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Science 5 July 1996:
Vol. 273. no. 5271, pp. 63 - 67
DOI: 10.1126/science.273.5271.63
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Articles

Replicative Senescence: Implications for in Vivo Aging and Tumor Suppression

James R. Smith * and Olivia M. Pereira-Smith

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.

The authors are at the Roy M. and Phyllis Gough Huffington Center on Aging, in the Division of Molecular Virology, and in the Departments of Cell Biology and Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030-3498, USA.
* To whom correspondence should be addressed.


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Inhibition of the Phosphoinositide 3-Kinase Pathway Induces a Senescence-like Arrest Mediated by p27Kip1.
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Insulin-like Growth Factor-I Extends in Vitro Replicative Life Span of Skeletal Muscle Satellite Cells by Enhancing G1/S Cell Cycle Progression via the Activation of Phosphatidylinositol 3'-Kinase/Akt Signaling Pathway.
M. V. Chakravarthy, T. W. Abraha, R. J. Schwartz, M. L. Fiorotto, and F. W. Booth (2000)
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Science. ISSN 0036-8075 (print), 1095-9203 (online)