Evidence map›Paper›PMID 32098957›Full record

ArticleNature communications2020

Measuring single cell divisions in human tissues from multi-region sequencing data.

Benjamin Werner, Jack Case, Marc J Williams, Ketevan Chkhaidze, Daniel Temko, Javier Fernández-Mateos, George D Cresswell, Daniel Nichol, William Cross, Inmaculada Spiteri and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 88 citations in OpenAlex.

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  16. Identifying genetic errors of immunity due to mosaicism.The Journal of experimental medicine · 2025
    Review
  17. Article
  18. Backtracking Cell Phylogenies in the Human Brain with Somatic Mosaic Variants.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 2 countries.

Benjamin WernerEvolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK. b.werner@qmul.ac.uk.ORCID http://orcid.org/0000-0002-6857-8699
Jack CaseEvolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK.
Marc J WilliamsEvolution and Cancer Laboratory, Centre for Cancer Genomics & Computational Biology, Barts Cancer Institute, Queen Mary University London, London, Charterhouse Square, London, EC1M 6BQ, UK.ORCID http://orcid.org/0000-0001-5524-4174
Ketevan ChkhaidzeEvolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK.
Daniel TemkoEvolution and Cancer Laboratory, Centre for Cancer Genomics & Computational Biology, Barts Cancer Institute, Queen Mary University London, London, Charterhouse Square, London, EC1M 6BQ, UK.
Javier Fernández-MateosEvolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK.
George D CresswellEvolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID http://orcid.org/0000-0003-3303-068X
Daniel NicholEvolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK.
William CrossEvolution and Cancer Laboratory, Centre for Cancer Genomics & Computational Biology, Barts Cancer Institute, Queen Mary University London, London, Charterhouse Square, London, EC1M 6BQ, UK.
Inmaculada SpiteriEvolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK.
Weini HuangGroup of Theoretical Biology, The State Key Laboratory of Biocontrol, School of Life Science, Sun Yat-sen University, 510060, Guangzhou, China.
Ian P M TomlinsonInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.ORCID http://orcid.org/0000-0003-3037-1470
Chris P BarnesDepartment of Cell and Developmental Biology, University College London, London, UK.ORCID http://orcid.org/0000-0002-9459-1395
Trevor A GrahamEvolution and Cancer Laboratory, Centre for Cancer Genomics & Computational Biology, Barts Cancer Institute, Queen Mary University London, London, Charterhouse Square, London, EC1M 6BQ, UK. t.graham@qmul.ac.uk.ORCID http://orcid.org/0000-0001-9582-1597
Andrea SottorivaEvolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK. andrea.sottoriva@icr.ac.uk.ORCID http://orcid.org/0000-0001-6709-9533
Institute of Cancer Research · GBQueen Mary University of London · GBSun Yat-sen University · CNUniversity College London · GBUniversity of Birmingham · GB

Funding

The Role of the Microbiome in Cancer Suppression and Susceptibility Across SpeciesU54CA217376 · NCI · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI MALEY, CARLO · 2018 to 2022
$8.6M
Cancer Research UK 19771Cancer Research UK 22909Cancer Research UK A19771Cancer Research UK A22909NCI NIH HHS U54 CA217376Wellcome Trust 202778/Z/16/ZWellcome Trust 209409/Z/17/Z
6 · The paper itself

Abstract

Both normal tissue development and cancer growth are driven by a branching process of cell division and mutation accumulation that leads to intra-tissue genetic heterogeneity. However, quantifying somatic evolution in humans remains challenging. Here, we show that multi-sample genomic data from a single time point of normal and cancer tissues contains information on single-cell divisions. We present a new theoretical framework that, applied to whole-genome sequencing data of healthy tissue and cancer, allows inferring the mutation rate and the cell survival/death rate per division. On average, we found that cells accumulate 1.14 mutations per cell division in healthy haematopoiesis and 1.37 mutations per division in brain development. In both tissues, cell survival was maximal during early development. Analysis of 131 biopsies from 16 tumours showed 4 to 100 times increased mutation rates compared to healthy development and substantial inter-patient variation of cell survival/death rates.

Indexed as

Mutation RateBayes TheoremBrainCell DivisionCell SurvivalGenetic HeterogeneityHematopoiesisHumansModels, GeneticMutation AccumulationNeoplasmsNeuronsReproducibility of ResultsSingle-Cell AnalysisWhole Genome Sequencing

Identifiers

PMID32098957
PMCPMC7042311
OpenAlexW3008012817

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.