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Clinical Cancer Research, ISSN 1078-0432, 01/2016, Volume 22, Issue 1 Supplement, pp. IA05 - IA05
Journal Article
Genome Biology, ISSN 1474-7596, 02/2016, Volume 17, Issue 1, pp. 31 - 31
Background: Analysis of somatic mutations provides insight into the mutational processes that have shaped the cancer genome, but such analysis currently... 
Esophageal carcinoma | Mutational signatures | Single samples | APOBEC | SIGNATURES | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | GENETICS & HEREDITY | HUMAN CANCER | Adenocarcinoma | Squamous cell carcinoma | Ultraviolet radiation | Evolution | Software | Genomes | Mutation | DNA repair | Deoxyribonucleic acid--DNA | Cancer | Esophagus | Tumors | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2010, Volume 5, Issue 2, pp. e8918 - 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 | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 07/2019, Volume 116, Issue 30, p. 15178
We derived a mouse model in which a mutant form of Nbn/Nbs1mid8 (hereafter Nbnmid8) exhibits severely impaired binding to the Mre11−Rad50 core of the Mre11... 
Genomic analysis | Acute lymphatic leukemia | Leukemia | CHK1 protein | p53 Protein | Lymphocytes T | Lymphatic leukemia | Hemopoiesis | Thymus | Blockage | Lymphocytes B | Hematopoiesis | MRE11 protein | Lymphocytes | Bone marrow | Mice | Mutation | Bcl-6 protein
Journal Article
2013, Second edition, ISBN 0199324794, xxvi, 559 pages
This second edition of Social Injustice and Public Health is a comprehensive, up-to-date, evidence-based resource on the relationship of social injustice to... 
Social medicine | Social justice | Social aspects | Public health | Social Medicine
Book
Journal of Clinical Investigation, ISSN 0021-9738, 03/2016, Volume 126, Issue 3, pp. 1052 - 1066
Journal Article
Journal Article
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 03/2009, Volume 106, Issue 11, pp. 4519 - 4524
Tumors with mutant BRAF and those with receptor tyrosine kinase (RTK) activation have similar levels of phosphorylated ERK, but only the former depend on ERK... 
Braf mutation | Mitogen-activated protein kinase | Extracellular signal-regulated kinase kinase inhibition | Dual specificity phosphatase | dual specificity phosphatase | mitogen-activated protein kinase, extracellular signal-regulated kinase kinase inhibition | Biological Sciences | BRAF mutation
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2010, Volume 107, Issue 33, pp. 14903 - 14908
Tumors with mutant BRAF and some with mutant RAS are dependent upon ERK signaling for proliferation, and their growth is suppressed by MAPK/ERK kinase (MEK)... 
Tumor cell line | Phosphorylation | Cell growth | Negative feedback | Genes | Cell lines | Melanoma | Genetic mutation | Tumors | Cancer | LUNG-CANCER | APOPTOSIS | KINASE KINASE-1/2 INHIBITOR | ACTIVATION | PATHWAY | MULTIDISCIPLINARY SCIENCES | IN-VIVO | B-RAF | MUTATIONS | MEK INHIBITORS | ADVANCED CANCERS | Diphenylamine - pharmacology | Oligonucleotide Array Sequence Analysis | Apoptosis - drug effects | Humans | Gene Expression Profiling | Extracellular Signal-Regulated MAP Kinases - metabolism | Diphenylamine - analogs & derivatives | Mitogen-Activated Protein Kinase Kinases - metabolism | Indoles - pharmacology | Benzamides - pharmacology | G1 Phase - genetics | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Reverse Transcriptase Polymerase Chain Reaction | Sulfonamides - pharmacology | Blotting, Western | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Cell Line, Tumor | Cell Proliferation - drug effects | Mutation | Amino Acid Substitution | Cell proliferation | Development and progression | Cellular signal transduction | Genetic aspects | Pharmacology | Research | Drug therapy | Proteins | Signal transduction | Kinases | Gene expression | Cells | Index Medicus | Biological Sciences
Journal Article
Journal Article
Science, ISSN 0036-8075, 10/2012, Volume 338, Issue 6104, pp. 221 - 221
Journal Article