Evidence map›Paper›PMID 23292359›Full record

ArticleBulletin of mathematical biology2013

A hybrid model of tumor-stromal interactions in breast cancer.

Yangjin Kim, Hans G Othmer

Abstract read
In one paragraph

Article in Bulletin of mathematical biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 71 citations in OpenAlex.

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  12. Collective invasion of glioma cells through OCT1 signalling and interaction with reactive astrocytes after surgery.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
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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

2 authors at 2 institutions in 2 countries.

Yangjin KimDepartment of Mathematics, Konkuk University, Seoul, 143-701, Republic of Korea.
Hans G Othmer
Konkuk University · KRUniversity of Minnesota · US

Funding

DYNAMIC PATTERN IN CHEMICALLY-REACTING SYSTEMSR01GM029123 · NIGMS · UNIVERSITY OF UTAH · PI OTHMER, HANS G · 1985 to 2018
$5.3M
NIGMS NIH HHS GM-29123NIGMS NIH HHS R01 GM029123
6 · The paper itself

Abstract

Ductal carcinoma in situ (DCIS) is an early stage noninvasive breast cancer that originates in the epithelial lining of the milk ducts, but it can evolve into comedo DCIS and ultimately, into the most common type of breast cancer, invasive ductal carcinoma. Understanding the progression and how to effectively intervene in it presents a major scientific challenge. The extracellular matrix (ECM) surrounding a duct contains several types of cells and several types of growth factors that are known to individually affect tumor growth, but at present the complex biochemical and mechanical interactions of these stromal cells and growth factors with tumor cells is poorly understood. Here we develop a mathematical model that incorporates the cross-talk between stromal and tumor cells, which can predict how perturbations of the local biochemical and mechanical state influence tumor evolution. We focus on the EGF and TGF-β signaling pathways and show how up- or down-regulation of components in these pathways affects cell growth and proliferation. We then study a hybrid model for the interaction of cells with the tumor microenvironment (TME), in which epithelial cells (ECs) are modeled individually while the ECM is treated as a continuum, and show how these interactions affect the early development of tumors. Finally, we incorporate breakdown of the epithelium into the model and predict the early stages of tumor invasion into the stroma. Our results shed light on the interactions between growth factors, mechanical properties of the ECM, and feedback signaling loops between stromal and tumor cells, and suggest how epigenetic changes in transformed cells affect tumor progression.

Indexed as

Models, BiologicalBreast NeoplasmsCarcinoma, Ductal, BreastCarcinoma, Intraductal, NoninfiltratingEpidermal Growth FactorFemaleHumansMathematical ConceptsNeoplasm InvasivenessSignal TransductionStromal CellsTransforming Growth Factor betaTumor MicroenvironmentEpidermal Growth FactorTransforming Growth Factor beta

Identifiers

PMID23292359
PMCPMC6421845
OpenAlexW2171996376

What OpenQuestion holds

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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.