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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-09-01
    Description: The strength and integrity of our bones depends on maintaining a delicate balance between bone resorption by osteoclasts and bone formation by osteoblasts. As we age or as a result of disease, this delicate balancing act becomes tipped in favor of osteoclasts so that bone resorption exceeds bone formation, rendering bones brittle and prone to fracture. A better understanding of the biology of osteoclasts and osteoblasts is providing opportunities for developing therapeutics to treat diseases of bone. Drugs that inhibit the formation or activity of osteoclasts are valuable for treating osteoporosis, Paget's disease, and inflammation of bone associated with rheumatoid arthritis or periodontal disease. Far less attention has been paid to promoting bone formation with, for example, growth factors or hormones, an approach that would be a valuable adjunct therapy for patients receiving inhibitors of bone resorption.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodan, G A -- Martin, T J -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1508-14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Research Laboratories, West Point, PA 19486, USA. St. Vincent's Institute of Medical Research, Melbourne 3065, Australia. gideon_rodan@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10968781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Diseases/*drug therapy/genetics/physiopathology/therapy ; Bone Resorption/drug therapy ; Calcitonin/therapeutic use ; Diphosphonates/therapeutic use ; Estrogen Receptor Modulators/therapeutic use ; Estrogens/therapeutic use ; Female ; Genetic Therapy ; Growth Substances/therapeutic use ; Humans ; Male ; Osteoclasts/drug effects ; Osteogenesis/drug effects ; Osteoporosis/*drug therapy/genetics/physiopathology/therapy ; Parathyroid Hormone/therapeutic use
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1983-09-23
    Description: Evidence is presented that a tumor-derived transforming growth factor is responsible for stimulating bone resorption and causing hypercalcemia in an animal tumor model of the hypercalcemia of malignancy. Both conditioned medium harvested from cultured tumor cells and tumor extracts of the transplantable rat Leydig cell tumor associated with hypercalcemia contained a macromolecular bone resorbing factor with the chemical characteristics of a tumor-derived transforming growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ibbotson, K J -- D'Souza, S M -- Ng, K W -- Osborne, C K -- Niall, M -- Martin, T J -- Mundy, G R -- AM-28149/AM/NIADDK NIH HHS/ -- CA-29537/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1292-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6577602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Resorption ; Calcium ; Cells, Cultured ; Culture Media ; Growth Substances/*physiology ; Hypercalcemia/*etiology ; Leydig Cell Tumor/complications/*physiopathology ; Male ; Neoplasm Proteins/*physiology ; Neoplasms, Experimental/complications/physiopathology ; Peptides/*physiology ; Rats ; Transforming Growth Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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