Abstract
Shortening of the ends of chromosomes limits a cell's lifespan. Some cancer cells avoid this fate through a mechanism called alternative lengthening of telomeres, molecular details of which have now been defined. See Article p.54 One aspect of cancer cells that contributes to their expansion and persistence is their ability to maintain telomere length as they continually divide. And one mechanism of telomere lengthening that does not utilize telomerase—and is found in more than one in ten cancers—is termed alternative lengthening of telomeres (ALT). Roger Greenberg and colleagues show here that a specialized replisome is formed in ALT-positive cancer cells that is capable of synthesizing long tracts of DNA at the telomere, proceeding from a double-strand break. This process is independent of many canonical replication- and homology-dependent repair components.
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