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Replicative senescence: implications for in vivo aging and tumor suppression.

Author information

Affiliations

  • 1. Roy M. and Phyllis Gough Huffington Center on Aging, Baylor College of Medicine, Houston, TX 77030-3498, USA.
      Authors
    • Smith JR 1
    (1 author)

Science, 01 Jul 1996, 273(5271):63-67
https://doi.org/10.1126/science.273.5271.63 PMID: 8658197 

Review

A comment on this article appears in "Mutation in embryonic stem cells." Science. 2001 Apr 20;292(5516):438-40.

Abstract 

Normal cells have limited proliferative potential in culture, a fact that has been the basis of their use as a model for replicative senescence for many years. Recent molecular analyses have identified numerous changes in gene expression that occur as cells become senescent, and the results indicate that multiple levels of control contribute to the irreversible growth arrest. These include repression of growth stimulatory genes, overexpression of growth inhibitory genes, and interference with downstream pathways. Studies with cell types other than fibroblasts will better define the role of cell senescence in the aging process and in tumorigenesis.

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Read article at publisher's site: https://doi.org/10.1126/science.273.5271.63

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