This Article Free Full Text (Free PDF) Free References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Foster, J. R. Search for Related Content PubMed PubMed Citation Articles by Foster, J. R. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Cancer Social Bookmarking                         What's this?

Cell Death and Cell Proliferation in the Control of Normal and Neoplastic Tissue Growth

Pathology Section, Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire SK10 4TJ, United Kingdom

The development of reliable methodology for the assessment of rates of cell replication and cell death has enabled the study of how these 2 fundamentally opposed processes work to form and maintain tissue and to remodel tissue following diseases resulting in cell loss. The balance between these 2 processes and the consequences of an imbalance are fundamental to a clearer understanding of how hyperplasia and neoplasia develop in tissues under the influence of chemicals and drugs. An understanding of the changes that occur in target organs and tissues following chemical or drug exposure has enabled a better understanding of the mechanism by which these chemicals are able to induce cancer after prolonged exposure. Studies of the control of cell replication and the changes that occur following drug exposure have defined 2 types of response, 1 in which the cell replicative response is sustained and the other in which the cell replicative response is transient and occurs during the first few days of exposure. Although regulatory and scientific opinion appears ready to accept sustained cell replicative processes as an increased risk factor in the development of cancer, the role played by transient increases in cell replication remains unclear. Concurrent events in target organs following treatment with chemicals that induce transient increases in cell replication have revealed that the rates of apoptosis are suppressed at the same time as the cell replication levels are induced. Additional evidence suggests that growth and antigrowth factors are central in controlling these responses. Escape from the regulatory action of these factors is postulated to be one of the ways in which nongenotoxic carcinogenic chemicals, such as the peroxisome proliferators and sodium phenobarbitone, may induce cancer, with apoptosis playing a key role in the process.

Key Words: Cell death • cell replication • cancer • transient • sustained • growth control

Toxicologic Pathology, Vol. 28, No. 3, 441-446 (2000)
DOI: 10.1177/019262330002800314


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				S. S. Sekhon, X. Tan, A. Micsenyi, W. C. Bowen, and S. P.S. Monga Fibroblast Growth Factor Enriches the Embryonic Liver Cultures for Hepatic Progenitors Am. J. Pathol., June 1, 2004; 164(6): 2229 - 2240. [Abstract] [Full Text] [PDF]

				L. Tryphonas and C. Gopinath A Synopsis of the Third International Federation of Societies of Toxicologic Pathologists Conference Toxicol Pathol, May 1, 2000; 28(3): 370 - 374. [PDF]