PerspectiveCANCER

Burning bridges in cancer genomes

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Science  17 Apr 2020:
Vol. 368, Issue 6488, pp. 240-241
DOI: 10.1126/science.abb4899

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Summary

Cancer is driven by mutations. A large fraction of mutations arise from unavoidable errors of DNA replication, which accumulate gradually over generations (1). Recent studies indicate that cancer genomes frequently harbor mutation signatures that result from chromothripsis. This is a sudden form of localized and massive chromosomal rearrangement, usually involving one or a few chromosomes. Chromothripsis is thought to arise through a single shattering event, after which tens to hundreds of chromosomal segments are joined in a random order and orientation. This one-off catastrophic event is common in cancer, with frequencies reaching 65% in certain cancer types (2). Until now, the mechanisms that explain this burst of mutagenesis remained largely unclear. On page 282 of this issue, Umbreit et al. (3) provide a unifying account of how extreme genome complexity is an outcome of a mutagenesis mechanism that involves aberrant DNA replication in human cells.

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