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Journal of Biomedicine and Biotechnology
Volume 1 (2001), Issue 1, Pages 28-37
Research article

Cellular Senescence: Ex Vivo p53-Dependent Asymmetric Cell Kinetics

1The Molecular Oncology Group, Division of Medical Science, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA
2Pharmacology Department, Division of Medical Science, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA
3Department of Radiation Oncology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
4Geron Corporation, Menlo Park, California 94025, USA
5Division of Bioengineering and Environmental Health and Center for Environmental Health Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA

Copyright © 2001 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Although senescence is a defining property of euploid mammalian cells, its physiologic basis remains obscure. Previously, cell kinetics properties of normal tissue cells have not been considered in models for senescence. We now provide evidence that senescence is in fact the natural consequence of normal in vivo somatic stem cell kinetics extended in culture. This concept of senescence is based on our discovery that cells engineered to conditionally express the well-recognized tumor suppressor protein and senescence factor, p53, exhibit asymmetric cell kinetics. In vivo, asymmetric cell kinetics are essential for maintenance of somatic stem cells; ex vivo, the same cell kinetics yield senescence as a simple kinetic endpoint. This new “asymmetric cell kinetics model” for senescence suggests novel strategies for the isolation and propagation of somatic tissue stem cells in culture.