The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Intermittent hypoxia is a key regulator of cancer cell and endothelial cell interplay in tumours
Open accessAbstract
Solid tumours are complex structures in which the interdependent relationship between tumour and endothelial cells modulates tumour development and metastasis dissemination. The tumour microenvironment plays an important role in this cell interplay, and changes in its features have a major impact on tumour growth as well as on anticancer therapy responsiveness. Different studies have shown irregular blood flow in tumours, which is responsible for hypoxia and reoxygenation phases, also called intermittent hypoxia. Intermittent hypoxia induces transient changes, the impact of which has been underestimated for a long time. Recent in vitro and in vivo studies have shown that intermittent hypoxia could positively modulate tumour development, inducing tumour growth, angiogenic processes, chemoresistance, and radioresistance. In this article, we review the effects of intermittent hypoxia on tumour and endothelial cells as well as its impacts on tumour development.
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Cited by
Regulation of Immunity and Inflammation by Hypoxia in Immunological Niches
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Metadata
- Authors
- Toffoli, S., & Michiels, C.
- Venue
- The FEBS Journal
- Publisher
- Wiley
- Published
- 2008-04-25
- Volume
- 275
- Issue
- 12
- Pages
- 2991-3002
- ISSN
- 1742-464X (ISSN-L)
- 1742-4658
- OpenAlex
- W1567827425
- Cited by
- 169
- References
- 8
- FWCI
- 2.12
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Toffoli, S., & Michiels, C. (2008). Intermittent hypoxia is a key regulator of cancer cell and endothelial cell interplay in tumours. The FEBS Journal. https://doi.org/10.1111/j.1742-4658.2008.06454.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.