ArticleIntegrative biology : quantitative biosciences from nano to macro2015
A cell-ECM screening method to predict breast cancer metastasis.
Article in Integrative biology : quantitative biosciences from nano to macro, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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.
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.
Who cites it
39 citing papers in PubMed, 73 citations in OpenAlex.
- Cell-Instructive Biomaterials with Native-Like Biochemical Complexity.Annual review of biomedical engineering · 2025Review
- Biomimetic Hydrogel Strategies for Cancer Therapy.Gels (Basel, Switzerland) · 2024Review
- Outlook and opportunities for engineered environments of breast cancer dormancy.Science advances · 2024Review
- Tenascin-C Activation of Lung Fibroblasts in a 3D Synthetic Lung Extracellular Matrix Mimic.Advanced materials (Deerfield Beach, Fla.) · 2023Article
- Polysaccharides and Structural Proteins as Components in Three-Dimensional Scaffolds for Breast Cancer Tissue Models: A Review.Bioengineering (Basel, Switzerland) · 2023Review
- Live Cell Lineage Tracing of Dormant Cancer Cells.Advanced healthcare materials · 2023Article
- Functional biomaterials for biomimetic 3D in vitro tumor microenvironment modeling.In vitro models · 2023Review
- Tenascin-C activation of lung fibroblasts in a 3D synthetic lung extracellular matrix mimic.bioRxiv : the preprint server for biology · 2023Article
- Challenges and Opportunities Modeling the Dynamic Tumor Matrisome.BME frontiers · 2023Review
- Systems approaches to uncovering the contribution of environment-mediated drug resistance.Current opinion in solid state & materials science · 2022Article
- Article
- Identification of Core Genes and Pathways in Melanoma Metastasis via Bioinformatics Analysis.International journal of molecular sciences · 2022Article
- Filamin A Is a Potential Driver of Breast Cancer MetastasisFrontiers in oncology · 2022Article
- Morphological Phenotyping of Organotropic Brain- and Bone-Seeking Triple Negative Metastatic Breast Tumor Cells.Frontiers in cell and developmental biology · 2022Article
- A poly(ethylene glycol) three-dimensional bone marrow hydrogel.Biomaterials · 2022Article
- Harnessing the power of antibodies to fight bone metastasis.Science advances · 2021Article
- Protein-Functionalized Poly(ethylene glycol) Hydrogels as Scaffolds for Monolayer Organoid Culture.Tissue engineering. Part C, Methods · 2021Article
- Review
- Best Practices for Preclinical In Vivo Testing of Cancer Nanomedicines.Advanced healthcare materials · 2020Review
- Vascularized Biomaterials to Study Cancer Metastasis.Advanced healthcare materials · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Breast cancer preferentially spreads to the bone, brain, liver, and lung. The clinical patterns of this tissue-specific spread (tropism) cannot be explained by blood flow alone, yet our understanding of what mediates tropism to these physically and chemically diverse tissues is limited. While the microenvironment has been recognized as a critical factor in governing metastatic colonization, the role of the extracellular matrix (ECM) in mediating tropism has not been thoroughly explored. We created a simple biomaterial platform with systematic control over the ECM protein density and composition to determine if integrin binding governs how metastatic cells differentiate between secondary tissue sites. Instead of examining individual behaviors, we compiled large patterns of phenotypes associated with adhesion to and migration on these controlled ECMs. In combining this novel analysis with a simple biomaterial platform, we created an in vitro fingerprint that is predictive of in vivo metastasis. This rapid biomaterial screen also provided information on how β1, α2, and α6 integrins might mediate metastasis in patients, providing insights beyond a purely genetic analysis. We propose that this approach of screening many cell-ECM interactions, across many different heterogeneous cell lines, is predictive of in vivo behavior, and is much simpler, faster, and more economical than complex 3D environments or mouse models. We also propose that when specifically applied toward the question of tissue tropism in breast cancer, it can be used to provide insight into certain integrin subunits as therapeutic targets.
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Registered trials
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.