Time, telomeres and tumours: is cellular senescence more than an anticancer mechanism?

Woodring E. Wright, Jerry W. Shay

Research output: Contribution to journalArticle

123 Citations (Scopus)

Abstract

Normal diploid cells, by definition, have a limited life span: they senesce after a set number of divisions both in vivo and in culture. It has been hypothesized that the molecular mechanism that measures the life span of a cell probably involves the shortening of telomeres that occurs with each round of DNA replication. This loss of telomeres is thought to induce antiproliferative signals that result in the induction of cellular senescence. In this article, Woodring Wright and Jerry Shay present a hypothesis for the mechanisms by which telomere shortening regulates cellular physiology and argue that cellular senescence is not only an anticancer mechanism but is also the cause of many of the degenerative changes of aging.

Original languageEnglish (US)
Pages (from-to)293-297
Number of pages5
JournalTrends in Cell Biology
Volume5
Issue number8
DOIs
StatePublished - 1995

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Telomere Shortening
Cell Aging
Telomere
Diploidy
DNA Replication
Neoplasms

ASJC Scopus subject areas

  • Cell Biology

Cite this

Time, telomeres and tumours : is cellular senescence more than an anticancer mechanism? / Wright, Woodring E.; Shay, Jerry W.

In: Trends in Cell Biology, Vol. 5, No. 8, 1995, p. 293-297.

Research output: Contribution to journalArticle

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