Evidence map›Paper›PMID 27856758›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Tissue-scale, personalized modeling and simulation of prostate cancer growth.

Guillermo Lorenzo, Michael A Scott, Kevin Tew, Thomas J R Hughes, Yongjie Jessica Zhang, Lei Liu, Guillermo Vilanova, Hector Gomez

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 93 citations in OpenAlex.

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  18. Folding drives cortical thickness variations.The European physical journal. Special topics · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Guillermo LorenzoDepartamento de Métodos Matemáticos e de Representación, Universidade da Coruña, 15071 A Coruña, Spain.
Michael A ScottDepartment of Civil and Environmental Engineering, Brigham Young University, Provo, UT 84602.
Kevin TewDepartment of Information Technology, Brigham Young University, Provo, UT 84602.
Thomas J R HughesInstitute for Computational Engineering and Sciences, The University of Texas at Austin, Austin, TX 78712-1229; hughes@ices.utexas.edu.
Yongjie Jessica ZhangDepartment of Mechanical Engineering, Carnegie Mellon University, Pittsburgh, PA 15213.
Lei LiuDepartment of Mechanical Engineering, Carnegie Mellon University, Pittsburgh, PA 15213.
Guillermo VilanovaDepartamento de Métodos Matemáticos e de Representación, Universidade da Coruña, 15071 A Coruña, Spain.
Hector GomezDepartamento de Métodos Matemáticos e de Representación, Universidade da Coruña, 15071 A Coruña, Spain.
Universidade da Coruña · ESBrigham Young University · USCarnegie Mellon University · USThe University of Texas at Austin · US

Funding

European Research Council 307201
6 · The paper itself

Abstract

Recently, mathematical modeling and simulation of diseases and their treatments have enabled the prediction of clinical outcomes and the design of optimal therapies on a personalized (i.e., patient-specific) basis. This new trend in medical research has been termed "predictive medicine." Prostate cancer (PCa) is a major health problem and an ideal candidate to explore tissue-scale, personalized modeling of cancer growth for two main reasons: First, it is a small organ, and, second, tumor growth can be estimated by measuring serum prostate-specific antigen (PSA, a PCa biomarker in blood), which may enable in vivo validation. In this paper, we present a simple continuous model that reproduces the growth patterns of PCa. We use the phase-field method to account for the transformation of healthy cells to cancer cells and use diffusion-reaction equations to compute nutrient consumption and PSA production. To accurately and efficiently compute tumor growth, our simulations leverage isogeometric analysis (IGA). Our model is shown to reproduce a known shape instability from a spheroidal pattern to fingered growth. Results of our computations indicate that such shift is a tumor response to escape starvation, hypoxia, and, eventually, necrosis. Thus, branching enables the tumor to minimize the distance from inner cells to external nutrients, contributing to cancer survival and further development. We have also used our model to perform tissue-scale, personalized simulation of a PCa patient, based on prostatic anatomy extracted from computed tomography images. This simulation shows tumor progression similar to that seen in clinical practice.

Indexed as

Cell ProliferationHumansKallikreinsMaleModels, BiologicalProstate-Specific AntigenProstatic NeoplasmsKallikreinsKLK3 protein, humanProstate-Specific Antigenisogeometric analysispersonalizedphase fieldprostate cancertissue scale

Identifiers

PMID27856758
PMCPMC5137692
OpenAlexW2556731147

What OpenQuestion holds

Textmetadata
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.