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Journal Article
Journal of the American Chemical Society, ISSN 0002-7863, 08/2013, Volume 135, Issue 31, pp. 11623 - 11633
Journal Article
Nature, ISSN 0028-0836, 08/2010, Volume 466, Issue 7307, pp. 765 - 768
Chronic myelogenous leukaemia (CML) can progress from a slow growing chronic phase to an aggressive blast crisis phase, but the molecular basis of this... 
CHRONIC MYELOGENOUS LEUKEMIA | MURINE MODEL | STEM-CELLS | TRANSLATIONAL REPRESSION | RNA | BINDING PROTEIN MUSASHI-1 | MULTIDISCIPLINARY SCIENCES | BCR-ABL | GENE-EXPRESSION | NUMB | CML BLAST CRISIS | RNA-Binding Proteins - genetics | Up-Regulation | Oncogene Proteins, Fusion - metabolism | Prognosis | Homeodomain Proteins - metabolism | Humans | Gene Expression Regulation, Neoplastic | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Nuclear Pore Complex Proteins - genetics | Cell Differentiation - genetics | RNA-Binding Proteins - biosynthesis | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Nerve Tissue Proteins - biosynthesis | Membrane Proteins - metabolism | Blast Crisis - pathology | Signal Transduction | Membrane Proteins - genetics | Nuclear Pore Complex Proteins - metabolism | Mice, Inbred C57BL | Tumor Suppressor Protein p53 - metabolism | Receptor, Notch1 - metabolism | Nerve Tissue Proteins - genetics | Disease Progression | Homeodomain Proteins - genetics | Nerve Tissue Proteins - metabolism | Fusion Proteins, bcr-abl - genetics | Membrane Proteins - biosynthesis | Animals | Oncogene Proteins, Fusion - genetics | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Blast Crisis - genetics | Mice | Blast Crisis - metabolism | Fusion Proteins, bcr-abl - metabolism | RNA-Binding Proteins - metabolism | Myelocytic leukemia | Molecular genetics | Physiological aspects | Development and progression | Nonlymphoid leukemia | Cellular signal transduction | Genetic aspects | Research | Genetic regulation | Gene expression | Medical research | Stem cells | Chronic illnesses | Index Medicus
Journal Article
1997, Cancer surveys, ISBN 0879695188, Volume 29., vi, 363
Book
Journal Article
Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 4795 - 13
Doxorubicin (DOX) is the mainstay chemotherapeutic agent against a variety of human neoplasmas. However, its clinical utility is limited by its marked... 
PROGRAMMED CELL-DEATH | MITOCHONDRIAL APOPTOSIS | OXIDATIVE STRESS | INDUCED CARDIOTOXICITY | INDUCED APOPTOSIS | MULTIDISCIPLINARY SCIENCES | IN-VIVO | HYDROGEN-PEROXIDE | NF-KAPPA-B | UP-REGULATION | BCL-2 FAMILY | Apoptosis - drug effects | Caspase 3 - metabolism | Cardiomyopathies - prevention & control | Male | NF-kappa B - metabolism | Cytochromes c - genetics | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - genetics | Proto-Oncogene Proteins c-akt - genetics | Tumor Suppressor Protein p53 - genetics | Cardiomyopathies - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | Caspase 3 - genetics | Apoptosis Regulatory Proteins - genetics | Flavonoids - pharmacology | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins c-akt - metabolism | bcl-2-Associated X Protein - genetics | Cardiotoxicity - prevention & control | Drug Administration Schedule | Signal Transduction | Cytochromes c - metabolism | Tumor Suppressor Protein p53 - metabolism | bcl-2-Associated X Protein - metabolism | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Cardiomyopathies - pathology | Antioxidants - pharmacology | Cardiotonic Agents - pharmacology | Rats, Sprague-Dawley | Doxorubicin - toxicity | Apoptosis Regulatory Proteins - metabolism | Gene Expression Regulation - drug effects | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | NF-kappa B - genetics | Myocytes, Cardiac - metabolism | Proto-Oncogene Proteins c-bcl-2 - genetics | Cardiomyopathies - chemically induced | Oxidative stress | NF-κB protein | Conduction | Bax protein | Bcl-2 protein | Cardiomyopathy | p53 Protein | Lipid peroxidation | Caspase | MAP kinase | JNK protein | AKT protein | Inflammation | Caspase-3 | Doxorubicin | Cytochrome c | Antioxidants | Molecular modelling | Rodents | Vascular endothelial growth factor | PTEN protein | Apoptosis | Cancer | Index Medicus
Journal Article
Journal Article
Genes and Development, ISSN 0890-9369, 05/2013, Volume 27, Issue 10, pp. 1101 - 1114
Tumorigenesis results from dysregulation of oncogenes and tumor suppressors that influence cellular proliferation, differentiation, apoptosis, and/or... 
Huwe1 | c-Myc | Mule | Ras | p21 | Miz1 | DNA-DAMAGE | KERATINOCYTE GROWTH | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | BASE EXCISION-REPAIR | HUWE1 UBIQUITIN LIGASE | NEGATIVE REGULATION | GENETICS & HEREDITY | ARF TUMOR-SUPPRESSOR | DIFFERENTIATION | MIZ-1 | HUMAN CANCER | Protein Inhibitors of Activated STAT - deficiency | Tetradecanoylphorbol Acetate - pharmacology | 9,10-Dimethyl-1,2-benzanthracene - pharmacology | Male | Protein Inhibitors of Activated STAT - metabolism | Cyclin-Dependent Kinase Inhibitor p15 - biosynthesis | Oncogene Protein p21(ras) - metabolism | Cyclin-Dependent Kinase Inhibitor p16 | Oncogene Protein p21(ras) - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Nuclear Proteins - deficiency | Protein Inhibitors of Activated STAT - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Nuclear Proteins - genetics | Protein Inhibitors of Activated STAT - antagonists & inhibitors | Skin Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis | Signal Transduction | Down-Regulation | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Skin Neoplasms - chemically induced | Proto-Oncogene Proteins c-myc - metabolism | Mice, Knockout | Skin Neoplasms - metabolism | Keratinocytes - pathology | Animals | Tumor Suppressor Protein p53 | Keratinocytes - drug effects | Keratinocytes - metabolism | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-myc - deficiency | Skin Neoplasms - genetics | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Ubiquitin-Protein Ligases - deficiency | Mice | Proto-Oncogene Proteins c-myc - genetics | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Genes, ras | Ubiquitin-Protein Ligases - genetics | Oncogene Protein p21(ras) - genetics | Carcinogenesis | Ras genes | Analysis | Index Medicus | Research Paper
Journal Article
Nature, ISSN 0028-0836, 08/2005, Volume 436, Issue 7052, pp. 807 - 811
The c-Myc oncoprotein promotes proliferation and apoptosis, such that mutations that disable apoptotic programmes often cooperate with MYC during... 
APOPTOSIS | ONCOGENE | GENE | MULTIDISCIPLINARY SCIENCES | IN-VIVO | N-TERMINAL DOMAIN | C-MYC | TRANSFORMING ACTIVITY | BURKITT-LYMPHOMA CELLS | TRANSACTIVATION DOMAIN | MUTATIONS | Cell Proliferation | Humans | Adoptive Transfer | Cyclin-Dependent Kinase Inhibitor p16 | Burkitt Lymphoma - pathology | Stem Cell Transplantation | Proto-Oncogene Proteins c-bcl-2 - metabolism | Bcl-2-Like Protein 11 | Burkitt Lymphoma - genetics | Membrane Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Tumor Suppressor Protein p53 - metabolism | Burkitt Lymphoma - metabolism | Mutation - genetics | Proto-Oncogene Proteins c-myc - metabolism | Animals | Apoptosis Regulatory Proteins | Carrier Proteins - metabolism | Genes, myc - genetics | Alleles | Mice | Proto-Oncogene Proteins c-myc - genetics | Tumor Suppressor Protein p14ARF - metabolism | Apoptosis | Proteins | Oncology | Mutation | Cellular biology | Tumors | Index Medicus | Proto-Oncogene Proteins c-myc/genetics/metabolism | Mutation/genetics | Tumor Suppressor Protein p14ARF/metabolism | Cell Cycle Proteins/metabolism | Proto-Oncogene Proteins/metabolism | Tumor Suppressor Protein p53/metabolism | Burkitt Lymphoma/genetics/metabolism/pathology | Genes; myc/genetics | Membrane Proteins/metabolism | Mice; Inbred C57BL | Proto-Oncogene Proteins c-bcl-2/metabolism | Carrier Proteins/metabolism
Journal Article
Nature Cell Biology, ISSN 1465-7392, 08/2009, Volume 11, Issue 8, pp. 973 - 979
Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cells. Paradoxically, senescent cells also secrete factors that alter... 
TUMOR SUPPRESSION | HUMAN-CELLS | HUMAN FIBROBLASTS | GROWTH-FACTOR | ONCOGENE-INDUCED SENESCENCE | CELLULAR SENESCENCE | CANCER | TUMORIGENESIS | P53 | TELOMERES | CELL BIOLOGY | RNA, Small Interfering - genetics | Humans | Male | Green Fluorescent Proteins - genetics | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Telomerase - genetics | Transfection | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Telomerase - metabolism | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Telomere - genetics | Cell Line | Green Fluorescent Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Enzyme-Linked Immunosorbent Assay | Cell Cycle Proteins - metabolism | Cells, Cultured | Cytokines - secretion | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cellular Senescence - physiology | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Interleukin-6 - secretion | Blotting, Western | Fibroblasts - radiation effects | Checkpoint Kinase 2 | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Signal Transduction - physiology | Fibroblasts - cytology | DNA Damage | Microscopy, Fluorescence | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Cytokines | DNA damage | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2013, Volume 8, Issue 7, pp. e68574 - e68574
F-box and WD repeat domain-containing 7 (Fbxw7/hAgo/hCdc4/Fbw7) is a p53-dependent tumor suppressor and leads to ubiquitination-mediated suppression of several... 
FBXW7 EXPRESSION | NETWORK | P53 GENE | MULTIDISCIPLINARY SCIENCES | MUTATION | TUMOR-SUPPRESSOR | DIFFERENTIATION | FBW7 | HCDC4 | CANCER | CLINICAL-SIGNIFICANCE | F-Box-WD Repeat-Containing Protein 7 | Genetic Therapy | Liver - pathology | Humans | Gene Expression Regulation, Neoplastic | Liver Neoplasms - therapy | Cyclin E - genetics | Tumor Suppressor Protein p53 - genetics | Tumor Suppressor Protein p53 - therapeutic use | RNA Interference | Carcinoma, Hepatocellular - genetics | Cell Cycle Proteins - genetics | Female | Liver Neoplasms - pathology | Liver Neoplasms - genetics | Signal Transduction | F-Box Proteins - metabolism | Liver - metabolism | Cell Cycle Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Animals | Mice, Nude | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Cell Line, Tumor | Adenoviruses, Human - genetics | Carcinoma, Hepatocellular - therapy | Mice | Mice, Inbred BALB C | Proto-Oncogene Proteins c-myc - genetics | Cyclin E - metabolism | Mutation | Ubiquitin-Protein Ligases - genetics | F-Box Proteins - genetics | Apoptosis | Carcinoma, Hepatocellular - metabolism | Ubiquitin | Hepatoma | Gene therapy | Tumor proteins | Adenoviruses | Cell culture | Biotechnology | Transcription factors | p53 Protein | c-Myc protein | Hepatocellular carcinoma | Myc protein | Tissues | Phase transitions | Cdc4 protein | Anticancer properties | Proteins | Liver cancer | Ubiquitination | Cell growth | Antitumor agents | Surgery | Cell cycle | Cyclin E | Recombinant | Enzymes | c-Jun protein | Pharmacology | Breast cancer | siRNA | Injection | Tumor cell lines | Chemical compounds | Medical prognosis | Cell lines | Proteasomes | Tumor suppressor genes | Protein expression | Index Medicus
Journal Article