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Endo180 at the cutting edge of bone cancer treatment and beyond

Sturge, Justin

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Abstract

Skeletal bone is an attractive site for secondary tumour growth and is also home to spontaneous primary cancer. Treatment of bone metastasis is focused on limiting the vicious cycle of bone destruction with bisphosphonates or inhibition of receptor activator of nuclear factor-κB ligand (RANKL) with the fully human monoclonal antibody denosumab. The estimated 1 million deaths/year where bone metastasis is present, and the high healthcare costs required for its management, have ignited intensive research into the cellular and molecular pathology of osteolysis, involving interplay between tumour cells, bone-forming osteoblasts and bone-degrading osteoclasts. Compared to bone metastasis, knowledge about the pathology of primary bone cancers is limited. In recent work published in this journal, Engelholm et al provide a unique insight into how this poorly understood disease manifests and destroys bone. For the first time they have demonstrated that a mouse monoclonal antibody targeting the collagen receptor Endo180 (CD280, MRC2 uPARAP) can prevent osteolysis and bone destruction in a syngeneic model of advanced osteosarcoma. Their convincing findings make an important contribution towards Endo180-based therapy being developed as an option for the treatment of bone cancer amongst other malignancies.

Journal Article Type Article
Publication Date Mar 1, 2016
Journal Journal of pathology
Print ISSN 0022-3417
Electronic ISSN 1096-9896
Publisher Wiley
Peer Reviewed Peer Reviewed
Volume 238
Issue 4
Pages 485-488
Institution Citation Sturge, J. (2016). Endo180 at the cutting edge of bone cancer treatment and beyond. Journal of Pathology, 238(4), 485-488. https://doi.org/10.1002/path.4673
DOI https://doi.org/10.1002/path.4673
Keywords Bone, Collagen, Endo180, Metastasis, Metastatic, Osteoblast, Osteoid, Osteolytic, Osteolysis, Osteosarcoma, Therapy
Publisher URL http://onlinelibrary.wiley.com/doi/10.1002/path.4673/abstract;jsessionid=2D092E94B84DEDA3B1B6860CC0563D26.f01t01
Copyright Statement © 2015 The Authors. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Additional Information This is a copy of an open access article published in Journal of pathology, 2016.

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Copyright Statement
© 2015 The Authors. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.



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