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Time, tumours and telomeres: Meeting on Cancer and Aging

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PMC
Keywords
  • Review Article
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  • Biology

Abstract

Time, tumours and telomeres meeting report ©2006 EUROPEAN MOLECULAR BIOLOGY ORGANIZATION EMBO reports VOL 7 | NO 5 | 2006 meeting report Time, tumours and telomeres Meeting on Cancer and Aging Toren Finkel1+, Jan Vijg2 & Jerry W. Shay3 1National Institutes of Health, Bethesda, Maryland, USA, 2Buck Institute for Age Research, Novato, California, USA, and 3University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA Introduction The crisp November air and beautiful Iberian city of Madrid served as the backdrop for the Cancer and Aging conference, held in the recently completed and ultra-modern CNIO (Centro Nacional de Investigaciones Oncologicas) facility. Thirty speakers and a similar number of invited guests heard presentations covering a range of topics including telomere biology, oxidative stress, genomic insta- bility and the hormonal regulation of cancer and ageing. The pre- sentations were short, lively and varied, providing—in deference to our Spanish hosts—a serving of intellectual tapas for the meet- ing participants. Central to many of the discussions were attempts to understand how and where the biology of cancer and ageing overlapped, and how each discipline could potentially inform the other. This report highlights just some of the interesting questions and new findings discussed at the meeting. Telomeres, telomerase, cancer and ageing The interface of cancer and ageing is traditionally located at the telo- mere. This complex of proteins and repetitive DNA sequences (TTAGGG in mammals) caps the end of eukaryotic linear chromo- somes and prevents their degradation. In cancer cells, and in normal stem cells, the enzyme telomerase continually adds repeats to telo- meres. Conversely, most somatic cells lack telomerase activity, which leads to a progressive shortening of the telomere with each cell divi- sion. When a small subset of telomeres becomes critically short, cells undergo permanent growth arrest. Erosion of telomere length is there- fore vi

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