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Articles by Tim H. H
Author Correction: Reliable detection of somatic mutations in solid tissues by laser-capture microdissection and low-input DNA sequencing
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
Single-cell transcriptomics reveals a distinct developmental state of KMT2A-rearranged infant B-cell acute lymphoblastic leukemia - Nature Medicine
Abstract KMT2A-rearranged infant ALL is an aggressive childhood leukemia with poor prognosis. Here, we investigated the developmental state of KMT2A-rearranged infant B-cell acute lymphoblastic leukemia (B-ALL) using bulk messenger RNA (mRNA) meta-analysis and examination of single lymphoblast transcriptomes against a developing bone marrow reference.
Author Correction: Inherent mosaicism and extensive mutation of human placentas - Nature
Correction to: Nature https://doi.org/10.1038/s41586-021-03345-1 Published online 10 March 2021 In the version of this article initially published, there was a plotting error affecting Fig. 1d,e and Extended Data Fig. 1b. SBS signature extraction was performed for the bulk placental samples on a per-placenta basis, but the results were plotted on a per-sample basis, duplicating the signature proportion estimates where multi-regional sampling was done.
Increased somatic mutation burdens in normal human cells due to defective DNA polymerases - Nature Genetics
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.
The mutational landscape of human somatic and germline cells - Nature
Abstract Over the course of an individual’s lifetime, normal human cells accumulate mutations1. Here we compare the mutational landscape in 29 cell types from the soma and germline using multiple samples from the same individuals. Two ubiquitous mutational signatures, SBS1 and SBS5/40, accounted for the majority of acquired mutations in most cell types, but their absolute and relative contributions varied substantially.
Extensive phylogenies of human development inferred from somatic mutations - Nature
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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