NDLI: Multiple myeloma disrupts the TRANCE/ osteoprotegerin cytokine axis to trigger bone destruction and promote tumor progression.

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Multiple myeloma disrupts the TRANCE/ osteoprotegerin cytokine axis to trigger bone destruction and promote tumor progression.

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Multiple myeloma disrupts the TRANCE/ osteoprotegerin cytokine axis to trigger bone destruction and promote tumor progression.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yaccoby, S. Sordillo, E. M. Michaeli, J. Choi, Y. Liau, D. F. Epstein, J. Pearse, R. N. Wong, B. R. Colman, N.
Description	Author Affiliation: Pearse RN ( Laboratories of Molecular Genetics and Immunology, and Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10021, USA. rnp2001@med.cornell.edu);
Abstract	Bone destruction, caused by aberrant production and activation of osteoclasts, is a prominent feature of multiple myeloma. We demonstrate that myeloma stimulates osteoclastogenesis by triggering a coordinated increase in the tumor necrosis factor-related activation-induced cytokine (TRANCE) and decrease in its decoy receptor, osteoprotegerin (OPG). Immunohistochemistry and in situ hybridization studies of bone marrow specimens indicate that in vivo, deregulation of the TRANCE-OPG cytokine axis occurs in myeloma, but not in the limited plasma cell disorder monoclonal gammopathy of unknown significance or in nonmyeloma hematologic malignancies. In coculture, myeloma cell lines stimulate expression of TRANCE and inhibit expression of OPG by stromal cells. Osteoclastogenesis, the functional consequence of increased TRANCE expression, is counteracted by addition of a recombinant TRANCE inhibitor, RANK-Fc, to marrow/myeloma cocultures. Myeloma-stroma interaction also has been postulated to support progression of the malignant clone. In the SCID-hu murine model of human myeloma, administration of RANK-Fc both prevents myeloma-induced bone destruction and interferes with myeloma progression. Our data identify TRANCE and OPG as key cytokines whose deregulation promotes bone destruction and supports myeloma growth.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	20
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Glycoproteins Pharmacology Acid Phosphatase Metabolism Animals Carrier Proteins Antagonists & Inhibitors Genetics Disease Progression Hodgkin Disease Pathology Isoenzymes Leukemia, Lymphocytic, Chronic, B-Cell Membrane Glycoproteins Mice Mice, SCID Osteoprotegerin Paraproteinemias RANK Ligand Receptor Activator Of Nuclear Factor-kappa B Receptors, Cytoplasmic And Nuclear Receptors, Tumor Necrosis Factor Reference Values Reverse Transcriptase Polymerase Chain Reaction Time Factors Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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