Cell death premature senescence

Fig. 12.12 With each cell division, the telomeies at the end of the chromosomes become shortened. The model shows that in order to stop senescence and death, both telomerase activity and blockage of the RB pathway are needed. Telomerase activity and blockage of the RB pathway are intimately linked, because the factors that block the RB pathway (the wyc oncogene and the E6 oncogene of the human papillomavirus, see Part 4) also upr late expression of hTERT.24 In contrast to normal differenbated cells, cancer cells have telomerase adivity. In this way, cancer cells overturn the life-sparvcontrolling clock and become immortal. Since, about 90% of all human cancers are derived from epithelial cells, it follows that in epithelial cancer cells the RB pathway has also been inactivated. To the contrary, when the tumour-suppressor p 53 accumulates, the cells age prematurely.25...

Caron, M., et al. (2007). Human lipodystrophies Unked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence. Cell Death Differ 14 1759-1767. 

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