Putting the stress on senescence.

[1]  Wenyi Wei,et al.  Role of p14ARF in Replicative and Induced Senescence of Human Fibroblasts , 2001, Molecular and Cellular Biology.

[2]  A. Berns,et al.  Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice , 2001, Nature.

[3]  D. Carrasco,et al.  Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis , 2001, Nature.

[4]  F. Zindy,et al.  Differential effects of p19Arf and p16Ink4a loss on senescence of murine bone marrow-derived preB cells and macrophages , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[5]  R. Alani,et al.  Id1 regulation of cellular senescence through transcriptional repression of p16/Ink4a , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[6]  R. DePinho,et al.  Telomere dysfunction and evolution of intestinal carcinoma in mice and humans , 2001, Nature Genetics.

[7]  E. Seto,et al.  Histone deacetylases in replicative senescence: evidence for a senescence‐specific form of HDAC‐2 , 2001, FEBS letters.

[8]  M. Blasco,et al.  Increased epidermal tumors and increased skin wound healing in transgenic mice overexpressing the catalytic subunit of telomerase, mTERT, in basal keratinocytes , 2001, The EMBO journal.

[9]  M. Blasco,et al.  The Absence of the DNA-Dependent Protein Kinase Catalytic Subunit in Mice Results in Anaphase Bridges and in Increased Telomeric Fusions with Normal Telomere Length and G-Strand Overhang , 2001, Molecular and Cellular Biology.

[10]  S. Lowe,et al.  Oncogenic ras activates the ARF-p53 pathway to suppress epithelial cell transformation , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[11]  F. Tamanini,et al.  Molecular Mechanisms of the Biological Clock in Cultured Fibroblasts , 2001, Science.

[12]  P. Yaswen,et al.  Expression of the telomerase catalytic subunit, hTERT, induces resistance to transforming growth factor β growth inhibition in p16INK4A(−) human mammary epithelial cells , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[13]  V. Paradis,et al.  Replicative senescence in normal liver, chronic hepatitis C, and hepatocellular carcinomas. , 2001, Human pathology.

[14]  G. Peters,et al.  Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence , 2001, Nature.

[15]  J. Shay,et al.  Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions. , 2001, Genes & development.

[16]  J. Shay,et al.  Cellular senescence as a tumor-protection mechanism: the essential role of counting. , 2001, Current opinion in genetics & development.

[17]  R. Bernards,et al.  Escape from premature senescence is not sufficient for oncogenic transformation by Ras , 2001, Nature Cell Biology.

[18]  D. Kurz,et al.  Cellular Senescence After Single and Repeated Balloon Catheter Denudations of Rabbit Carotid Arteries , 2001, Arteriosclerosis, thrombosis, and vascular biology.

[19]  A. Lloyd,et al.  Lack of Replicative Senescence in Normal Rodent Glia , 2001, Science.

[20]  A. Lloyd,et al.  Lack of Replicative Senescence in Cultured Rat Oligodendrocyte Precursor Cells , 2001, Science.

[21]  J. Axelman,et al.  Human embryonic germ cell derivatives express a broad range of developmentally distinct markers and proliferate extensively in vitro. , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[22]  T. Jacks,et al.  Targeted disruption of the three Rb-related genes leads to loss of G(1) control and immortalization. , 2000, Genes & development.

[23]  A. V. van Rossum,et al.  Ablation of the retinoblastoma gene family deregulates G(1) control causing immortalization and increased cell turnover under growth-restricting conditions. , 2000, Genes & development.

[24]  J. Weitzman,et al.  JunD protects cells from p53-dependent senescence and apoptosis. , 2000, Molecular cell.

[25]  Marc J. van de Vijver,et al.  Senescence bypass screen identifies TBX2, which represses Cdkn2a (p19ARF) and is amplified in a subset of human breast cancers , 2000, Nature Genetics.

[26]  D. Kurz,et al.  Senescence-associated (beta)-galactosidase reflects an increase in lysosomal mass during replicative ageing of human endothelial cells. , 2000, Journal of cell science.

[27]  E. Medrano,et al.  Cellular and molecular mechanisms of stress-induced premature senescence (SIPS) of human diploid fibroblasts and melanocytes , 2000, Experimental Gerontology.

[28]  M. Diaz,et al.  Id-1 delays senescence but does not immortalize keratinocytes. , 2000, The Journal of biological chemistry.

[29]  M. Blasco,et al.  Mammalian Ku86 protein prevents telomeric fusions independently of the length of TTAGGG repeats and the G‐strand overhang , 2000, EMBO reports.

[30]  M. Blasco,et al.  Telomerase-deficient mice with short telomeres are resistant to skin tumorigenesis , 2000, Nature Genetics.

[31]  S. Lowe,et al.  PML is induced by oncogenic ras and promotes premature senescence. , 2000, Genes & development.

[32]  D. Hanahan Cancer: Benefits of bad telomeres , 2000, Nature.

[33]  Lynda Chin,et al.  Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice , 2000, Nature.

[34]  A. Bounacer,et al.  Evidence for a Telomere-Independent “Clock” Limiting RAS Oncogene-Driven Proliferation of Human Thyroid Epithelial Cells , 2000, Molecular and Cellular Biology.

[35]  M. Roussel,et al.  Disruption of the ARF transcriptional activator DMP1 facilitates cell immortalization, Ras transformation, and tumorigenesis. , 2000, Genes & development.

[36]  Pier Paolo Pandolfi,et al.  PML regulates p53 acetylation and premature senescence induced by oncogenic Ras , 2000, Nature.

[37]  M. Benson,et al.  Expression of senescence-associated beta-galactosidase in enlarged prostates from men with benign prostatic hyperplasia. , 2000, Urology.

[38]  E. Wagner,et al.  JunB suppresses cell proliferation by transcriptional activation of p16INK4a expression , 2000, The EMBO journal.

[39]  Gregory J. Hannon,et al.  Cell biology: Risky immortalization by telomerase , 2000, Nature.

[40]  J. McDougall,et al.  Genetic and epigenetic changes in human epithelial cells immortalized by telomerase. , 2000, The American journal of pathology.

[41]  M. Serrano,et al.  Tumor suppressors and oncogenes in cellular senescence☆ , 2000, Experimental Gerontology.

[42]  D. Beach,et al.  p16INK4A and p19ARF act in overlapping pathways in cellular immortalization , 2000, Nature Cell Biology.

[43]  R. Reddel The role of senescence and immortalization in carcinogenesis. , 2000, Carcinogenesis.

[44]  W. Hahn,et al.  Human Keratinocytes That Express hTERT and Also Bypass a p16INK4a-Enforced Mechanism That Limits Life Span Become Immortal yet Retain Normal Growth and Differentiation Characteristics , 2000, Molecular and Cellular Biology.

[45]  M. Blasco,et al.  Telomeres and telomerase. , 1999, Genes & development.

[46]  Lynda Chin,et al.  p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis , 1999, Cell.

[47]  V. Ferrans,et al.  Ras Proteins Induce Senescence by Altering the Intracellular Levels of Reactive Oxygen Species* , 1999, The Journal of Biological Chemistry.

[48]  G. Nolan,et al.  Analysis of Genomic Integrity and p53-Dependent G1Checkpoint in Telomerase-Induced Extended-Life-Span Human Fibroblasts , 1999, Molecular and Cellular Biology.

[49]  D. Broccoli,et al.  p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2. , 1999, Science.

[50]  M. Hande,et al.  Telomere Length Dynamics and Chromosomal Instability in Cells Derived from Telomerase Null Mice , 1999, The Journal of cell biology.

[51]  R. DePinho,et al.  The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus , 1999, Nature.

[52]  M. White,et al.  Absence of cancer–associated changes in human fibroblasts immortalized with telomerase , 1999, Nature Genetics.

[53]  Xu-Rong Jiang,et al.  Telomerase expression in human somatic cells does not induce changes associated with a transformed phenotype , 1999, Nature Genetics.

[54]  T. Kiyono,et al.  Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells , 1998, Nature.

[55]  S. Lowe,et al.  Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling. , 1998, Genes & development.

[56]  D. Woods,et al.  Senescence of human fibroblasts induced by oncogenic Raf. , 1998, Genes & development.

[57]  M. Serrano,et al.  p19ARF links the tumour suppressor p53 to Ras , 1998, Nature.

[58]  T. Lange Telomeres and Senescence: Ending the Debate , 1998 .

[59]  C. Harley,et al.  Extension of life-span by introduction of telomerase into normal human cells. , 1998, Science.

[60]  L. Hayflick How and why we age , 1994, Experimental Gerontology.

[61]  María A Blasco,et al.  Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA , 1997, Cell.

[62]  S. Lowe,et al.  Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a , 1997, Cell.

[63]  Human fibroblast commitment to a senescence-like state in response to histone deacetylase inhibitors is cell cycle dependent. , 1996, Molecular and cellular biology.

[64]  C Roskelley,et al.  A biomarker that identifies senescent human cells in culture and in aging skin in vivo. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[65]  G. Wahl,et al.  DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts. , 1994, Genes & development.