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10.1182/blood-2017-03-773341 http://scihub22266oqcxt.onion/10.1182/blood-2017-03-773341 C5492093!5492093 !28515094     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28515094 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibiting the osteocyte-specific protein sclerostin increases bone mass and fracture resistance in multiple myeloma |pdf=|usr=}}{{28515094 }} gab.com Text Inhibiting the osteocyte-specific protein sclerostin increases bone mass and fracture resistance in multiple myeloma JO: Blood http://www.kidney.de/pget.php?&tw=1&pmid=28515094 #FOAvip Multiple myeloma (MM) is a plasma cell cancer that develops in the skeleton causing profound bone destruction and fractures. The bone disease is mediated by increased osteoclastic bone resorption and suppressed bone formation. Bisphosphonates used for treatment inhibit bone resorption and prevent bone loss but fail to influence bone formation and do not replace lost bone, so patients continue to fracture. Stimulating bone formation to increase bone mass and fracture resistance is a priority; however, targeting tumor-derived modulators of bone formation has had limited success. Sclerostin is an osteocyte-specific Wnt antagonist that inhibits bone formation. We hypothesized that inhibiting sclerostin would prevent development of bone disease and increase resistance to fracture in MM. Sclerostin was expressed in osteocytes from bones from naive and myeloma-bearing mice. In contrast, sclerostin was not expressed by plasma cells from 630 patients with myeloma or 54 myeloma cell lines. Mice injected with 5TGM1-eGFP, 5T2MM, or MM1.S myeloma cells demonstrated significant bone loss, which was associated with a decrease in fracture resistance in the vertebrae. Treatment with anti-sclerostin antibody increased osteoblast numbers and bone formation rate but did not inhibit bone resorption or reduce tumor burden. Treatment with anti-sclerostin antibody prevented myeloma-induced bone loss, reduced osteolytic bone lesions, and increased fracture resistance. Treatment with anti-sclerostin antibody and zoledronic acid combined increased bone mass and fracture resistance when compared with treatment with zoledronic acid alone. This study defines a therapeutic strategy superior to the current standard of care that will reduce fractures for patients with MM. Twit Text FOAVip Inhibiting the osteocyte-specific protein sclerostin increases bone mass and fracture resistance in multiple myeloma ????Blood http://www.kidney.de/pget.php?&tw=1&pmid=28515094 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28515094 #FOAvip English Wikipedia <ref>{{Cite pmid|28515094 }}</ref> Inhibiting the osteocyte-specific protein sclerostin increases bone mass and fracture resistance in multiple myeloma #MMPMID28515094 McDonald MM ; Reagan MR ; Youlten SE ; Mohanty ST ; Seckinger A ; Terry RL ; Pettitt JA ; Simic MK ; Cheng TL ; Morse A ; Le LMT ; Abi-Hanna D ; Kramer I ; Falank C ; Fairfield H ; Ghobrial IM ; Baldock PA ; Little DG ; Kneissel M ; Vanderkerken K ; Bassett JHD ; Williams GR ; Oyajobi BO ; Hose D ; Phan TG ; Croucher PI Blood 2017[Jun]; 129 (26 ): 3452-3464 PMID28515094 show ga Multiple myeloma (MM) is a plasma cell cancer that develops in the skeleton causing profound bone destruction and fractures. The bone disease is mediated by increased osteoclastic bone resorption and suppressed bone formation. Bisphosphonates used for treatment inhibit bone resorption and prevent bone loss but fail to influence bone formation and do not replace lost bone, so patients continue to fracture. Stimulating bone formation to increase bone mass and fracture resistance is a priority; however, targeting tumor-derived modulators of bone formation has had limited success. Sclerostin is an osteocyte-specific Wnt antagonist that inhibits bone formation. We hypothesized that inhibiting sclerostin would prevent development of bone disease and increase resistance to fracture in MM. Sclerostin was expressed in osteocytes from bones from naive and myeloma-bearing mice. In contrast, sclerostin was not expressed by plasma cells from 630 patients with myeloma or 54 myeloma cell lines. Mice injected with 5TGM1-eGFP, 5T2MM, or MM1.S myeloma cells demonstrated significant bone loss, which was associated with a decrease in fracture resistance in the vertebrae. Treatment with anti-sclerostin antibody increased osteoblast numbers and bone formation rate but did not inhibit bone resorption or reduce tumor burden. Treatment with anti-sclerostin antibody prevented myeloma-induced bone loss, reduced osteolytic bone lesions, and increased fracture resistance. Treatment with anti-sclerostin antibody and zoledronic acid combined increased bone mass and fracture resistance when compared with treatment with zoledronic acid alone. This study defines a therapeutic strategy superior to the current standard of care that will reduce fractures for patients with MM. |Adaptor Proteins, Signal Transducing [MESH] |Animals [MESH] |Antibodies/pharmacology/therapeutic use [MESH] |Bone Density/*drug effects [MESH] |Bone Morphogenetic Proteins/*antagonists & inhibitors/immunology [MESH] |Cell Line, Tumor [MESH] |Diphosphonates/therapeutic use [MESH] |Fractures, Bone/*prevention & control [MESH] |Genetic Markers/immunology [MESH] |Humans [MESH] |Imidazoles/therapeutic use [MESH] |Mice [MESH] |Multiple Myeloma/complications [MESH] |Osteocytes/*chemistry [MESH] |Osteogenesis/*drug effects [MESH] |Tumor Cells, Cultured [MESH]Inhibiting the osteocyte-specific protein sclerostin increases bone ma(epmc).pdf DeepDyve Pubget Overpricing