Evidence map›Paper›PMID 42139303›Full record

ArticlePLoS computational biology2026

Exploring the relationship between vascular remodelling and tumour growth using agent-based modelling.

Nicholas Fan, Joshua A Bull, Helen M Byrne

Abstract read
In one paragraph

Article in PLoS computational biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Nicholas FanWolfson Centre for Mathematical Biology, Mathematical Institute, University of Oxford, Oxford, United Kingdom.ORCID https://orcid.org/0009-0002-6039-3902
Joshua A BullWolfson Centre for Mathematical Biology, Mathematical Institute, University of Oxford, Oxford, United Kingdom.ORCID https://orcid.org/0000-0003-1475-2898
Helen M ByrneWolfson Centre for Mathematical Biology, Mathematical Institute, University of Oxford, Oxford, United Kingdom.ORCID https://orcid.org/0000-0003-1771-5910

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We develop a multiscale agent-based model (ABM) to investigate the effect that mechanical interactions between proliferating tumour cells and the surrounding vasculature have on the oxygen supply to the tumour microenvironment (TME), the tumour's growth dynamics, and its response to radiotherapy. Our model extends existing models of tumour spheroid growth by incorporating vessel deformation due to mechanical forces between vessel walls and neighbouring tumour cells. These forces generate an effective pressure which compresses vessels, driving occlusion and pruning. This, in turn, leads to a hypoxic oxygen landscape which stimulates angiogenesis. A key feature of our model is the treatment of mechanical cell interactions with the tumour microenvironment, which we represent with two forces. The first is Stokes' drag which is widely used in ABMs to represent resistance to cell movement. The second is a friction force which accounts for resistance due to the continual breaking and reforming of cell-extracellular matrix (ECM) adhesions. The importance of this friction force is demonstrated by numerical simulation. When Stokes' drag dominates, pressure gradients dissipate across the tissue and vessel compression is negligible. By contrast, as the strength of the friction force increases, larger pressure gradients form, leading to significant vessel compression. We perform extensive numerical simulations to investigate how model parameters that control vascular remodelling and friction influence tumour vascularisation, which we spatially quantify using the cross-pair correlation function. This, in turn, alters the oxygen landscape and drives changes in tumour morphology. Finally, we highlight the importance of accounting for both mechanisms when simulating tumour responses to treatment with radiotherapy. We observe that vascular remodelling critically alters the tumour's susceptibility to treatment and post-radiotherapy regrowth. Tumour regrowth is especially impacted by vessel remodelling, with certain vascular landscapes able to rebound quickly post-radiotherapy, resulting in fast tumour regrowth.

Indexed as

Models, BiologicalNeoplasmsNeovascularization, PathologicVascular RemodelingAnimalsCell ProliferationComputational BiologyComputer SimulationExtracellular MatrixHumansOxygenTumor MicroenvironmentOxygen

Identifiers

PMID42139303
PMCPMC13354106

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.