Evidence map›Paper›PMID 36894662›Full record

ArticleNature ecology & evolution2023

State-dependent evolutionary models reveal modes of solid tumour growth.

Maya A Lewinsohn, Trevor Bedford, Nicola F Müller, Alison F Feder

Open access · hybridAbstract read
In one paragraph

Article in Nature ecology & evolution, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

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  11. Quantitative and sensitive sequencing of somatic mutations induced by a maize transposon.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  14. Bayesian phylodynamic inference of population dynamics with dormancy.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  15. Bayesian phylodynamic inference of population dynamics with dormancy.bioRxiv : the preprint server for biology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Maya A LewinsohnDepartment of Genome Sciences, University of Washington, Seattle, WA, USA. lewinsom@uw.edu.ORCID http://orcid.org/0000-0002-3275-5681
Trevor BedfordDepartment of Genome Sciences, University of Washington, Seattle, WA, USA.
Nicola F MüllerVaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, WA, USA. nicola.felix.mueller@gmail.com.ORCID http://orcid.org/0000-0002-2927-1002
Alison F FederDepartment of Genome Sciences, University of Washington, Seattle, WA, USA. affeder@uw.edu.ORCID http://orcid.org/0000-0003-2915-089X
University of Washington · USCape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZAHoward Hughes Medical Institute · US

Funding

Real-time tracking of virus evolution for vaccine strain selection and epidemiological investigationR35GM119774 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BEDFORD, TREVOR BC · 2016 to 2025
$4.1M
A phylodynamic time machine for solid tumorsDP2CA280623 · NCI · UNIVERSITY OF WASHINGTON · PI FEDER, ALISON F · 2022 to 2025
$2.3M
6 · The paper itself

Abstract

Spatial properties of tumour growth have profound implications for cancer progression, therapeutic resistance and metastasis. Yet, how spatial position governs tumour cell division remains difficult to evaluate in clinical tumours. Here, we demonstrate that faster division on the tumour periphery leaves characteristic genetic patterns, which become evident when a phylogenetic tree is reconstructed from spatially sampled cells. Namely, rapidly dividing peripheral lineages branch more extensively and acquire more mutations than slower-dividing centre lineages. We develop a Bayesian state-dependent evolutionary phylodynamic model (SDevo) that quantifies these patterns to infer the differential division rates between peripheral and central cells. We demonstrate that this approach accurately infers spatially varying birth rates of simulated tumours across a range of growth conditions and sampling strategies. We then show that SDevo outperforms state-of-the-art, non-cancer multi-state phylodynamic methods that ignore differential sequence evolution. Finally, we apply SDevo to single-time-point, multi-region sequencing data from clinical hepatocellular carcinomas and find evidence of a three- to six-times-higher division rate on the tumour edge. With the increasing availability of high-resolution, multi-region sequencing, we anticipate that SDevo will be useful in interrogating spatial growth restrictions and could be extended to model non-spatial factors that influence tumour progression.

Indexed as

NeoplasmsBayes TheoremHumansPhylogeny

Identifiers

PMID36894662
PMCPMC10089931
OpenAlexW4323669978

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.