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NATURE REVIEWS CANCER, ISSN 1474-175X, 01/2010, Volume 10, Issue 1, pp. 51 - 57
The importance of cellular senescence, which is a stress response that stably blocks proliferation, is increasingly being recognized. Senescence is prevalent... 
P53-DEPENDENT CELLULAR SENESCENCE | INDUCE SENESCENCE | TELOMERE DYSFUNCTION | RAS ONCOGENE | ONCOLOGY | IN-VIVO | DNA-DAMAGE | MOUSE MODEL | DEVELOPMENTAL DEFECTS | ONCOGENE-INDUCED SENESCENCE | CANCER-THERAPY
Journal Article
Nature, ISSN 0028-0836, 02/2013, Volume 494, Issue 7437, pp. 361 - 365
Journal Article
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
Journal Article
Journal Article
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 374 - 379
Cellular senescence has been recently shown to have an important role in opposing tumour initiation and promotion. Senescence induced by oncogenes or by loss... 
BOX PROTEIN SKP2 | TUMOR SUPPRESSION | PATHWAY | MULTIDISCIPLINARY SCIENCES | IN-VIVO | PTEN | ACCUMULATION | ONCOGENE-INDUCED SENESCENCE | EXPRESSION | CANCER | P53 | Proto-Oncogene Proteins p21(ras) - genetics | Cellular Senescence - drug effects | Male | Prostate - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | S-Phase Kinase-Associated Proteins - antagonists & inhibitors | Adenovirus E1A Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Fibroblasts | Prostatic Neoplasms - prevention & control | Prostatic Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - metabolism | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | PTEN Phosphohydrolase - deficiency | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | PTEN Phosphohydrolase - metabolism | SKP Cullin F-Box Protein Ligases - metabolism | S-Phase Kinase-Associated Proteins - metabolism | Tumor Suppressor Protein p53 - deficiency | Animals | Activating Transcription Factor 4 - metabolism | Adenovirus E1A Proteins - genetics | Prostate - cytology | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | S-Phase Kinase-Associated Proteins - genetics | Mice | Cell Transformation, Neoplastic - drug effects | Prevention | Care and treatment | Physiological aspects | Aging | Tumor suppressor genes | Genetic aspects | Research | Cells | Tumors | Cell cycle | Apoptosis | Index Medicus
Journal Article
Current Drug Targets, ISSN 1389-4501, 03/2016, Volume 17, Issue 4, pp. 460 - 466
Senescence was originally identified by the finite lifespan of normal cells that is a consequence of telomere shortening with each cycle of DNA replication.... 
Chemotherapy | Senescence | p16 | DNA damage | p21 | Tumor cell | p53 | DNA-DAMAGE RESPONSE | tumor cell | TUMOR-CELLS | ONCOGENE-INDUCED SENESCENCE | chemotherapy | BREAST-CANCER CELLS | ACCELERATED CELLULAR SENESCENCE | PREMATURE SENESCENCE | THERAPY | ENDOTHELIAL-CELLS | IN-VIVO | PHARMACOLOGY & PHARMACY | p16(INK4A) | HETEROCHROMATIC FOCI | p21(WAF-1)
Journal Article