Risky immortalization by telomerase

Abstract

Senescence naturally limits the proliferation of mammalian cells in culture, possibly by shortening the telomere regions at the ends of chromosomes during cell division^1,2. In support of this idea, introducing TERT, the catalytic subunit of telomerase — the enzyme that maintains chromosome ends — into certain cell types can extend their lifespan and potentially immortalize them^3,4. It has been proposed that treatment with exogenous TERT might be useful for cell-based therapies by allowing indefinite expansion of normal human cells without damaging their genomes^5,6. But we show here that TERT-driven cell proliferation is not genoprotective because it is associated with activation of the c-myc oncogene.