ArticleCell cycle (Georgetown, Tex.)2009
Biological impact of mechanical stimuli on tumor metastasis.
Article in Cell cycle (Georgetown, Tex.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Toward a role for the acoustic field in cells interaction.Frontiers in systems neuroscience · 2025Article
- ZINC4085554 inhibits cancer cell adhesion by interfering with the interaction of Akt1 and FAK.Oncology letters · 2019Article
- Mimicking biophysical stimuli within bone tumor microenvironment.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2015Article
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- A novel flow bioreactor for in vitro microvascularization.Tissue engineering. Part C, Methods · 2010Article
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 1 institution in 2 countries.
Funding
Abstract
Increasing evidence suggests tumor cell exposure to mechanical stimuli during the perioperative period as well as throughout the normal disease process may have a discernable impact on tumor metastasis and patient outcome. In vitro studies have demonstrated that transient exposure to increased extracellular pressure and shear forces modulates integrin binding affinity and stimulates cancer cell adhesion through a cytoskeleton- and focal adhesion complex-dependent signaling mechanism. More prolonged exposure to elevated pressures stimulates tumor cell proliferation by a distinct signaling pathway. Whether pressure effects on cell adhesion and proliferation pose biological ramifications in vivo remained unknown. We recently reported that pressure activation of malignant cells does indeed have a biological impact on surgical wound implantation, tumor development and tumor-free survival in a murine colon tumor model. Moreover, this effect can be disrupted by preoperative administration of colchicine. Taken together with previous work from our laboratory and others, these findings suggest that further elucidation of the mechanical signaling pathways governing pressure-stimulated tumor cell adhesion and proliferation may identify novel therapeutic targets for the treatment and prevention of tumor metastasis.
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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.