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Normal cells can divide only a limited number of times because the protective caps on their chromosomes, telomeres, wear down. About 90% of cancers switch the cap-rebuilding enzyme telomerase back on, often through TERT promoter mutations, and roughly 10% use an alternative lengthening route (ALT), so they divide indefinitely; imetelstat is the first approved telomerase inhibitor.
About 90% of cancers reactivate telomerase (TERT), often via TERT promoter mutations (glioblastoma, melanoma, bladder, thyroid) or amplification; ~10% use alternative lengthening of telomeres (ALT) through homologous recombination, associated with ATRX/DAXX loss (sarcomas, pancreatic NETs, gliomas). Telomerase inhibition (imetelstat, an oligonucleotide) reached approval in lower-risk MDS (2024) and is in phase 3 in myelofibrosis; ALT cells are sensitive to ATR inhibition. TERT promoter mutation is a diagnostic and prognostic marker and a candidate for ctDNA detection in bladder cancer and glioma.
The plastic tips on shoelaces fray a little every time you tie them; when they are gone the lace unravels and the shoe is thrown out. Cancer cells carry a machine that keeps re-tipping the laces.
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