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Apoptosis (the 1992 Frank Rose Memorial Lecture)

Apoptosis (the 1992 Frank Rose Memorial Lecture) Apoptosis is a mode of cell death with characteristic structural features. These appear to result from a set of discrete cellular events that are regulated by gene expression. Oncogenesis and oncosuppressor genes are involved in this regulation. The role of c-myc is of particular interest, as it can act as a bivalent regulator, determining either cell proliferation or apoptosis, depending on whether free movement around the cell cycle is supported (by growth factors) or is limited by growth factor deprivation or treatment with other cycle-blocking agents. In vivo, c-myc expression may be associated with a 'high-turnover' state in which cell proliferation and apoptosis co-exist. Certain other oncogenes (e.g. ras, bcl-2) rescue cells from susceptibility to apoptosis and so convert this high-turnover state into rapid population expansion. One role of the oncosuppressor gene p53 may be to initiate apoptosis by causing G 1/S arrest in cells expressing c-myc. Some aspects of resistance and sensitivity to chemotherapeutic agents can be explained on the basis of movement between the population-expansion and the high-turnover states, perhaps through modulation of the expression of these and other genes. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Cancer Springer Journals

Apoptosis (the 1992 Frank Rose Memorial Lecture)

Wyllie, AH
British Journal of Cancer , Volume 67 (2) – Feb 1, 1993
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References (60)

Publisher
Springer Journals
Copyright
Copyright © 1993 by Cancer Research Campaign
Subject
Biomedicine; Biomedicine, general; Cancer Research; Epidemiology; Molecular Medicine; Oncology; Drug Resistance
ISSN
0007-0920
eISSN
1532-1827
DOI
10.1038/bjc.1993.40
Publisher site
See Article on Publisher Site

Abstract

Apoptosis is a mode of cell death with characteristic structural features. These appear to result from a set of discrete cellular events that are regulated by gene expression. Oncogenesis and oncosuppressor genes are involved in this regulation. The role of c-myc is of particular interest, as it can act as a bivalent regulator, determining either cell proliferation or apoptosis, depending on whether free movement around the cell cycle is supported (by growth factors) or is limited by growth factor deprivation or treatment with other cycle-blocking agents. In vivo, c-myc expression may be associated with a 'high-turnover' state in which cell proliferation and apoptosis co-exist. Certain other oncogenes (e.g. ras, bcl-2) rescue cells from susceptibility to apoptosis and so convert this high-turnover state into rapid population expansion. One role of the oncosuppressor gene p53 may be to initiate apoptosis by causing G 1/S arrest in cells expressing c-myc. Some aspects of resistance and sensitivity to chemotherapeutic agents can be explained on the basis of movement between the population-expansion and the high-turnover states, perhaps through modulation of the expression of these and other genes.

Journal

British Journal of Cancer – Springer Journals

Published: Feb 1, 1993

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