J Campisi

Summary

Affiliation: Lawrence Berkeley National Laboratory
Country: USA

Publications

  1. ncbi request reprint Suppressing cancer: the importance of being senescent
    Judith Campisi
    Lawrence Berkeley National Laboratory, Life Sciences Division, 1 Cyclotron Road, Berkeley, CA 94720 and Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Science 309:886-7. 2005
  2. doi request reprint Aging and cancer cell biology, 2008
    Judith Campisi
    Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Aging Cell 7:281-4. 2008
  3. pmc Bloom syndrome cells undergo p53-dependent apoptosis and delayed assembly of BRCA1 and NBS1 repair complexes at stalled replication forks
    Albert R Davalos
    Lawrence Berkeley National Laboratory, Life Sciences Division, Berkeley, CA 94720, USA
    J Cell Biol 162:1197-209. 2003
  4. pmc Regulation and localization of the Bloom syndrome protein in response to DNA damage
    O Bischof
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    J Cell Biol 153:367-80. 2001
  5. pmc Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin
    Michael C Velarde
    Buck Institute for Research on Aging, Novato, CA 94945, USA
    Aging (Albany NY) 4:3-12. 2012
  6. pmc p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes
    Albert R Davalos
    Lawrence Berkeley National Laboratory, Life Sciences Division, Berkeley, CA 94720, USA
    J Cell Biol 201:613-29. 2013
  7. pmc Comprehensive microRNA profiling in B-cells of human centenarians by massively parallel sequencing
    Saurabh Gombar
    Department of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    BMC Genomics 13:353. 2012
  8. ncbi request reprint Aging, tumor suppression and cancer: high wire-act!
    Judith Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Mech Ageing Dev 126:51-8. 2005
  9. ncbi request reprint Cancer and ageing: rival demons?
    Judith Campisi
    Lawrence Berkeley National Laboratory, Life Sciences Division, 1 Cyclotron Road, Berkeley, California 94720, USA
    Nat Rev Cancer 3:339-49. 2003
  10. ncbi request reprint Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors
    Judith Campisi
    Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Cell 120:513-22. 2005

Research Grants

  1. SENESCENCE AND LONGEVITY MODULATING GENES
    Judith Campisi; Fiscal Year: 1999
  2. Senescence and Longevity Modulating Genes, WRN and BLM
    Judith Campisi; Fiscal Year: 2006
  3. Role of WRN in Longevity Assurance
    Judith Campisi; Fiscal Year: 2005
  4. Role of WRN in Longevity Assurance
    Judith Campisi; Fiscal Year: 2007
  5. SENESCENCE AND LONGEVITY MODULATING GENES
    Judith Campisi; Fiscal Year: 2002
  6. Training in Basic Aging Research and Age-Related Disease
    Judith Campisi; Fiscal Year: 2007
  7. Senescence and Longevity Modulating Genes, WRN and BLM
    Judith Campisi; Fiscal Year: 2007
  8. CELLULAR SENESCENCE AND CONTROL OF GENE EXPRESSION
    Judith Campisi; Fiscal Year: 2007
  9. Role of WRN in Longevity Assurance
    Judith Campisi; Fiscal Year: 2006
  10. Senescence and Longevity Modulating Genes, WRN and BLM
    Judith Campisi; Fiscal Year: 2005

Detail Information

Publications93

  1. ncbi request reprint Suppressing cancer: the importance of being senescent
    Judith Campisi
    Lawrence Berkeley National Laboratory, Life Sciences Division, 1 Cyclotron Road, Berkeley, CA 94720 and Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Science 309:886-7. 2005
  2. doi request reprint Aging and cancer cell biology, 2008
    Judith Campisi
    Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Aging Cell 7:281-4. 2008
    ..These articles reveal the expected complexities, but also surprising conservation, in mechanisms that link cancer and aging...
  3. pmc Bloom syndrome cells undergo p53-dependent apoptosis and delayed assembly of BRCA1 and NBS1 repair complexes at stalled replication forks
    Albert R Davalos
    Lawrence Berkeley National Laboratory, Life Sciences Division, Berkeley, CA 94720, USA
    J Cell Biol 162:1197-209. 2003
    ..These findings suggest that BLM is an early responder to damaged replication forks. Moreover, p53 eliminates cells that rapidly assemble BRCA1/NBS1 without BLM, suggesting that BLM is essential for timely BRCA1/NBS1 function...
  4. pmc Regulation and localization of the Bloom syndrome protein in response to DNA damage
    O Bischof
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    J Cell Biol 153:367-80. 2001
    ..Our findings suggest that BLM is part of a dynamic nuclear matrix-based complex that requires PML and functions during G2 in undamaged cells and recombinational repair after DNA damage...
  5. pmc Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin
    Michael C Velarde
    Buck Institute for Research on Aging, Novato, CA 94945, USA
    Aging (Albany NY) 4:3-12. 2012
    ..Our results support the idea that mitochondrial oxidative stress and cellular senescence contribute to aging skin phenotypes in vivo...
  6. pmc p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes
    Albert R Davalos
    Lawrence Berkeley National Laboratory, Life Sciences Division, Berkeley, CA 94720, USA
    J Cell Biol 201:613-29. 2013
    ..Our findings identify senescence as a novel biological setting in which HMGB1 functions and link HMGB1 redistribution to p53 activity and senescence-associated inflammation...
  7. pmc Comprehensive microRNA profiling in B-cells of human centenarians by massively parallel sequencing
    Saurabh Gombar
    Department of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    BMC Genomics 13:353. 2012
    ..Despite their demonstrated roles in age-associated pathologies, little is known about the role of miRNAs in human aging and longevity...
  8. ncbi request reprint Aging, tumor suppression and cancer: high wire-act!
    Judith Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Mech Ageing Dev 126:51-8. 2005
    ....
  9. ncbi request reprint Cancer and ageing: rival demons?
    Judith Campisi
    Lawrence Berkeley National Laboratory, Life Sciences Division, 1 Cyclotron Road, Berkeley, California 94720, USA
    Nat Rev Cancer 3:339-49. 2003
    ..Recent evidence indicates that some mammalian tumour-suppressor mechanisms contribute to ageing. How might this have happened, and what are its implications for our ability to control cancer and ageing?..
  10. ncbi request reprint Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors
    Judith Campisi
    Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Cell 120:513-22. 2005
    ..Thus, the senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate...
  11. ncbi request reprint Cellular senescence: when bad things happen to good cells
    Judith Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, California 94720, USA
    Nat Rev Mol Cell Biol 8:729-40. 2007
    ....
  12. ncbi request reprint Aging and cancer cell biology, 2007
    Judith Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Aging Cell 6:261-3. 2007
    ....
  13. ncbi request reprint Cellular senescence and apoptosis: how cellular responses might influence aging phenotypes
    Judith Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Exp Gerontol 38:5-11. 2003
    ..Both processes are essential for the viability and fitness of young organisms, but may contribute to aging phenotypes, including certain age-related diseases...
  14. ncbi request reprint Cellular senescence as a tumor-suppressor mechanism
    J Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Trends Cell Biol 11:S27-31. 2001
    ..Recent findings have revealed the complexities of the senescence phenotype and unexpected possible consequences for the organism...
  15. ncbi request reprint Cellular senescence, cancer and aging: the telomere connection
    J Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, Mailstop 84 171, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Exp Gerontol 36:1619-37. 2001
    ....
  16. ncbi request reprint From cells to organisms: can we learn about aging from cells in culture?
    J Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, Mailstop 84 171, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Exp Gerontol 36:607-18. 2001
    ..Cross-species comparisons suggest there is a relationship between the senescence of cells in culture and organismal life span, but the relationship is neither quantitative nor direct...
  17. ncbi request reprint Cancer, aging and cellular senescence
    J Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    In Vivo 14:183-8. 2000
    ..Thus, mutation accumulation may synergize with the accumulation of senescent cells, leading to increasing risk for developing cancer that is a hallmark of mammalian aging...
  18. ncbi request reprint Cancer and aging: yin, yang, and p53
    Judith Campisi
    Lawrence Berkeley National Laboratory, MS 84 171, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Sci Aging Knowledge Environ 2002:pe1. 2002
    ..This new discovery is discussed in light of previous findings related to mechanisms of aging...
  19. ncbi request reprint Aging, chromatin, and food restriction--connecting the dots
    J Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Science 289:2062-3. 2000
    ..In her Perspective, Campisi comments on new work showing that caloric restriction increases longevity in yeast by activating the SIR2 gene, which alters the compactness of chromatin and thus regulates gene expression (Lin et al.)...
  20. pmc Senescent fibroblasts promote epithelial cell growth and tumorigenesis: a link between cancer and aging
    A Krtolica
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Proc Natl Acad Sci U S A 98:12072-7. 2001
    ..Our findings suggest that, although cellular senescence suppresses tumorigenesis early in life, it may promote cancer in aged organisms, suggesting it is an example of evolutionary antagonistic pleiotropy...
  21. pmc Ku acts in a unique way at the mammalian telomere to prevent end joining
    H L Hsu
    Department of Cell and Molecular Biology, Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Genes Dev 14:2807-12. 2000
    ..We propose that Ku localizes to internal regions of the telomere via a high-affinity interaction with TRF1. Therefore, Ku acts in a unique way at the telomere to prevent end joining...
  22. pmc Regulation of a senescence checkpoint response by the E2F1 transcription factor and p14(ARF) tumor suppressor
    G P Dimri
    Department of Cell Biology, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Mol Cell Biol 20:273-85. 2000
    ....
  23. ncbi request reprint C. elegans clk-2, a gene that limits life span, encodes a telomere length regulator similar to yeast telomere binding protein Tel2p
    C S Lim
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Curr Biol 11:1706-10. 2001
    ..In mammals, telomere length and structure can influence cellular, and possibly organismal, aging. Here, we show that clk-2 encodes a regulator of telomere length in C. elegans...
  24. pmc Mitochondrial DNA damage induces apoptosis in senescent cells
    R M Laberge
    Buck Institute for Research on Aging, Novato, CA, USA
    Cell Death Dis 4:e727. 2013
    ..Thus, cellular senescence and mtDNA damage are outcomes of synthetic nucleoside analog treatment, indicating that the GCV-HSVtk combination can be used effectively to promote the targeted formation or eradication of senescent cells. ..
  25. ncbi request reprint Regulation of cellular senescence by p53
    K Itahana
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Eur J Biochem 268:2784-91. 2001
    ..Despite the well-documented central role for p53 in the senescence response, many questions remain regarding how p53 senses senescence-inducing stimuli and how it elicits the senescent phenotype...
  26. ncbi request reprint TANK2, a new TRF1-associated poly(ADP-ribose) polymerase, causes rapid induction of cell death upon overexpression
    P G Kaminker
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    J Biol Chem 276:35891-9. 2001
    ..The cell death was prevented by the PARP inhibitor 3-aminobenzamide. In vivo, TANK2 may differ from TANK1 in its intrinsic or regulated PARP activity or its substrate specificity...
  27. pmc Characterization of the human and mouse WRN 3'-->5' exonuclease
    S Huang
    Life Sciences Division, Mailstop 84 144, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Nucleic Acids Res 28:2396-405. 2000
    ..Finally, we show that hWRN forms a trimer and interacts with the proliferating cell nuclear antigen in vitro. These findings provide new data on the biochemical activities of WRN that may help elucidate its role(s) in DNA metabolism...
  28. ncbi request reprint Werner syndrome protein is regulated and phosphorylated by DNA-dependent protein kinase
    S M Yannone
    Life Sciences Division, Department of Molecular and Cellular Biology, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    J Biol Chem 276:38242-8. 2001
    ..These data suggest that DNA-PK and WRN may function together in DNA metabolism and implicate WRN function in non-homologous end joining...
  29. pmc How does proliferative homeostasis change with age? What causes it and how does it contribute to aging?
    Judith Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    J Gerontol A Biol Sci Med Sci 64:164-6. 2009
    ..New molecular tools and model organisms, some already on the horizon, will need to be developed to better understand the roles of apoptosis and cellular senescence in age-associated changes in proliferative homeostasis...
  30. ncbi request reprint Oncogene-induced senescence pathways weave an intricate tapestry
    Paul Yaswen
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Rd, Berkeley, CA 94720, USA
    Cell 128:233-4. 2007
    ..They show that the p38-regulated/activated protein kinase (PRAK) induces senescence downstream of oncogenic Ras by directly phosphorylating and activating the tumor-suppressor protein p53...
  31. pmc p53-dependent integration of telomere and growth factor deprivation signals
    Alain Beliveau
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Proc Natl Acad Sci U S A 104:4431-6. 2007
    ..Our findings provide a previously unrecognized mechanistic explanation for the observation that ectopically expressed hTERT conveys growth advantages to cells, without having to postulate nontelomeric functions for the enzyme...
  32. pmc Two faces of p53: aging and tumor suppression
    Francis Rodier
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Nucleic Acids Res 35:7475-84. 2007
    ..Here, we discuss the role of p53 as a key regulator of the DNA damage responses, and discuss how p53 integrates the outcome of the DNA damage response to optimally balance tumor suppression and longevity...
  33. ncbi request reprint Aging and cancer cell biology, 2009
    Judith Campisi
    Buck Institute for Age Research, Novato, CA 94945, USA
    Aging Cell 8:221-5. 2009
    ....
  34. pmc A novel pathway for mammary epithelial cell invasion induced by the helix-loop-helix protein Id-1
    P Y Desprez
    Department of Cell and Molecular Biology, Life Sciences Division, Berkeley National Laboratory, University of California, Berkeley, California 94720, USA
    Mol Cell Biol 18:4577-88. 1998
    ..This Id-1-regulated invasive phenotype could contribute to involution of the mammary gland and possibly to the development of invasive breast cancer...
  35. ncbi request reprint TIN2, a new regulator of telomere length in human cells
    S H Kim
    Department of Cell and Molecular Biology, Lawrence Berkeley National Laboratory, Berkeley, California, USA
    Nat Genet 23:405-12. 1999
    ..Our findings suggest that TRF1 is insufficient for control of telomere length in human cells, and that TIN2 is an essential mediator of TRF1 function...
  36. pmc Environmental stress, ageing and glial cell senescence: a novel mechanistic link to Parkinson's disease?
    S J Chinta
    Buck Institute for Research on Aging, Novato, CA, USA
    J Intern Med 273:429-36. 2013
    ....
  37. ncbi request reprint Integrating epithelial cancer, aging stroma and cellular senescence
    A Krtolica
    Lawrence Berkeley National Laboratory, Life Sciences Division, Mailstop 84 171, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Adv Gerontol 11:109-16. 2003
    ..Recent evidence lends support to this idea, and suggests that cellular senescence may be an example of evolutionary antagonistic pleiotropy...
  38. ncbi request reprint Selective cleavage of BLM, the bloom syndrome protein, during apoptotic cell death
    O Bischof
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley California 94720, USA
    J Biol Chem 276:12068-75. 2001
    ..The results suggest that BLM, but not WRN, is an early selected target during the execution of apoptosis...
  39. ncbi request reprint ATR and ATM-dependent movement of BLM helicase during replication stress ensures optimal ATM activation and 53BP1 focus formation
    Albert R Davalos
    Lawrence Berkeley National Laboratory, Life Sciences Division, Berkeley, California 94720, USA
    Cell Cycle 3:1579-86. 2004
    ..BLM recruits 53BP1 to these lesions independent of its helicase activity, and optimal activation of ATM requires both p53 and BLM helicase activities...
  40. pmc Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor
    Jean Philippe Coppe
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA
    PLoS Biol 6:2853-68. 2008
    ..Moreover, they suggest a cell-nonautonomous mechanism by which p53 can restrain, and oncogenic RAS can promote, the development of age-related cancer by altering the tissue microenvironment...
  41. pmc Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion
    Francis Rodier
    Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Nat Cell Biol 11:973-9. 2009
    ..Thus, in addition to orchestrating cell-cycle checkpoints and DNA repair, a new and important role of the DDR is to allow damaged cells to communicate their compromised state to the surrounding tissue...
  42. ncbi request reprint Telomeres, aging and cancer: in search of a happy ending
    Sahn ho Kim Sh
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, California, CA 94720, USA
    Oncogene 21:503-11. 2002
    ..Here, we discuss what is known about the basis for the links between telomeres, aging and cancer, and some of the known and proposed consequences of telomere dysfunction and maintenance for mammalian cells and organisms...
  43. pmc A human-like senescence-associated secretory phenotype is conserved in mouse cells dependent on physiological oxygen
    Jean Philippe Coppe
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, United States of America
    PLoS ONE 5:e9188. 2010
    ..Our findings underscore critical mouse-human differences in oxygen sensitivity, identify conditions to use mouse cells to model human cellular senescence, and reveal novel conserved features of the SASP...
  44. pmc Control of the replicative life span of human fibroblasts by p16 and the polycomb protein Bmi-1
    Koji Itahana
    Life Sciences Division, Lawrence Berkeley National Laboratory, California 94720, USA
    Mol Cell Biol 23:389-401. 2003
    ..Our data suggest that Bmi-1 extends the replicative life span of human fibroblasts by suppressing the p16-dependent senescence pathway...
  45. ncbi request reprint Cancer and aging: a model for the cancer promoting effects of the aging stroma
    Ana Krtolica
    Lawrence Berkeley National Laboratory, Life Sciences Division, Mailstop 84 171, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Int J Biochem Cell Biol 34:1401-14. 2002
    ..Recent evidence lends support to this idea, and suggests that senescent stromal fibroblasts may be particularly adept at creating a tissue environment that can promote the development of age-related epithelial cancers...
  46. ncbi request reprint Cancer and aging: the importance of telomeres in genome maintenance
    Francis Rodier
    Lawrence Berkeley National Laboratory, Life Sciences Division, 1 Cyclotron Rd, Berkeley, CA 94720, USA
    Int J Biochem Cell Biol 37:977-90. 2005
    ..Here, we review what is known about the structure and function of telomeres in mammalian cells, particularly human cells, and how telomere dysfunction may arise and contribute to cancer and aging phenotypes...
  47. ncbi request reprint Analysis of tumor suppressor gene-induced senescence
    Judith Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, CA, USA
    Methods Mol Biol 223:155-72. 2003
  48. pmc Does damage to DNA and other macromolecules play a role in aging? If so, how?
    Judith Campisi
    Lawrence Berkeley National Laboratory, Life Sciences Division, 1 Cyclotron Road, Berkeley, CA 94720, USA
    J Gerontol A Biol Sci Med Sci 64:175-8. 2009
    ..New tools and approaches are on the horizon and will need to be developed and implemented before we can fully understand whether and to what extent macromolecular damage drives aging phenotypes...
  49. ncbi request reprint Stromal-epithelial interactions in aging and cancer: senescent fibroblasts alter epithelial cell differentiation
    Simona Parrinello
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    J Cell Sci 118:485-96. 2005
    ....
  50. ncbi request reprint The senescence-associated secretory phenotype: the dark side of tumor suppression
    Jean Philippe Coppe
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Annu Rev Pathol 5:99-118. 2010
    ..The most significant of these effects is the acquisition of a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression...
  51. ncbi request reprint Telomere length mediates the effects of telomerase on the cellular response to genotoxic stress
    Miguel A Rubio
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Exp Cell Res 298:17-27. 2004
    ..Our findings identify a mechanism and conditions under which telomerase and telomeres affect the response of human cells to genotoxic agents and may have important implications for anti-cancer interventions...
  52. ncbi request reprint Oxygen sensitivity severely limits the replicative lifespan of murine fibroblasts
    Simona Parrinello
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Nat Cell Biol 5:741-7. 2003
    ..Our results identify oxygen sensitivity as a critical difference between mouse and human cells, explaining their proliferative differences in culture, and possibly their different rates of cancer and ageing...
  53. ncbi request reprint Meeting report: Translational Research at the Aging and Cancer Interface
    Christopher C Benz
    Buck Institute for Age Research, Novato, California, USA
    Cancer Res 67:4560-3. 2007
  54. ncbi request reprint Reversible manipulation of telomerase expression and telomere length. Implications for the ionizing radiation response and replicative senescence of human cells
    Miguel A Rubio
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    J Biol Chem 277:28609-17. 2002
    ..Our results support a role for telomere structure, rather than length, in replicative senescence...
  55. pmc Puzzles, promises and a cure for ageing
    Jan Vijg
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, California 94945, USA
    Nature 454:1065-71. 2008
    ..A better understanding of the targets of such interventions, as well as the proximate causes of ageing-related degeneration and disease, is essential before we can evaluate if abrogation of human senescence is a realistic prospect...
  56. ncbi request reprint Secretion of vascular endothelial growth factor by primary human fibroblasts at senescence
    Jean Philippe Coppe
    Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    J Biol Chem 281:29568-74. 2006
    ..Our findings may in part explain why senescent cells stimulate tumorigenesis in vivo and support the idea that senescent cells may facilitate age-associated cancer development by secreting factors that promote malignant progression...
  57. pmc Senescent cells as a source of inflammatory factors for tumor progression
    Albert R Davalos
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Cancer Metastasis Rev 29:273-83. 2010
    ..Here, we summarize our knowledge of the SASP and the impact it has on tissue microenvironments and ability to stimulate tumor progression...
  58. pmc Telomere dysfunction and cell survival: roles for distinct TIN2-containing complexes
    Sahn Ho Kim
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    J Cell Biol 181:447-60. 2008
    ..Our findings suggest that distinct TIN2 complexes exist and that TIN2-15C-sensitive subcomplexes are particularly important for cell survival in the absence of functional p53...
  59. pmc Reversal of human cellular senescence: roles of the p53 and p16 pathways
    Christian M Beausejour
    Lawrence Berkeley National Laboratory, MS 84 171, 1 Cyclotron Road, Berkeley, CA 94720, USA
    EMBO J 22:4212-22. 2003
    ..Our results indicate that the senescence response to telomere dysfunction is reversible and is maintained primarily by p53. However, p16 provides a dominant second barrier to the unlimited growth of human cells...
  60. pmc Higher-order nuclear organization in growth arrest of human mammary epithelial cells: a novel role for telomere-associated protein TIN2
    Patrick Kaminker
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, California 94945, USA
    J Cell Sci 118:1321-30. 2005
    ..Here we show that a novel extra-telomeric organization of TIN2 is associated with the control of cell proliferation and identify TIN2 as an important regulator of mammary epithelial differentiation...
  61. pmc MicroRNAs miR-146a/b negatively modulate the senescence-associated inflammatory mediators IL-6 and IL-8
    Dipa Bhaumik
    Buck Institute for Age Research, Novato, CA 94945, USA
    Aging (Albany NY) 1:402-11. 2009
    ....
  62. ncbi request reprint The thorny path linking cellular senescence to organismal aging
    Christopher K Patil
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Mech Ageing Dev 126:1040-5. 2005
  63. pmc Inflammatory networks during cellular senescence: causes and consequences
    Adam Freund
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Trends Mol Med 16:238-46. 2010
    ..We also summarize the cellular pathways/processes that are known to regulate this phenotype--namely, the DNA damage response, microRNAs, key transcription factors and kinases and chromatin remodeling...
  64. ncbi request reprint A role for p53 in maintaining and establishing the quiescence growth arrest in human cells
    Koji Itahana
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    J Biol Chem 277:18206-14. 2002
    ..Our data indicate that p53 is activated during both quiescence and senescence. They further suggest that p53 activity contributes, albeit not exclusively, to the quiescent growth arrest...
  65. pmc Cell surface-bound IL-1alpha is an upstream regulator of the senescence-associated IL-6/IL-8 cytokine network
    Arturo V Orjalo
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Proc Natl Acad Sci U S A 106:17031-6. 2009
    ..Thus, cell surface IL-1alpha is an essential cell-autonomous regulator of the senescence-associated IL-6/IL-8 cytokine network...
  66. pmc A novel form of the telomere-associated protein TIN2 localizes to the nuclear matrix
    Patrick G Kaminker
    Buck Institute for Age Research, Novato, California, USA
    Cell Cycle 8:931-9. 2009
    ..Our results suggest a dual role for TIN2 in mediating the function of the shelterin complex and tethering telomeres to the nuclear matrix...
  67. ncbi request reprint Caspase-independent cytochrome c release is a sensitive measure of low-level apoptosis in cell culture models
    Joshua C Goldstein
    Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Aging Cell 4:217-22. 2005
    ..Further, apoptosis increased subtly but measurably when human mammary epithelial and skin fibroblast cells entered crisis, indicating that cell death during crisis is largely non-apoptotic...
  68. ncbi request reprint Quantification of epithelial cells in coculture with fibroblasts by fluorescence image analysis
    Ana Krtolica
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Cytometry 49:73-82. 2002
    ..Proc Natl Acad Sci USA 98:12072-12077, 2001), we developed methods to quantify the proliferation of epithelial cells cocultured with fibroblasts...
  69. pmc The human telomere-associated protein TIN2 stimulates interactions between telomeric DNA tracts in vitro
    Sahn Ho Kim
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA
    EMBO Rep 4:685-91. 2003
    ..Unlike TRF1, TIN2 did not form homodimers. We propose that TIN2 alters the conformation of TRF1, which favours a tertiary telomeric structure that hinders telomerase from gaining access to telomeres...
  70. ncbi request reprint TIN2 mediates functions of TRF2 at human telomeres
    Sahn Ho Kim
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    J Biol Chem 279:43799-804. 2004
    ..TIN2 mutants defective in binding of TRF1 or TRF2 induce a DNA damage response and destabilize TRF1 and TRF2 at telomeres in human cells. Our findings suggest that the functions of TRF1 and TRF2 are linked by TIN2...
  71. ncbi request reprint Aging and genome maintenance: lessons from the mouse?
    Paul Hasty
    Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, TX 78245, USA
    Science 299:1355-9. 2003
    ..Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans...
  72. ncbi request reprint The aging factor in health and disease: the promise of basic research on aging
    Robert N Butler
    International Longevity Center USA, Alliance for Health and the Future, and Department of Geriatrics, Mount Sinai Medical Center, New York, NY 10028, USA
    Aging Clin Exp Res 16:104-11; discussion 111-2. 2004
  73. ncbi request reprint Mechanisms of cellular senescence in human and mouse cells
    Koji Itahana
    Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
    Biogerontology 5:1-10. 2004
    ....
  74. ncbi request reprint Between Scylla and Charybdis: p53 links tumor suppression and aging
    Judith Campisi
    Mech Ageing Dev 123:567-73. 2002
  75. pmc Zinc-finger protein-targeted gene regulation: genomewide single-gene specificity
    Siyuan Tan
    Sangamo BioSciences, Inc, Point Richmond Tech Center II, 501 Canal Boulevard, Richmond, CA 94804, USA
    Proc Natl Acad Sci U S A 100:11997-2002. 2003
    ..These data demonstrate the utility of ZFP TFs as precise tools for target validation, and highlight their potential as clinical therapeutics...
  76. ncbi request reprint Methods to detect biomarkers of cellular senescence: the senescence-associated beta-galactosidase assay
    Koji Itahana
    Department of Radiation Oncology, School of Medicine, The University of North Carolina, Chapel Hill, NC, USA
    Methods Mol Biol 371:21-31. 2007
    ..Because it is easy to detect, SA-beta-gal is currently a widely used biomarker of senescence. Here we describe a method to detect SA-beta-gal in detail, including some recent modifications...
  77. ncbi request reprint WRN, the protein deficient in Werner syndrome, plays a critical structural role in optimizing DNA repair
    Lishan Chen
    Department of Pathology, University of Washington, Seattle, WA 98195 7470, USA
    Aging Cell 2:191-9. 2003
    ..Another human RECQ helicase, BLM, suppressed HR but had little or no effect on NHEJ, suggesting that mammalian RECQ helicases have distinct functions that can finely regulate recombination events...
  78. ncbi request reprint Genomic instability, aging, and cellular senescence
    Rita A Busuttil
    Sam and Ann Barshop Center for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78245, USA
    Ann N Y Acad Sci 1019:245-55. 2004
    ....
  79. pmc A role for fibroblasts in mediating the effects of tobacco-induced epithelial cell growth and invasion
    Jean Philippe Coppe
    California Pacific Medical Center, Research Institute, San Francisco, CA 94107, USA
    Mol Cancer Res 6:1085-98. 2008
    ..Thus, tobacco may not only initiate mutagenic changes in epithelial cells but also promote the growth and invasion of mutant cells by creating a procarcinogenic stromal environment...
  80. ncbi request reprint Cancer and aging: more puzzles, more promises?
    Mikhail V Blagosklonny
    Cell Cycle 7:2615-8. 2008
    ..Here, we discuss the relationship between aging and cancer, the mechanism of metformin action, and the prospects of using this compound for life span extension in humans...
  81. ncbi request reprint Ageing: balancing regeneration and cancer
    Christian M Beausejour
    Nature 443:404-5. 2006
  82. pmc Collaboration of Werner syndrome protein and BRCA1 in cellular responses to DNA interstrand cross-links
    Wen Hsing Cheng
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Nucleic Acids Res 34:2751-60. 2006
    ..These findings suggest that WRN and BRCA1 act in a coordinated manner to facilitate repair of DNA ICLs...
  83. ncbi request reprint Fragile fugue: p53 in aging, cancer and IGF signaling
    Judith Campisi
    Nat Med 10:231-2. 2004
  84. ncbi request reprint The Bmi-1 oncogene induces telomerase activity and immortalizes human mammary epithelial cells
    Goberdhan P Dimri
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, New England Medical Center, Boston, Massachusetts 02111, USA
    Cancer Res 62:4736-45. 2002
    ..These data suggest that Bmi-1 regulates telomerase expression in MECs and plays a role in the development of human breast cancer...
  85. ncbi request reprint Time to talk SENS: critiquing the immutability of human aging
    Aubrey D N J de Grey
    Department of Genetics, University of Cambridge, Cambridge, UK
    Ann N Y Acad Sci 959:452-62; discussion 463-5. 2002
    ..Given the major demographic consequences if it came about, this possibility merits urgent debate...
  86. ncbi request reprint Oxygen accelerates the accumulation of mutations during the senescence and immortalization of murine cells in culture
    Rita A Busuttil
    Sam and Ann Barshop Center for Longevity and Aging Studies, University of Texas Health Science Center, STCBM, San Antonio, TX 78245, USA
    Aging Cell 2:287-94. 2003
    ..These findings demonstrate for the first time the impact of oxidative stress on the genomic integrity of murine cells during senescence and immortalization...
  87. ncbi request reprint Lack of WRN results in extensive deletion at nonhomologous joining ends
    Junko Oshima
    Department of Pathology, University of Washington, Seattle, Washington, 98195, USA
    Cancer Res 62:547-51. 2002
    ..This extensive deletion phenotype was complemented by wild-type WRN. These results suggest that WRN can out-compete other exonucleases that participate in double-strand break repair or stabilize the broken DNA end...
  88. ncbi request reprint Correction of cellular phenotypes of Hutchinson-Gilford Progeria cells by RNA interference
    Shurong Huang
    Department of Pathology, University of Washington, Box 357470, HSB K 543, 1959 NE Pacific Ave, Seattle, WA, 98195 7470, USA
    Hum Genet 118:444-50. 2005
    ..These findings provide a rationale for potential gene therapy...
  89. ncbi request reprint Vintage gerontology. Cell biologist Judith Campisi's lab has fermented new insights into cancer and the biology of aging
    Ingfei Chen
    Sci Aging Knowledge Environ 2004:nf6. 2004
  90. ncbi request reprint Mutant frequencies and spectra depend on growth state and passage number in cells cultured from transgenic lacZ-plasmid reporter mice
    Rita A Busuttil
    Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, STCBM Building, Suite 2 200, 15355 Lambda, San Antonio, TX 78245, USA
    DNA Repair (Amst) 5:52-60. 2006
    ..In long-term cultures, the locus is less suitable for studying induced mutations owing to the instability of the cell population...
  91. ncbi request reprint No restriction points in life and science
    Mikhail V Blagosklonny
    Cell Cycle 1:100-2. 2002
  92. pmc Generation and characterization of telomere length maintenance in tankyrase 2-deficient mice
    Y Jeffrey Chiang
    Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Building 10, 4B36, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Mol Cell Biol 26:2037-43. 2006
    ....

Research Grants20

  1. SENESCENCE AND LONGEVITY MODULATING GENES
    Judith Campisi; Fiscal Year: 1999
    ..The long range goal is to identify human longevity assurance genes and to know enough about their function to develop rational strategies for therapeutics or interventions. ..
  2. Senescence and Longevity Modulating Genes, WRN and BLM
    Judith Campisi; Fiscal Year: 2006
    ..Our studies will provide important insights into how WRN and BLM postpone the development of aging phenotypes and the development of cancer in humans. ..
  3. Role of WRN in Longevity Assurance
    Judith Campisi; Fiscal Year: 2005
    ..abstract_text> ..
  4. Role of WRN in Longevity Assurance
    Judith Campisi; Fiscal Year: 2007
    ..abstract_text> ..
  5. SENESCENCE AND LONGEVITY MODULATING GENES
    Judith Campisi; Fiscal Year: 2002
    ..The long range goal is to identify human longevity assurance genes and to know enough about their function to develop rational strategies for therapeutics or interventions. ..
  6. Training in Basic Aging Research and Age-Related Disease
    Judith Campisi; Fiscal Year: 2007
    ..S. population. ..
  7. Senescence and Longevity Modulating Genes, WRN and BLM
    Judith Campisi; Fiscal Year: 2007
    ..Our studies will provide important insights into how WRN and BLM postpone the development of aging phenotypes and the development of cancer in humans. ..
  8. CELLULAR SENESCENCE AND CONTROL OF GENE EXPRESSION
    Judith Campisi; Fiscal Year: 2007
    ....
  9. Role of WRN in Longevity Assurance
    Judith Campisi; Fiscal Year: 2006
    ..abstract_text> ..
  10. Senescence and Longevity Modulating Genes, WRN and BLM
    Judith Campisi; Fiscal Year: 2005
    ..Our studies will provide important insights into how WRN and BLM postpone the development of aging phenotypes and the development of cancer in humans. ..
  11. Senescence and Longevity Modulating Genes, WRN and BLM
    Judith Campisi; Fiscal Year: 2004
    ..Our studies will provide important insights into how WRN and BLM postpone the development of aging phenotypes and the development of cancer in humans. ..
  12. Role of WRN in Longevity Assurance
    Judith Campisi; Fiscal Year: 2004
    ..abstract_text> ..
  13. SENESCENCE AND LONGEVITY MODULATING GENES
    Judith Campisi; Fiscal Year: 2003
    ..The long range goal is to identify human longevity assurance genes and to know enough about their function to develop rational strategies for therapeutics or interventions. ..
  14. SENESCENCE AND LONGEVITY MODULATING GENES
    Judith Campisi; Fiscal Year: 2001
    ..The long range goal is to identify human longevity assurance genes and to know enough about their function to develop rational strategies for therapeutics or interventions. ..
  15. SENESCENCE AND LONGEVITY MODULATING GENES
    Judith Campisi; Fiscal Year: 2000
    ..The long range goal is to identify human longevity assurance genes and to know enough about their function to develop rational strategies for therapeutics or interventions. ..