Main description:

As cells mature they naturally stop dividing and enter a period called senescence. But cellular senescence can also be induced prematurely by certain oncogenes involved in cancer development. Cellular senescence, a growth-arrest program that limits the lifespan of mammalian cells and prevents unlimited cell proliferation, is attracting considerable interest because of its links to tumor suppression.

Contents:

Introduction: J Sedivy. Section 1. Senescence signals. 1. Telomere biology and biochemistry: 1, J Karlseder; 2, T de Lange; 3, L Harrington. 2. Short telomere-driven senescence: 1, F d'Adda di Fagagna; 2, N Sharpless; 3, V Bohr. 3. Oncogene-induced senescence: 1, M Serrano; 2, J Bartek; 3, G, Ferbeyre. 4. Stress-induced senescence: 1, T Finkel; 2, V Gorbunova; 3, E Hara; 4, F Ishikawa. 5. Modulation of senescence by extracellular growth factors: 1, P Adams. Section 2. The senescent phenotype. 6. The senescent phenotype and its evolution: 1, J Campisi. 7. Chromatin structure in senescent cells: 1, E Medrano; 2. M Narita. 8. A comparison of senescence in mouse and human cells: 1, C Greider; 2, M Blasco. Section 3. The physiological consequences of senescence. 9. Tumor suppression: 1, G Peters; 2, N Sharpless; 3, S Chang. 10. Tissue aging: 1, L Rudolph; 2, A Trumpp. 11. Senescence as a potential therapeutic tool: 1, C Schmitt; 2, S Lowe.