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Most human somatic cells contain no or very low levels of telomerase.
However, most human somatic cells lack sufficient telomerase activity to prevent telomere shortening that occurs with every replicative cycle [5].
In most human somatic cells insufficient telomerase is expressed to counteract the end replication problem.
The level of telomerase activity in most human somatic cells is so weak that telomere attrition is unavoidable.
Most human somatic cells lose telomeric repeat sequences with each cell division, which leads to replicative senescence [ 4, 5].
Most human somatic cells do not divide indefinitely but enter a terminal growth arrest termed replicative senescence.
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While hTERT is not expressed in most normal human somatic tissues, hTR is expressed constitutively in most human tissues (Kim et al, 1994; Shay and Bacchetti, 1997).
Telomerase activity is absent in most human adult somatic cells.
Telomerase, a RNA-dependent DNA polymerase silent in most normal human somatic cells, is frequently activated during the oncogenic process [18], [19].
However, telomerase is not expressed in most normal human somatic cells making them vulnerable to the aging related replicative senescence and potential telomere dysfunction during crisis that has been implicated in carcinogenesis [1], [19].
The expression of telomerase is suppressed in most normal human somatic cells, but is reactivated during tumorigenesis.
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