Evidence map›Paper›PMID 25473842›Full record

ArticlePLoS computational biology2014

Lattice-based model of ductal carcinoma in situ suggests rules for breast cancer progression to an invasive state.

Eline Boghaert, Derek C Radisky, Celeste M Nelson

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. A Multiscale Agent-Based Model of Ductal Carcinoma In Situ.IEEE transactions on bio-medical engineering · 2020
    Article
  5. Article
  6. A checkpoint-oriented cell cycle simulation model.Cell cycle (Georgetown, Tex.) · 2019
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Multiscale mechanobiology: computational models for integrating molecules to multicellular systems.Integrative biology : quantitative biosciences from nano to macro · 2015
    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

3 authors at 2 institutions in 1 country.

Eline BoghaertDepartment of Chemical and Biological Engineering, Princeton University, Princeton, New Jersey, United States of America.
Derek C RadiskyDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida, United States of America.
Celeste M NelsonDepartment of Chemical and Biological Engineering, Princeton University, Princeton, New Jersey, United States of America; Department of Molecular Biology, Princeton University, Princeton, New Jersey, United States of America.
Princeton University · USMayo Clinic in Florida · US

Funding

The Role of CHFR in Tumorigenesis and Paclitaxel-Sensitivity in Breast CancerP50CA116201 · NCI · MAYO CLINIC ROCHESTER · PI PETER C LUCAS · 2005 to 2026
$49.9M
Mechanical Regulation of Mesenchyme and Mammalian Lung DevelopmentR01HL120142 · NHLBI · PRINCETON UNIVERSITY · PI NELSON, CELESTE M · 2014 to 2017
$1.6M
Spatial patterning of branching morphogenesisR01GM083997 · NIGMS · PRINCETON UNIVERSITY · PI NELSON, CELESTE M · 2008 to 2012
$1.4M
Mechanical regulation of branching morphogenesisR21HL110335 · NHLBI · PRINCETON UNIVERSITY · PI NELSON, CELESTE M · 2011 to 2012
$443k
Exogenous Fluid Forces and Branching of the Mammalian LungR21HL118532 · NHLBI · PRINCETON UNIVERSITY · PI NELSON, CELESTE M · 2014 to 2015
$442k
NCI NIH HHS CA116201NCI NIH HHS P50 CA116201NHLBI NIH HHS HL110335NHLBI NIH HHS HL118532NHLBI NIH HHS HL120142NHLBI NIH HHS R01 HL120142NHLBI NIH HHS R21 HL110335NHLBI NIH HHS R21 HL118532NIGMS NIH HHS GM083997NIGMS NIH HHS R01 GM083997
6 · The paper itself

Abstract

Ductal carcinoma in situ (DCIS) is a heterogeneous group of non-invasive lesions of the breast that result from abnormal proliferation of mammary epithelial cells. Pathologists characterize DCIS by four tissue morphologies (micropapillary, cribriform, solid, and comedo), but the underlying mechanisms that distinguish the development and progression of these morphologies are not well understood. Here we explored the conditions leading to the emergence of the different morphologies of DCIS using a two-dimensional multi-cell lattice-based model that incorporates cell proliferation, apoptosis, necrosis, adhesion, and contractility. We found that the relative rates of cell proliferation and apoptosis governed which of the four morphologies emerged. High proliferation and low apoptosis favored the emergence of solid and comedo morphologies. In contrast, low proliferation and high apoptosis led to the micropapillary morphology, whereas high proliferation and high apoptosis led to the cribriform morphology. The natural progression between morphologies cannot be investigated in vivo since lesions are usually surgically removed upon detection; however, our model suggests probable transitions between these morphologies during breast cancer progression. Importantly, cribriform and comedo appear to be the ultimate morphologies of DCIS. Motivated by previous experimental studies demonstrating that tumor cells behave differently depending on where they are located within the mammary duct in vivo or in engineered tissues, we examined the effects of tissue geometry on the progression of DCIS. In agreement with our previous experimental work, we found that cells are more likely to invade from the end of ducts and that this preferential invasion is regulated by cell adhesion and contractility. This model provides additional insight into tumor cell behavior and allows the exploration of phenotypic transitions not easily monitored in vivo.

Indexed as

Models, BiologicalApoptosisBreast NeoplasmsCarcinoma, Intraductal, NoninfiltratingCell AdhesionComputational BiologyFemaleHumansNeoplasm InvasivenessPhenotypeTumor Cells, Cultured

Identifiers

PMID25473842
PMCPMC4256017
OpenAlexW2068716083

What OpenQuestion holds

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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.