Evidence map›Paper›PMID 19566124›Full record

ArticleMathematical biosciences and engineering : MBE2009

A spatial model of tumor-host interaction: application of chemotherapy.

Peter Hinow, Philip Gerlee, Lisa J McCawley, Vito Quaranta, Madalina Ciobanu, Shizhen Wang, Jason M Graham, Bruce P Ayati, Jonathan Claridge, Kristin R Swanson and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Mathematical biosciences and engineering : MBE, 2009. 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
2.1field-weighted citation impact, top 15% 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, 91 citations in OpenAlex.

  1. Article
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  16. BioMed research international · 2017
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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

12 authors at 6 institutions in 2 countries.

Peter HinowInstitute for Mathematics and its Applications, University of Minnesota, Minneapolis, MN 55455, USA. hinow@ima.umn.edu
Philip Gerlee
Lisa J McCawley
Vito Quaranta
Madalina Ciobanu
Shizhen Wang
Jason M Graham
Bruce P Ayati
Jonathan Claridge
Kristin R Swanson
Mary Loveless
Alexander R A Anderson
Vanderbilt University · USUniversity of Minnesota · USUniversity of Iowa · USUniversity of Washington · USCity Of Hope National Medical Center · USUniversity of Copenhagen · DK

Funding

TrainingU54CA113007 · NCI · VANDERBILT UNIVERSITY · PI ESTRADA-RODGERS, LOURDES · 2004 to 2014
$19.2M
NCI NIH HHS U54 CA113007NCI NIH HHS U54 CA 11307
6 · The paper itself

Abstract

In this paper we consider chemotherapy in a spatial model of tumor growth. The model, which is of reaction-diffusion type, takes into account the complex interactions between the tumor and surrounding stromal cells by including densities of endothelial cells and the extra-cellular matrix. When no treatment is applied the model reproduces the typical dynamics of early tumor growth. The initially avascular tumor reaches a diffusion limited size of the order of millimeters and initiates angiogenesis through the release of vascular endothelial growth factor (VEGF) secreted by hypoxic cells in the core of the tumor. This stimulates endothelial cells to migrate towards the tumor and establishes a nutrient supply sufficient for sustained invasion. To this model we apply cytostatic treatment in the form of a VEGF-inhibitor, which reduces the proliferation and chemotaxis of endothelial cells. This treatment has the capability to reduce tumor mass, but more importantly, we were able to determine that inhibition of endothelial cell proliferation is the more important of the two cellular functions targeted by the drug. Further, we considered the application of a cytotoxic drug that targets proliferating tumor cells. The drug was treated as a diffusible substance entering the tissue from the blood vessels. Our results show that depending on the characteristics of the drug it can either reduce the tumor mass significantly or in fact accelerate the growth rate of the tumor. This result seems to be due to complicated interplay between the stromal and tumor cell types and highlights the importance of considering chemotherapy in a spatial context.

Indexed as

Models, ImmunologicalAntineoplastic AgentsComputer SimulationDocetaxelEndothelial CellsHumansNeoplasmsNeovascularization, PathologicTaxoidsVascular Endothelial Growth Factor AAntineoplastic AgentsDocetaxelTaxoidsVascular Endothelial Growth Factor A

Identifiers

PMID19566124
PMCPMC2981353
OpenAlexW2002379387

What OpenQuestion holds

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LicenceTDM
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.