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Nature Protocols, Apr 2023 This is a preview of a remote PDF: https://www.nature.com/articles/s41596-023-00816-9.pdf Ellis, Peter, Moore, Luiza, Sanders, Mathijs A., Butler, Timothy M., Brunner, Simon F., Lee-Six, Henry, Osborne, Robert, Farr, Ben, Coorens, Tim H. H., Lawson, Andrew R. J., Cagan, Alex, Stratton, Mike R., Martincorena, Inigo, Campbell, Peter J.. , Nature Protocols, DOI: 10.1038/s41596-023-00816-9
Abstract Mutation accumulation in somatic cells contributes to cancer development and is proposed as a cause of aging. DNA polymerases Pol ε and Pol δ replicate DNA during cell division. However, in some cancers, defective proofreading due to acquired POLE/POLD1 exonuclease domain mutations causes markedly elevated somatic mutation burdens with distinctive mutational signatures. Germline POLE/POLD1 mutations cause familial cancer predisposition.
Abstract Starting from the zygote, all cells in the human body continuously acquire mutations. Mutations shared between different cells imply a common progenitor and are thus naturally occurring markers for lineage tracing1,2. Here we reconstruct extensive phylogenies of normal tissues from three adult individuals using whole-genome sequencing of 511 laser capture microdissections.
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