Human Ageing and Telomeres

  1. Derek J. Chadwick Organizer and
  2. Gail Cardew Organizer
  1. Calvin B. Harley

Published Online: 28 SEP 2007

DOI: 10.1002/9780470515433.ch9

Ciba Foundation Symposium 211 - Telomeres and Telomerase

Ciba Foundation Symposium 211 - Telomeres and Telomerase

How to Cite

Harley, C. B. (2007) Human Ageing and Telomeres, in Ciba Foundation Symposium 211 - Telomeres and Telomerase (eds D. J. Chadwick and G. Cardew), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470515433.ch9

Author Information

  1. Geron Corporation, 230 Constitution Drive, Menlo Park, CA 94025, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471972785

Online ISBN: 9780470515433



  • human ageing;
  • telomerase mortality;
  • telomerase repression;
  • telomeric DNA;
  • cell senescence


Telomerase expression is repressed early in development in all normal somatic human tissues investigated to date, whereas activity and the expression of the RNA component for this enzyme are upregulated in almost all cases of malignant transformation and late-stage cancer. The telomere hypothesis of ageing and immortalization postulates that sufficient telomere loss on one or more chromosomes in normal somatic cells triggers cell senescence, whereas reactivation of the enzyme is necessary for cell immortalization. Measurements of telomere length and telomerase activity in cancer and during normal and accelerated human ageing in skin, blood, haemopoietic, skeletal muscle, vascular and CNS tissues support this model. Tissue culture studies of cell ageing and transformation have added to our understanding of telomere dynamics in these processes. Evolution of telomerase repression and mortality in somatic cells of long-lived organisms is consistent with antagonistic pleiotropy models in which cell senescence is a tumour suppressor mechanism: stringent repression of telomerase has a beneficial early effect in reducing the probability of cancer, but a deleterious, unselected late effect in its contributions to age-related disease.