Osteosarcoma metastasis: Evidence for ACP5 downregulation and osteoclast involvement

Endo-Munoz, Liliana, Cumming, Andrew, Cueva, Claudia, Ng, Charlotte, Strutton, Geoffrey, Evdokiou, Andreas, Sommerville, Scott, Dickinson, Ian, Guminski, Alexander and Saunders, Nicholas (2008). Osteosarcoma metastasis: Evidence for ACP5 downregulation and osteoclast involvement. In: AACR Annual Meeting 2008. American Association for Cancer Research Annual Meeting, San Diego, CA, U.S.A., (). April 12-16, 2008.

Author Endo-Munoz, Liliana
Cumming, Andrew
Cueva, Claudia
Ng, Charlotte
Strutton, Geoffrey
Evdokiou, Andreas
Sommerville, Scott
Dickinson, Ian
Guminski, Alexander
Saunders, Nicholas
Title of paper Osteosarcoma metastasis: Evidence for ACP5 downregulation and osteoclast involvement
Conference name American Association for Cancer Research Annual Meeting
Conference location San Diego, CA, U.S.A.
Conference dates April 12-16, 2008
Proceedings title AACR Annual Meeting 2008
Publication Year 2008
Sub-type Poster
Volume 49
Formatted Abstract/Summary
 Osteosarcoma (OS) is the most common primary bone tumour in the pediatric age group. Pulmonary metastasis, which can be present in up to 50% of cases, is the major fatal complication of osteosarcoma. While the long-term survival of patients without metastasis is 65-70%, the long-term survival of patients who develop metastasis is only 10-20%. Our gene expression profiling study of primary osteosarcoma biopsies identified tartrate-resistant acid phosphatase 5 (ACP5, TRAP), a marker of osteoclasts, which at the time of diagnosis, predicts with 93% accuracy those patients in our group that will progress to lung metastasis. These results have been confirmed by immunohistochemistry in the original patient biopsies. Furthermore, within the metastatic patient group, the time for the development of detectable metastasis correlates directly with the level of ACP5 expression. We have also shown that the loss of ACP5 is associated with a loss of osteoclasts, and that in vitro, this loss of osteoclasts correlates with enhanced osteosarcoma cell migration. We have used nine different osteosarcoma cell lines to set up an orthotopic mouse model in which manipulation of osteoclast number and activity, with zoledronic acid or with a low calcium diet, is able to modulate the tumorigenicity and metastatic potential of osteosarcoma. Our findings suggest that the loss of osteoclasts and concomitant downregulation of ACP5 may contribute to OS metastasis, and that modulators of osteoclast number and activity may have a significant impact in patients at risk of metastasis.
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Conference Paper
Collection: UQ Diamantina Institute Publications
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Created: Thu, 03 Nov 2011, 12:07:15 EST by Liliana Munoz on behalf of UQ Diamantina Institute