Direct crosstalk between cancer and osteoblast lineage cells fuels metastatic growth in bone via auto-amplification of IL-6 and RANKL signaling pathways. (Q39010800)

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scientific article published on September 2014

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English	Direct crosstalk between cancer and osteoblast lineage cells fuels metastatic growth in bone via auto-amplification of IL-6 and RANKL signaling pathways.	scientific article published on September 2014

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12 March 2020

Direct crosstalk between cancer and osteoblast lineage cells fuels metastatic growth in bone via auto-amplification of IL-6 and RANKL signaling pathways (English)

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12 March 2020

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12 March 2020

Markus J Seibel

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12 March 2020

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Yu Zheng

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12 March 2020

Shu-Oi Chow

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12 March 2020

Katja Boernert

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12 March 2020

Dennis Basel

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12 March 2020

Anastasia Mikuscheva

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12 March 2020

Sarah Kim

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12 March 2020

Colette Fong-Yee

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12 March 2020

Trupti Trivedi

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12 March 2020

Robert L Sutherland

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12 March 2020

Hong Zhou

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12 March 2020

Frank Buttgereit

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12 March 2020

publication date

1 September 2014

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12 March 2020

Journal of Bone and Mineral Research

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12 March 2020

29

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12 March 2020

9

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12 March 2020

1938-1949

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12 March 2020

Metastatic bone disease: clinical features, pathophysiology and treatment strategies

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https://api.crossref.org/works/10.1002%2FJBMR.2231

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Tumor-derived interleukin-8 stimulates osteolysis independent of the receptor activator of nuclear factor-kappaB ligand pathway

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Osteoblasts are a major source of inflammatory cytokines in the tumor microenvironment of bone metastatic breast cancer

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Regulation of cancer cell migration and bone metastasis by RANKL.

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The interleukin-6/soluble interleukin-6 receptor system induces parathyroid hormone-related protein in human osteoblastic cells

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Osteoclast differentiation factor RANKL controls development of progestin-driven mammary cancer

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Parathyroid hormone-related protein (PTHrP)-(1-139) isoform is efficiently secreted in vitro and enhances breast cancer metastasis to bone in vivo.

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T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-γ

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