期刊
JOURNAL OF BONE AND MINERAL RESEARCH
卷 25, 期 12, 页码 2357-2370出版社
WILEY
DOI: 10.1002/jbmr.142
关键词
ACTIVIN-A; BREAST CANCER; MYELOMA METASTASIS
资金
- Fonds voor Wetenschappelijk Onderzoek Vlaanderen
- Biotechnology and Biological Sciences Research Council
- Arthritis Research Campaign Acceleron Pharma
- Multiple Myeloma Research Foundation
Cancers that grow in bone, such as myeloma and breast cancer metastases, cause devastating osteolytic bone destruction These cancers hijack bone remodeling by stimulating osteoclastic bone resorption and suppressing bone formation Currently, treatment is targeted primarily at blocking bone resorption, but this approach has achieved only limited success Stimulating osteoblastic bone formation to promote repair is a novel alternative approach We show that a soluble activin receptor type IIA fusion protein (ActRIIA muFc) stimulates osteoblastogenesis (p < 01), promotes bone formation (p < 01) and increases bone mass in vivo (p < 001) We show that the development of osteolytic bone lesions in mice bearing murine myeloma cells is caused by both increased resorption (p < 05) and suppression of bone formation (p < 01) ActRIIA muFc treatment stimulates osteoblastogenesis (p < 01), prevents myeloma-induced suppression of bone formation (p < 05), blocks the development of osteolytic bone lesions (p < 05), and increases survival (p < 05) We also show, in a murine model of breast cancer bone metastasis, that ActRIIA muFc again prevents bone destruction (p < 001) and inhibits bone metastases (p < 05) These findings show that stimulating osteoblastic bone formation with ActRIIA muFc blocks the formation of osteolytic bone lesions and bone metastases in models of myeloma and breast cancer and paves the way for new approaches to treating this debilitating aspect of cancer (C) 2010 American Society for Bone and Mineral Research
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