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Journal of Hepatology, ISSN 0168-8278, 04/2018, Volume 68, Issue 4, pp. 867 - 867
It has come to our attention that the PITER framework investigator, Alessandro Federico, was incorrectly listed as F. Alessandro in the original manuscript.... 
Senescence
Journal Article
2013, ISBN 0817317880, Volume 9780817386580, ages cm
Book
Journal of Cell Science, ISSN 0021-9533, 10/2017, Volume 130, Issue 19, pp. e1903 - e1903
Journal Article
2004, ISBN 9780195140354, 1295
Explains human aging from genes to clinical disease. With over 4,000 references, this book explores both the fundamental processes of aging and the resultant... 
Aging | Cells
eBook
1999, ISBN 9780195125931, xv, 234
In this work, the various theories of ageing are explained and assessed. The author presents case accounts about disorders that open windows on to the ageing... 
Aging | Cells | Apoptosis | Molecular aspects
Book
2004, 1st ed., ISBN 9780444515834, vii, 178
Book
2003, Biology of aging and its modulation, ISBN 1402013698, Volume 5, 333
Book
1994, ISBN 9780521382991, xii, 322
The maximum life span of multicellular organisms varies greatly: for a fruitfly it is about 30 days, for a dog about 20 years, and for a human about 100 years.... 
Aging | Genetic aspects | Cells
Book
Journal Article
2001, 1st ed., Advances in cell aging and gerontology, ISBN 0444504958, Volume 7., viii, 272
Book
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 04/2015, Volume 19, Issue 4, pp. 734 - 743
Human mesenchymal stem cells (h MSC s) are adult multipotent stem cells located in various tissues, including the bone marrow. In contrast to terminally... 
actinomycin D | damage | mesenchymal stem cell | DNA | senescence‐associated secretory phenotype | stress‐induced premature senescence | Actinomycin D | Mesenchymal stem cell | Senescence-associated secretory phenotype | Stress-induced premature senescence | DNA damage | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | ACTIVATION | SECRETORY PHENOTYPE | PROLIFERATION | senescence-associated secretory phenotype | CELLULAR SENESCENCE | CANCER | CELL BIOLOGY | stress-induced premature senescence | GROWTH | HUMAN FIBROBLASTS | ACTINOMYCIN-D | ATAXIA-TELANGIECTASIA | Interleukin-8 - genetics | Antibiotics, Antineoplastic - pharmacology | Gene Expression - drug effects | Humans | Cell Survival - genetics | Cellular Senescence - drug effects | Immunoblotting | Intracellular Signaling Peptides and Proteins - metabolism | Cell Differentiation - genetics | beta-Galactosidase - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cell Survival - drug effects | Cellular Senescence - genetics | Mesenchymal Stromal Cells - drug effects | Interleukin-6 - genetics | Cells, Cultured | Mesenchymal Stromal Cells - metabolism | DNA - metabolism | Reverse Transcriptase Polymerase Chain Reaction | DNA - genetics | Microscopy, Confocal | Cell Differentiation - drug effects | Cell Line, Tumor | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | DNA Damage | Histones - metabolism | Tumor Suppressor p53-Binding Protein 1 | Dactinomycin - pharmacology | DNA synthesis | Stem cells | Bone marrow | Senescence | Deoxyribonucleic acid--DNA | Index Medicus | Original
Journal Article
06/2013
Mechanistic insights into how enduring menstrual cycle hormonal signaling promotes tumorigenesis are emerging. We performed a genome-wide screen in primary... 
Senescence | Hormones
Dissertation
Journal Article
Autophagy, ISSN 1554-8627, 03/2015, Volume 11, Issue 3, pp. 527 - 537
Telomere dysfunction plays a complex role in tumorigenesis. While dysfunctional telomeres can block the proliferation of incipient cancer clones by inducing... 
TIFs, telomere dysfunction-induced foci | TDIS, telomere dysfunction-induced senescence | RBBP8/CtIP, retinoblastoma binding protein 8 | autophagy | telomeres | B2M, β-2-microglobulin | TERT, telomerase reverse transcriptase | chromosome fusions | ACD/Tpp1, adrenocortical dysplasia homolog (mouse) | SA-β-Gal, senescence-associated β-galactosidase | SASP | SASP, senescence associated secretory phenotype | HBSS, Hank's buffered salt solution | OIS, oncogene-induced senescence | senescence | ATG5, autophagy-related 5, ATG7, autophagy-related 7 | telomerase | genome instability | HMECs, human mammary epithelial cells | MEFs, mouse embryonic fibroblasts | MT-HsTER, mutant template-Homo sapiens template-containing RNA | MT-MmTER, mutant template-Mus musculus template-containing RNA | Telomeres | Senescence | Chromosome fusions | Genome instability | Autophagy | Telomerase | CANCER-CELLS | FUSION | TIFs | mutant template-Homo sapiens template-containing RNA | DNA-DAMAGE | Hank's buffered salt solution | autophagy-related 5 | CELL BIOLOGY | 2-microglobulin | human mammary epithelial cells | senescence associated secretory phenotype | TERT | RBBP8 | CtIP | telomere dysfunction-induced foci | mouse embryonic fibroblasts | SA--Gal | ATG7 | B2M | oncogene-induced senescence | ATG5 | adrenocortical dysplasia homolog (mouse) | MEFs | ACD | MT-MmTER | MECHANISM | BIOMARKER | BARRIER | telomere dysfunction-induced senescence | HMECs | MT-HsTER | senescence-associated -galactosidase | CELLULAR SENESCENCE | retinoblastoma binding protein 8 | autophagy-related 7 | mutant template-Mus musculus template-containing RNA | OIS | Tpp1 | HBSS | telomerase reverse transcriptase | TDIS | Genomic Instability | Cell Proliferation | Enzyme-Linked Immunosorbent Assay | Microtubule-Associated Proteins - genetics | Telomere - ultrastructure | Genomics | Humans | In Situ Hybridization, Fluorescence | Mice, Knockout | Chromosomes - ultrastructure | Autophagy-Related Protein 7 | Phenotype | Animals | Autophagy-Related Protein 5 | Cellular Senescence | DNA Repair | Mice | Interleukin-8 - metabolism | Interleukin-6 - metabolism | Microscopy, Fluorescence | Fibroblasts - metabolism | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2010, Volume 5, Issue 2, pp. e9188 - e9188
Cellular senescence irreversibly arrests cell proliferation in response to oncogenic stimuli. Human cells develop a senescence-associated secretory phenotype... 
HUMAN-FIBROBLASTS | EPITHELIAL-CELLS | DNA-DAMAGE | IN-VIVO | TRIGGERS SENESCENCE | BIOLOGY | GENE-EXPRESSION | GROWTH-FACTOR | CANCER PROGRESSION | CELLULAR SENESCENCE | REPLICATIVE SENESCENCE | Genomic Instability | Fibroblasts - secretion | Matrix Metalloproteinases - genetics | Proteome - genetics | Epithelial Cells - metabolism | Species Specificity | Fibroblasts - physiology | Humans | Insulin-Like Growth Factor Binding Protein 6 - genetics | Transplantation, Heterologous | Intracellular Signaling Peptides and Proteins - metabolism | Oxygen - metabolism | Neoplasms, Experimental - pathology | Epithelial Cells - physiology | Epithelial Cells - secretion | Neoplasms, Experimental - genetics | Insulin-Like Growth Factor Binding Protein 6 - metabolism | Proteomics - methods | Interleukin-6 - metabolism | Intracellular Signaling Peptides and Proteins - genetics | DNA-Binding Proteins | Fibroblasts - metabolism | Cellular Senescence - genetics | Interleukin-6 - genetics | Oxygen - physiology | Mice, Inbred C57BL | Cells, Cultured | Chromosomal Proteins, Non-Histone | Cellular Senescence - physiology | Tumor Burden | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Phenotype | Animals | Mice, Nude | Mice | DNA Damage | Matrix Metalloproteinases - metabolism | Neoplasms, Experimental - metabolism | Tumor Suppressor p53-Binding Protein 1 | Proteome - metabolism | Physiological aspects | Genetic aspects | Cytokines | Cells | Cell proliferation | Cell culture | Senescence | Matrix metalloproteinases | Laboratories | Epithelial cells | DNA damage | Radiation | Genomes | Genotype & phenotype | Cell growth | Cell cycle | Fibroblasts | Aging | Physiology | Life sciences | Tumorigenesis | Vascular endothelial growth factor | Telomerase | Age | Deoxyribonucleic acid--DNA | Phenotypes | Oxygen | Secretion | Breast cancer | Gene expression | Studies | Chemokines | Esophageal cancer | Tumors | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article