Cell cycle and apoptosis.
Journal: 2001/January - Neoplasia
ISSN: 1522-8002
PUBMED: 11005563
Abstract:
In multicellular organisms, cell proliferation and death must be regulated to maintain tissue homeostasis. Many observations suggest that this regulation may be achieved, in part, by coupling the process of cell cycle progression and programmed cell death by using and controlling a shared set of factors. An argument in favor of a link between the cell cycle and apoptosis arises from the accumulated evidence that manipulation of the cell cycle may either prevent or induce an apoptotic response. This linkage has been recognized for tumor suppressor genes such as p53 and RB, the dominant oncogene, c-Myc, and several cyclin-dependent kinases (Cdks) and their regulators. These proteins that function in proliferative pathways may also act to sensitize cells to apoptosis. Indeed, unregulated cell proliferation can result in pathologic conditions including neoplasias if it is not countered by the appropriate cell death. Translating the knowledge gained by studying the connection between cell death and cell proliferation may aid in identifying novel therapies to circumvent disease progression or improve clinical outcome.
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Neoplasia 2(4): 291-299

Cell Cycle and Apoptosis<sup><a href="#FN1" rid="FN1" class=" fn">1</a></sup>

Department of Pathology, Anatomy and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Suite 226, 1020 Locust Street, Philadelphia, PA 19107
Address all correspondence to: Antonio Giordano, MD, PhD, Department of Pathology, Anatomy and Cell Biology, Jefferson Medical College, JAH Room 226, Philadelphia, PA 19107. E-mail: ude.ujt.icj.cal@nadroiga
Department of Pathology, Anatomy and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Suite 226, 1020 Locust Street, Philadelphia, PA 19107
Address all correspondence to: Antonio Giordano, MD, PhD, Department of Pathology, Anatomy and Cell Biology, Jefferson Medical College, JAH Room 226, Philadelphia, PA 19107. E-mail: ude.ujt.icj.cal@nadroiga
Received 1999 Sep 3; Revised 2000 Jul 7; Accepted 2000 Jul 10.

Abstract

In multicellular organisms, cell proliferation and death must be regulated to maintain tissue homeostasis. Many observations suggest that this regulation may be achieved, in part, by coupling the process of cell cycle progression and programmed cell death by using and controlling a shared set of factors. An argument in favor of a link between the cell cycle and apoptosis arises from the accumulated evidence that manipulation of the cell cycle may either prevent or induce an apoptotic response. This linkage has been recognized for tumor suppressor genes such as p53 and RB, the dominant oncogene, c-Myc, and several cyclin-dependent kinases (Cdks) and their regulators. These proteins that function in proliferative pathways may also act to sensitize cells to apoptosis. Indeed, unregulated cell proliferation can result in pathologic conditions including neoplasias if it is not countered by the appropriate cell death. Translating the knowledge gained by studying the connection between cell death and cell proliferation may aid in identifying novel therapies to circumvent disease progression or improve clinical outcome.

Keywords: apoptosis, cell cycle, c-myc, p53, pRb, Cdks
Abstract

Acknowledgements

The authors thank Marco Tafani for critically reading the manuscript and for his comments. M. K. was supported by NCI training grant 5 T32 CA 09137.

Acknowledgements

Footnotes

This work was supported by grants from the National Institutes of Health awarded to A. G. and in part by The Sbarro Institute.

Footnotes

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