Evidence map›Paper›PMID 34161319›Full record

ArticlePLoS computational biology2021

Multiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.

Sahar Jafari Nivlouei, M Soltani, João Carvalho, Rui Travasso, Mohammad Reza Salimpour, Ebrahim Shirani

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
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 at 3 institutions in 3 countries.

Sahar Jafari NivloueiDepartment of Mechanical Engineering, Isfahan University of Technology, Isafahan, Iran.
M SoltaniDepartment of Mechanical Engineering, K. N. Toosi University of Technology, Tehran, Iran.ORCID 0000-0003-0878-6274
João CarvalhoCFisUC, Department of Physics, University of Coimbra, Coimbra, Portugal.ORCID 0000-0001-9955-4131
Rui TravassoCFisUC, Department of Physics, University of Coimbra, Coimbra, Portugal.ORCID 0000-0001-6078-0721
Mohammad Reza SalimpourDepartment of Mechanical Engineering, Isfahan University of Technology, Isafahan, Iran.ORCID 0000-0002-5871-8360
Ebrahim ShiraniDepartment of Mechanical Engineering, Isfahan University of Technology, Isafahan, Iran.ORCID 0000-0001-9491-4935
Isfahan University of Technology · IRUniversity of Coimbra · PTUniversity of Waterloo · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dynamics of tumor growth and associated events cover multiple time and spatial scales, generally including extracellular, cellular and intracellular modifications. The main goal of this study is to model the biological and physical behavior of tumor evolution in presence of normal healthy tissue, considering a variety of events involved in the process. These include hyper and hypoactivation of signaling pathways during tumor growth, vessels' growth, intratumoral vascularization and competition of cancer cells with healthy host tissue. The work addresses two distinctive phases in tumor development-the avascular and vascular phases-and in each stage two cases are considered-with and without normal healthy cells. The tumor growth rate increases considerably as closed vessel loops (anastomoses) form around the tumor cells resulting from tumor induced vascularization. When taking into account the host tissue around the tumor, the results show that competition between normal cells and cancer cells leads to the formation of a hypoxic tumor core within a relatively short period of time. Moreover, a dense intratumoral vascular network is formed throughout the entire lesion as a sign of a high malignancy grade, which is consistent with reported experimental data for several types of solid carcinomas. In comparison with other mathematical models of tumor development, in this work we introduce a multiscale simulation that models the cellular interactions and cell behavior as a consequence of the activation of oncogenes and deactivation of gene signaling pathways within each cell. Simulating a therapy that blocks relevant signaling pathways results in the prevention of further tumor growth and leads to an expressive decrease in its size (82% in the simulation).

Indexed as

Models, BiologicalAlgorithmsAnimalsCell ProliferationComputational BiologyComputer SimulationHumansMolecular Targeted TherapyNeoplasm InvasivenessNeoplasmsNeovascularization, PathologicSignal TransductionSystems AnalysisTumor HypoxiaVascular Endothelial Growth Factor AVascular Endothelial Growth Factor A

Identifiers

PMID34161319
PMCPMC8259971
OpenAlexW3176013527

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.