug effects | Repressor Proteins - metabolism | Oncogenes - genetics | Insulator Elements - genetics | Glioma - enzymology | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Isocitrate Dehydrogenase - genetics | DNA Methylation - genetics | Down-Regulation - drug effects | Mutation - genetics | CRISPR-Cas Systems - genetics | Insulator Elements - drug effects | Phenotype | Isocitrate Dehydrogenase - chemistry | Receptor, Platelet-Derived Growth Factor alpha - genetics | CCCTC-Binding Factor | CpG Islands - genetics | Protein Binding | Isocitrate Dehydrogenase - metabolism | Cell Proliferation - drug effects | Enhancer Elements, Genetic - genetics | Glutarates - metabolism | Cell Transformation, Neoplastic - drug effects | Chromatin - genetics | DNA Methylation - drug effects | Glioma - drug therapy | Complications and side effects | Care and treatment | Platelet-derived growth factor | Gliomas | Analysis | Influence | Genetic aspects | Research | Methylation | Oncogenes | DNA methylation | Epigenetics | Genomes | Mutation | Gene expression | Binding sites | Deoxyribonucleic acid--DNA | Tumors
Journal Article
Journal Article
Acta neuropathologica, ISSN 1432-0533, 2018, Volume 135, Issue 4, pp. 601 - 615
textabstractThe optimal treatment for patients with low-grade glioma (LGG) WHO grade II remains controversial. Overall survival ranges from 2 to over 15 years... 
TMZ | DNA methylation | DDR genes | MGMT-STP27 | Randomized trial | Low-grade glioma | Pathology | Neurosciences | Medicine & Public Health | CELLS | METHYLATION | MGMT | SENSITIVITY | MISMATCH REPAIR | PATHOLOGY | TUMORS | NEUROSCIENCES | CLINICAL NEUROLOGY | TEMOZOLOMIDE | GLIOBLASTOMA | RADIOTHERAPY | EXPRESSION | Epigenesis, Genetic | Humans | Brain Neoplasms - pathology | DNA Repair Enzymes - genetics | Male | Glioma - genetics | Temozolomide - therapeutic use | Neoplasm Grading | DNA Methylation - radiation effects | Glioma - pathology | Tumor Suppressor Proteins - genetics | Glioma - therapy | Adult | Female | Promoter Regions, Genetic | Discoidin Domain Receptors - genetics | Brain Neoplasms - genetics | Isocitrate Dehydrogenase - genetics | Treatment Outcome | Antineoplastic Agents, Alkylating - therapeutic use | DNA Modification Methylases - genetics | DNA | Progression-Free Survival | Brain Neoplasms - therapy | CpG Islands | DNA Methylation - drug effects | Medical colleges | Medical research | Care and treatment | DNA damage | Genes | Medicine, Experimental | Genetic aspects | Radiotherapy | Methylation | Cancer | Preservation | Brain tumors | Genotoxicity | Cognitive ability | Genomes | Radiation therapy | Survival | Quality of life | Glioma | Temozolomide | Isocitrate dehydrogenase | Deoxyribonucleic acid--DNA | CpG islands | Original Paper
Journal Article
Nature genetics, ISSN 1546-1718, 2016, Volume 48, Issue 7, pp. 768 - 776
Glioblastoma (GBM) is the most common and aggressive primary brain tumor. To better understand how GBM evolves, we analyzed longitudinal genomic and... 
GENE FUSIONS | TGF-BETA | CANCER GENOMICS | LANDSCAPE | GLIOMA | GENETICS & HEREDITY | GENOMIC ALTERATIONS | MSH6 MUTATIONS | SEQUENCING DATA | BRAIN-TUMORS | TEMOZOLOMIDE | Cell Proliferation | Dacarbazine - therapeutic use | Genomics | Humans | Brain Neoplasms - pathology | DNA Repair Enzymes - genetics | Gene Expression Regulation, Neoplastic | Transcriptome | Neoplasm Recurrence, Local - drug therapy | Clonal Evolution - genetics | Neoplasm Recurrence, Local - pathology | Neoplasm Grading | Glioblastoma - genetics | Tumor Suppressor Proteins - genetics | Dacarbazine - analogs & derivatives | Brain Neoplasms - genetics | Isocitrate Dehydrogenase - genetics | Survival Rate | Brain Neoplasms - drug therapy | Mutation - genetics | Antineoplastic Agents, Alkylating - therapeutic use | Latent TGF-beta Binding Proteins - genetics | DNA Modification Methylases - genetics | Transforming Growth Factor beta - genetics | Glioblastoma - pathology | Neoplasm Recurrence, Local - genetics | Biomarkers, Tumor - genetics | Temozolomide | Glioblastoma - drug therapy | Longitudinal Studies | Molecular targeted therapy | Care and treatment | Gene mutations | Development and progression | Genetic aspects | Genetic transcription | Glioblastoma multiforme | Health aspects | Methods | Brain cancer | Genomes | Gene expression | Cancer therapies | Studies | Archives & records | DNA methylation | Mathematical models | Mutation | Deoxyribonucleic acid--DNA | Tumors | Cancer
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 2010, Volume 5, Issue 2, p. e8918
Background: Glioblastoma multiforme (GBM) is the most common and aggressive type of brain tumor in humans and the first cancer with comprehensive genomic... 
GLIOMAS | PROTEIN-INTERACTION NETWORKS | HUMAN-DISEASE | BIOLOGICAL NETWORKS | METABOLIC NETWORKS | MULTIDISCIPLINARY SCIENCES | FUNCTIONAL MODULES | GENES | CANCER GENOME | PIKE-A | INTEGRATED ANALYSIS | Genetic Predisposition to Disease | Humans | Brain Neoplasms - genetics | Signal Transduction - genetics | Gene Regulatory Networks | GTP-Binding Proteins - genetics | Tumor Suppressor Protein p53 - genetics | Phosphatidylinositol 3-Kinases - genetics | Algorithms | Glioblastoma - genetics | Retinoblastoma Protein - genetics | Models, Genetic | Software | GTPase-Activating Proteins - genetics | Mutation | Genes | Brain tumors | Genomics | Natural language interfaces | Genomes | Protein-protein interactions | Technology application | Mobile communication systems | Wireless communication systems | Language processing | Analysis | Genetic aspects | Computational linguistics | Tumor proteins | Health aspects | Protein kinases | Cancer | Brain | Copy number | Modules | p53 Protein | Brain cancer | Glioblastoma | Biology | Metastasis | Software development tools | Kinases | Proteins | Signal transduction | Alterations | Pathways | Cellular communication | Network analysis | Phylogenetics | Bioinformatics | Deoxyribonucleic acid--DNA | Cartography | Nucleotide sequence | Retinoblastoma protein | Metabolism | Gene expression | Glioblastoma multiforme | 1-Phosphatidylinositol 3-kinase | Endothelium | Signaling | Hypotheses | Passengers | Protein interaction | Tumors | Deoxyribonucleic acid | DNA
Journal Article
Nature (London), ISSN 1476-4687, 2008, Volume 455, Issue 7216, pp. 1061 - 1068
Journal Article