Springer Science & Business Media, Sep 17, 1999 - Science - 208 pages
The problem of the long-term proliferation of cells is a seminal one. It has always been a hot subject in biology, a source of far-reaching hypotheses, even more so now when explanations for the mechanisms of cell prolifera tive mortality or immortality seem within our reach. A question which is still debated is whether an infinite division potential can be a normal trait or is always the result of modifications leading to abnormal cell growth and escape from homeostasis. In general, investigators have been advocates of one of the two extremes, universal limited or unlim ited normal proliferative potential. Since the long-term proliferative potential of cells concerns regulation of development, regeneration of tissues, and homeostatic control of cell growth, in brief survival of living organisms, and since the regulation of these processes is so different along the evolutionary scale, it is not surpris ing that there does not seem to be any universal trait. The question of whether cells are endowed with finite or infinite prolifera tive phenotypes has to be seen using the perspective of comparative biology.
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Acad Sci USA apoptosis autogamy binding Cancer Res cell cycle cell division cell population cellular aging cellular senescence chromosome clonal age clones culture cyclin differentiation diploid division potential DNA damage DNA repair epithelial cells eukaryotes Exp Cell Res family tree finitely proliferative function genetic genome growth haploid Harley CB Hayflick heat shock protein homologous HSPs human cells human fibroblasts human mammary epithelial immortal HMECs immortal human inactivation induced involved keratinocytes kinase large T antigen lifespan Macieira-Coelho macronucleus mammalian mammary epithelial cells Matsumura mechanism meiosis mitosis Mol Cell Biol molecular mortalin mutations Natl Acad Sci normal cells normal human Oncogene oxidative Paramecium Pereira-Smith phenotype Proc Natl Acad proliferation proliferative potential RecA recombination replicative senescence sequences Shay JW small t antigen soma somatic cells span Stampfer stem cells studies SV40 large synthesis telomerase activity telomere telomere length telomere shortening tion tissues transcription transformation viral virus vitro vivo Wadhwa
Page 203 - Serrano, M., Lin, AW, McCurrach, ME, Beach, D., and Lowe, SW (1997) Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a.