The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
A causal role for endothelin-1 in the pathogenesis of osteoblastic bone metastases
Open accessAbstract
Osteoblastic bone metastases are common in prostate and breast cancer patients, but mechanisms by which tumor cells stimulate new bone formation are unclear. We identified three breast cancer cell lines that cause osteoblastic metastases in a mouse model and secrete endothelin-1. Tumor-produced endothelin-1 stimulates new bone formation in vitro and osteoblastic metastases in vivo via the endothelin A receptor. Treatment with an orally active endothelin A receptor antagonist dramatically decreased bone metastases and tumor burden in mice inoculated with ZR-75-1 cells. Tumor-produced endothelin-1 may have a major role in the establishment of osteoblastic bone metastases, and endothelin A receptor blockade represents effective treatment.
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Cites
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Cited by
The role of Dickkopf-1 in bone development, homeostasis, and disease
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Self-citationOsteoblast differentiation profiles define sex specific gene expression patterns in craniosynostosis
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Metadata
- Authors
- Yin, J. J., Mohammad, K. S., Käkönen, S. M., Harris, S., Wu-Wong, J. R., Wessale, J. L., Padley, R. J., Garrett, I. R., Chirgwin, J. M., & Guise, T. A.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2003-08-26
- Volume
- 100
- Issue
- 19
- Pages
- 10954-10959
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2023659903
- Cited by
- 381
- References
- 27
- FWCI
- 10.38
- Type
- journal article
- Language
- en
- Open access
- green
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- Yin, J. J., Mohammad, K. S., Käkönen, S. M., Harris, S., Wu-Wong, J. R., Wessale, J. L., Padley, R. J., Garrett, I. R., Chirgwin, J. M., & Guise, T. A. (2003). A causal role for endothelin-1 in the pathogenesis of osteoblastic bone metastases. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1830978100
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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