Evidence map›Paper›PMID 37792732›Full record

ArticlePLoS computational biology2023

Mechanistic characterization of oscillatory patterns in unperturbed tumor growth dynamics: The interplay between cancer cells and components of tumor microenvironment.

Aymara Sancho-Araiz, Zinnia P Parra-Guillen, Jean Bragard, Sergio Ardanza, Victor Mangas-Sanjuan, Iñaki F Trocóniz

Abstract read
In one paragraph

Article in PLoS computational biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

6 authors.

Aymara Sancho-AraizPharmacometrics & Systems Pharmacology Group, Department of Pharmaceutical Technology and Chemistry, School of Pharmacy and Nutrition, University of Navarra, Pamplona, Spain.ORCID 0000-0001-7139-165X
Zinnia P Parra-GuillenPharmacometrics & Systems Pharmacology Group, Department of Pharmaceutical Technology and Chemistry, School of Pharmacy and Nutrition, University of Navarra, Pamplona, Spain.
Jean BragardDepartment of Physics and Applied Math. University of Navarra, Pamplona, Spain.ORCID 0000-0003-3450-9609
Sergio ArdanzaDepartment of Physics and Applied Math. University of Navarra, Pamplona, Spain.
Victor Mangas-SanjuanDepartment of Pharmacy and Pharmaceutical Technology and Parasitology, Faculty of Pharmacy, University of Valencia, Valencia, Spain.
Iñaki F TrocónizPharmacometrics & Systems Pharmacology Group, Department of Pharmaceutical Technology and Chemistry, School of Pharmacy and Nutrition, University of Navarra, Pamplona, Spain.ORCID 0000-0003-3700-8658

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mathematical modeling of unperturbed and perturbed tumor growth dynamics (TGD) in preclinical experiments provides an opportunity to establish translational frameworks. The most commonly used unperturbed tumor growth models (i.e. linear, exponential, Gompertz and Simeoni) describe a monotonic increase and although they capture the mean trend of the data reasonably well, systematic model misspecifications can be identified. This represents an opportunity to investigate possible underlying mechanisms controlling tumor growth dynamics through a mathematical framework. The overall goal of this work is to develop a data-driven semi-mechanistic model describing non-monotonic tumor growth in untreated mice. For this purpose, longitudinal tumor volume profiles from different tumor types and cell lines were pooled together and analyzed using the population approach. After characterizing the oscillatory patterns (oscillator half-periods between 8-11 days) and confirming that they were systematically observed across the different preclinical experiments available (p<10-9), a tumor growth model was built including the interplay between resources (i.e. oxygen or nutrients), angiogenesis and cancer cells. The new structure, in addition to improving the model diagnostic compared to the previously used tumor growth models (i.e. AIC reduction of 71.48 and absence of autocorrelation in the residuals (p>0.05)), allows the evaluation of the different oncologic treatments in a mechanistic way. Drug effects can potentially, be included in relevant processes taking place during tumor growth. In brief, the new model, in addition to describing non-monotonic tumor growth and the interaction between biological factors of the tumor microenvironment, can be used to explore different drug scenarios in monotherapy or combination during preclinical drug development.

Indexed as

Models, BiologicalNeoplasmsAnimalsCell Line, TumorCell ProliferationMiceModels, TheoreticalTumor Microenvironment

Identifiers

PMID37792732
PMCPMC10550146

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LicenceCC BY
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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.