ArticleBiophysical journal2016
Physical Mechanisms of Cancer in the Transition to Metastasis.
Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Integrin αBiomaterials · 2018Article
- Cellular Contraction Can Drive Rapid Epithelial Flows.Biophysical journal · 2017Article
- Establishment and characterization of a novel highly aggressive gallbladder cancer cell line, TJ-GBC2.Cancer cell international · 2017Article
- Biophysical Properties and Motility of Human Mature Dendritic Cells Deteriorated by Vascular Endothelial Growth Factor through Cytoskeleton Remodeling.International journal of molecular sciences · 2016Article
- The Inelastic Hierarchy: Multiscale Biomechanics of Weak Bonds.Biophysical journal · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Whether a tumor is metastatic is one of the most significant factors that influence the prognosis for a cancer patient. The transition from a nonmetastatic tumor to a metastatic one is accompanied by a number of genetic and proteomic changes within the tumor cells. These protein-level changes conspire to produce behavioral changes in the cells: cells that had been relatively stationary begin to move, often as a group. In this study we ask the question of what cell-level biophysical changes are sufficient to initiate evasion away from an otherwise static tumor. We use a mathematical model developed to describe the biophysics of epithelial tissue to explore this problem. The model is first validated against in vitro wound healing experiments with cancer cell lines. Then we simulate the behavior of a group of mutated cells within a sea of healthy tissue. We find that moderate increases in adhesion between the cell and extracellular matrix (ECM) accompanied by a decrease in cell-cell adhesion and/or Rho family of small GTPase activation can cause a group of cells to break free from a tumor and spontaneously migrate. This result may explain why some metastatic cells have been observed to upregulate integrin, downregulate cadherin, and activate Rho family signaling.
Indexed as
Identifiers
What OpenQuestion holds
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.