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Peter Diamond

Researcher at University of Adelaide

Publications -  19
Citations -  1173

Peter Diamond is an academic researcher from University of Adelaide. The author has contributed to research in topics: Cold-shock domain & Osteolysis. The author has an hindex of 16, co-authored 18 publications receiving 1109 citations.

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Elevated Serum Levels of Stromal-Derived Factor-1α Are Associated with Increased Osteoclast Activity and Osteolytic Bone Disease in Multiple Myeloma Patients

TL;DR: It is proposed that inhibition of the CXCR4-SDF-1α axis may provide an effective means of treatment for MM-induced osteolysis and serve to recruit osteoclast precursors to local sites within the bone marrow and enhance their motility and bone-resorbing activity.
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A novel monoclonal antibody (STRO-3) identifies an isoform of tissue nonspecific alkaline phosphatase expressed by multipotent bone marrow stromal stem cells.

TL;DR: Using retroviral expression cloning, it is determined that STRO-3 binds to tissue nonspecific alkaline phosphatase (TNSALP), a cell-surface glycoprotein usually associated with cells of the osteoblast lineage that may represent a marker of immature BMSSCs in vivo.
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The emerging role of hypoxia, HIF-1 and HIF-2 in multiple myeloma

TL;DR: The emerging role of hypoxia and the HIFs in the pathogenesis of multiple myeloma (MM), an incurable hematological malignancy of BM PCs, which reside within the hypoxic BM microenvironment is discussed.
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A multi-protein complex containing cold shock domain (Y-box) and polypyrimidine tract binding proteins forms on the vascular endothelial growth factor mRNA. Potential role in mRNA stabilization.

TL;DR: The identification of complexes, binding to the VEGFmRNA 5'- and 3'-UTR, that contain cold shock domain (CSD) and polypyrimidine tract binding (PTB) RNA binding proteins are reported, suggesting a combined transcriptional/post-transcriptional role for these proteins in V EGF and other growth factor gene regulation.
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The tyrosine kinase inhibitor dasatinib dysregulates bone remodeling through inhibition of osteoclasts in vivo

TL;DR: It is shown that dasatinib increases trabecular bone volume at least in part by inhibiting osteoclast activity, suggesting that d asatinib therapy may result in dysregulated bone remodeling.