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Toshihiro Hashimoto

Researcher at Tokushima Bunri University

Publications -  252
Citations -  6756

Toshihiro Hashimoto is an academic researcher from Tokushima Bunri University. The author has contributed to research in topics: Aspergillus niger & Cytotoxic T cell. The author has an hindex of 42, co-authored 252 publications receiving 6278 citations. Previous affiliations of Toshihiro Hashimoto include Korean Council for University Education & Tamkang University.

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Myeloma cells suppress bone formation by secreting a soluble Wnt inhibitor, sFRP-2.

TL;DR: In addition to enhanced osteolysis, MM cells also suppress bone formation at least in part through an inhibition of the canonical Wnt pathway by secreting sFRP-2, suggesting a predominant role for MM cell-derived sFRp-2 in the impairment of bone formation by MM.
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Osteoclasts enhance myeloma cell growth and survival via cell-cell contact: a vicious cycle between bone destruction and myeloma expansion.

TL;DR: It is demonstrated that peripheral blood mononuclear cell-derived OCs enhanced growth and survival of primary MM cells as well as MM cell lines more potently than stromal cells, and that OCs protected MM cells from apoptosis induced by serum depletion or doxorubicin.
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Role for macrophage inflammatory protein (MIP)-1α and MIP-1β in the development of osteolytic lesions in multiple myeloma

TL;DR: Results suggest that MIP-1α and Mip-1β may be major osteoclast-activating factors produced by MM cells, and C-C chemokines, macrophage inflammatory protein (MIP)–1 α and MIP -1β, in MM cell-induced osteolysis.
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Myeloma Cell-Osteoclast Interaction Enhances Angiogenesis Together with Bone Resorption: A Role for Vascular Endothelial Cell Growth Factor and Osteopontin

TL;DR: Osteoclast-derived osteopontin and VEGF from myeloma cells cooperatively enhance angiogenesis and also induce osteoclastogenic activity by vascular endothelial cells, suggesting the presence of a close link between myelomas cells, osteoclasts, and vascular endothelium cells to form a vicious cycle between bone destruction, angiogenic, and myelomatic expansion.