Antisense inhibition of macrophage inflammatory protein 1-alpha blocks bone destruction in a model of myeloma bone disease. - Wikidata - awgldk - TriplyDB

Antisense inhibition of macrophage inflammatory protein 1-alpha blocks bone destruction in a model of myeloma bone disease.

Antisense inhibition of macrophage inflammatory protein 1-alpha blocks bone destruction in a model of myeloma bone disease.

http://www.wikidata.org/entity/Q36169814

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Osteoimmunology: interactions of the bone and immune system Mechanism of Action of Bortezomib and the New Proteasome Inhibitors on Myeloma Cells and the Bone Microenvironment: Impact on Myeloma-Induced Alterations of Bone Remodeling CCL9/MIP-1gamma and its receptor CCR1 are the major chemokine ligand/receptor species expressed by osteoclasts Tgf-Beta inhibition restores terminal osteoblast differentiation to suppress myeloma growth Osteoclast-gene expression profiling reveals osteoclast-derived CCR2 chemokines promoting myeloma cell migration.Growth factors in multiple myeloma: a comprehensive analysis of their expression in tumor cells and bone marrow environment using Affymetrix microarrays.Activin A promotes multiple myeloma-induced osteolysis and is a promising target for myeloma bone disease Saturated fatty acids enhance osteoclast survival Multiple myeloma mesenchymal stromal cells: Contribution to myeloma bone disease and therapeutics Bone disease in multiple myeloma: pathophysiology and management.The effects of promoter methylation on downregulation of DAZAP2 in multiple myeloma cell lines.MIP-1δ activates NFATc1 and enhances osteoclastogenesis: involvement of both PLCγ2 and NFκB signaling.Metastasis and bone loss: advancing treatment and prevention.Osteolytic bone resorption in adult T-cell leukemia/lymphoma.New insights, recent advances, and current challenges in the biological treatment of multiple myeloma.Relative roles of direct regeneration versus paracrine effects of human cardiosphere-derived cells transplanted into infarcted mice.Inhibitory effects of osteoblasts and increased bone formation on myeloma in novel culture systems and a myelomatous mouse model Homing and mobilization of hematopoietic stem cells and hematopoietic cancer cells are mirror image processes, utilizing similar signaling pathways and occurring concurrently: circulating cancer cells constitute an ideal target for concurrent treatm New insights into the pathophysiology and management of bone disease in multiple myeloma.Bone anabolic agents for the treatment of multiple myeloma.Targeting bone as a therapy for myeloma.Effects of parathyroid hormone-related protein and macrophage inflammatory protein-1α in Jurkat T-cells on tumor formation in vivo and expression of apoptosis regulatory genes in vitro The high rate of bone resorption in multiple myeloma is due to RANK (receptor activator of nuclear factor-kappaB) and RANK Ligand expression.Glycosphingolipid synthesis inhibition limits osteoclast activation and myeloma bone disease.MLN3897, a novel CCR1 inhibitor, impairs osteoclastogenesis and inhibits the interaction of multiple myeloma cells and osteoclasts.Myeloma bone disease: pathophysiology and management.CCR1 blockade reduces tumor burden and osteolysis in vivo in a mouse model of myeloma bone disease Bone lesions and macrophage inflammatory protein-1 alpha (MIP-1a) in human multiple myeloma.Significance of macrophage inflammatory protein-1 alpha (MIP-1alpha) in multiple myeloma.Osteoclast precursors, RANKL/RANK, and immunology.The role of immune cells and inflammatory cytokines in Paget's disease and multiple myeloma.Advances in the management of myeloma bone disease.Novel therapeutic strategies targeting growth factor signalling cascades in multiple myeloma.Clinical utilization of chemokines to combat cancer: the double-edged sword.Role of the microenvironment in multiple myeloma bone disease.Chemokines in multiple myeloma Cellular mechanisms of multiple myeloma bone disease Genetic polymorphisms of EPHX1, Gsk3beta, TNFSF8 and myeloma cell DKK-1 expression linked to bone disease in myeloma Mechanisms of multiple myeloma bone disease.The pathogenesis of the bone disease of multiple myeloma.

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Antisense inhibition of macrophage inflammatory protein 1-alpha blocks bone destruction in a model of myeloma bone disease.

http://www.wikidata.org/entity/Q36169814

description

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G D Roodman

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P2860

Structures of human genes coding for cytokine LD78 and their expression

Macrophage inflammatory protein-1alpha is an osteoclastogenic factor in myeloma that is independent of receptor activator of nuclear factor kappaB ligand.

Cloning and identification of human Sca as a novel inhibitor of osteoclast formation and bone resorption.

Advances in therapy of multiple myeloma: lessons from acute leukemia.

Interleukin 6. A potential autocrine/paracrine factor in Paget's disease of bone

Cell-cell contact between marrow stromal cells and myeloma cells via VCAM-1 and alpha(4)beta(1)-integrin enhances production of osteoclast-stimulating activity.

Differential use of very late antigen-4 and -5 integrins by hematopoietic precursors and myeloma cells to adhere to transforming growth factor-beta1-treated bone marrow stroma.

Bisphosphonates induce apoptosis in human myeloma cell lines: a novel anti-tumour activity.

Development of an in vivo model of human multiple myeloma bone disease.

Cell adhesion mediated drug resistance (CAM-DR): role of integrins and resistance to apoptosis in human myeloma cell lines.

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