PROSTATE, cilt.36, sa.4, ss.264-271, 1998 (SCI-Expanded)
BACKGROUND. Telomeres that protect chromosomes at both ends are shortened with each somatic cell division through replication-dependent sequence loss at DNA termini. The chromosomes with shortened telomeres tend to become unstable, leading to cell death. Due largely to reactivation/upregulation of telomerase, a ribonucleoprotein that adds nucleotide sequences onto chromosome ends, cancer cells become immortal and neoplastically transformed.