Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Nelson, J.B. et al.

New bone formation in an osteoblastic tumor model is increased by endothelin-1 overexpression and decreased by endothelin A receptor blockade.

OBJECTIVES: The osteoblastic response of bone to metastatic prostate cancer is both characteristic and enigmatic. The potent vasoconstrictor endothelin-1 ( ET-1), produced by prostate cancer, has been identified as a potential factor in new bone formation. METHODS: Using a novel method to quantitate new bone formation induced by the WISH tumor, we examined the effects of ET-1 overexpression and endothelin receptor antagonists on the osteoblastic response. RESULTS: WISH, a human tumor cell line derived from amnion, produces ET-1 mRNA and protein and induces abundant new bone formation and splenomegaly in vivo. Stable transfection of WISH with an ET-1 overexpression cDNA construct produced clones that secreted 18-fold more bioactive ET-1 than vector-only controls. After 14 days of growth in the lower leg of nu/nu mice, ET-1 overexpressing tumors produced significantly more new bone than vector-only controls. Conversely, areas of new bone formation were significantly less in animals treated with a selective endothelin A (ET(A)) receptor antagonist A127722. CONCLUSIONS: The activity of ET-1 in this osteoblastic model provides a unique target for therapy.[1]

References

New bone formation in an osteoblastic tumor model is increased by endothelin-1 overexpression and decreased by endothelin A receptor blockade. Nelson, J.B., Nguyen, S.H., Wu-Wong, J.R., Opgenorth, T.J., Dixon, D.B., Chung, L.W., Inoue, N. Urology (1999) [Pubmed]

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