Author

Philip S. Robinson

University of CambridgeORCID 0000-0002-6237-7159Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:human· 6 Approach:statistical model· 6 Assay:whole-genome sequencing· 5 Research Focus:variant calling· 4 Research Focus:phylogenetics / evolution· 2 Research Focus:differential expression· 1 Assay:whole-exome sequencing· 1

Frequent Co-Authors

Peter J. CampbelliD· 6 shared Tim H. H. CoorensiD· 6 shared Michael R. StrattoniD· 5 shared Henry Lee-SixiD· 4 shared Iñigo MartincorenaiD· 4 shared Luiza MooreiD· 4 shared Mathijs Arnoud SandersiD· 4 shared Yvette E. Hooks· 4 shared

Activity by Year

2020-2022 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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6 shared papersGenomics

Peter J. CampbellORCID

Mutual co-authors in cluster

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6 papers

Recent·Most cited

Inherited MUTYH mutations cause elevated somatic mutation rates and distinctive mutational signatures in normal human cells

Philip S. Robinson, Laura E. Thomas, Federico Abascal, Hyunchul Jung, Luke M. R. Harvey, Hannah D. West, Sigurgeir Ólafsson, Bernard C. H. Lee, Tim H. H. Coorens, Henry Lee-Six, Laura Butlin, Nicola Lander, Rebekah Truscott, Mathijs Arnoud Sanders, Stefanie V. Lensing, , Michael R. Stratton

This study shows that inherited MUTYH mutations increase somatic mutation rates and specific mutational signatures in normal human cells, contributing to cancer risk without causing premature aging.

Nature Communications · Jul 8, 2022Peer-reviewedGenomics

Elevated somatic mutation burdens in normal human cells due to defective DNA polymerases

Philip S. Robinson, Tim H. H. Coorens, Claire Palles, Emily Mitchell, Federico Abascal, Sigurgeir Ólafsson, Bernard C. H. Lee, Andrew R. J. Lawson, Henry Lee-Six, Luiza Moore, Mathijs Arnoud Sanders, James Hewinson, Lynn M. Martin, Claudia Maria Assunta Pinna, Sara Galavotti, , Michael R. Stratton

The paper shows that germline mutations in POLE or POLD1 lead to elevated mutation burdens in normal human cells and tissues, but do not cause premature aging or other phenotypic features beyond early-onset cancer.

Nature Genetics · Sep 30, 2021Peer-reviewedGenomics

Life without mismatch repair

Mathijs Arnoud Sanders, Harald S. Vöhringer, Victoria J. Forster, Luiza Moore, Brittany B. Campbell, Yvette E. Hooks, Melissa Edwards, Vanessa Bianchi, Tim H. H. Coorens, Timothy M. Butler, Henry Lee-Six, Philip S. Robinson, Christoffer Flensburg, Rebecca A. Bilardi, Ian J. Majewski, , Peter J. Campbell

The paper quantifies mismatch repair (MMR) activity in human tissues by analyzing mutation rates in individuals with constitutional MMR deficiency, revealing genotype-specific mutational signatures and the role of MMR components in DNA repair.

bioRxiv · Apr 14, 2021 · PreprintGenomics

Extensive phylogenies of human development reveal variable embryonic patterns

Tim H. H. Coorens, Luiza Moore, Philip S. Robinson, Rashesh Sanghvi, Joseph Christopher, James Hewinson, Alex Cagan, Thomas R. W. Oliver, Matthew D. C. Neville, Yvette E. Hooks, Ayesha Noorani, Thomas J. Mitchell, Rebecca Claire Fitzgerald, Peter J. Campbell, Iñigo Martincorena, , Michael R. Stratton

The paper reconstructs phylogenies of human development using whole-genome sequencing to show variable embryonic patterns and lineage asymmetries across individuals and tissues.

bioRxiv · Nov 25, 2020 · PreprintGenomics

Somatic evolution in non-neoplastic IBD-affected colon

Sigurgeir Ólafsson, Rebecca E. McIntyre, Tim H. H. Coorens, Timothy M. Butler, Hyunchul Jung, Philip S. Robinson, Henry Lee-Six, Mathijs Arnoud Sanders, Kenneth Arestang, Claire Dawson, Monika Tripathi, Konstantina Strongili, Yvette E. Hooks, Michael R. Stratton, Miles Parkes, , Carl A. Anderson

The paper analyzes somatic mutations in colonic crypts of IBD patients and controls, finding higher mutation rates and clonal expansions in IBD-affected tissue.

Cell · Jul 21, 2020Peer-reviewedGenetics

Lineage tracing of human embryonic development and foetal haematopoiesis through somatic mutations

Michael Spencer Chapman, Anna Maria Ranzoni, Brynelle Myers, Nick Williams, Tim H. H. Coorens, Emily Mitchell, Timothy M. Butler, Kevin J. Dawson, Yvette E. Hooks, Luiza Moore, Jyoti Nangalia, Philip S. Robinson, Elizabeth Hook, Peter J. Campbell, Ana Cvejic

This study uses whole-genome sequencing of single-cell haematopoietic colonies to trace lineage and divergence of embryonic and extra-embryonic tissues in human fetal development.

bioRxiv · May 29, 2020 · PreprintGenomics