Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0279530 (bone cancer)
 1,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mobilization of calcium from the bone to the extracellular fluid proceeds in parallel with the dissolution of bone matrix, and is subject to the same influences. The role of circulating hormones has been discussed, and the importance of the skeleton as a store of calcium, even though skeletal calcium release is a relatively slow process in maturity. The major circulating hormones stimulating the processes are parathyroid hormone, 1,25-dihydroxyvitamin D3, and epidermal growth factor related substances. These represent three different classes of hormone with respect to their initial mechanisms of action. The most potent known hormonal inhibitor of bone resorption is the peptide, calcitonin, which acts directly upon the osteoclasts to inhibit their activity and generation. Local factors are undoubtedly important in the regulation of bone resorption, especially the prostaglandins. Prostaglandin E2 is the most potent bone resorber of the arachidonic acid metabolites, and is much more likely to be important locally than as a circulating factor especially in disease states such as metastatic bone cancer and arthritis. In understanding the ways in which drugs can influence bone mineral release it is important to appreciate how bone cells interact to resorb mineral and matrix. In this review the view is presented that cells of the osteoblast lineage (perhaps at the stage of osteocytes, or 'lining' cells) are the prime target of the resorbing hormones. Once having been acted upon, they initiate events which result in activation of osteoclasts. If this involves the passage of a message from osteoblast/osteocyte to osteoclast, it will be important to define this in further research.
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PMID:Drug and hormone effects on calcium release from bone. 635 42

Chordoma is a rare bone cancer originating from embryologic notochordal remnants. Clival chordomas show different dural penetration ability, with serious dural penetration exhibiting poorer prognosis. The molecular mechanism of dural penetration is not clear. We analyzed lncRNA and mRNA profiles in 12 chordoma patients with different degrees of dural penetration using expression microarrays. The differentially expressed lncRNAs and mRNAs were used to construct a lncRNA-mRNA co-expression network. LncRNAs were classified into lincRNA, enhancer-like lncRNA, or antisense lncRNA. Biological functions for lncRNAs were predicted according to the lncRNA-mRNA network and adjacent coding genes by pathway analysis. The 2760 lncRNAs and 3988 mRNAs were differentially expressed in chordomas between two groups of patients with and without dural penetration. Possible pathway involvement of the significance among the 55 lncRNAs located in the lncRNA-mRNA network, 24 lincRNAs, 7 enhancer-like lncRNAs, and 14 antisense lncRNAs include cell adhesion, metastasis, invasion, proliferation, and apoptosis. Expression of 10 lncRNAs and mRNAs, and epidermal growth factor mRNA with two identified lncRNAs were subsequently verified by qRT-PCR in chordoma tissues. Our report predicts the biological functions of many lncRNAs which may be used as diagnostic and prognostic biomarkers as well as therapeutic targets during the process of dural penetration in chordoma.
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PMID:LncRNA and mRNA expression profiles reveal the potential roles of lncRNA contributing to regulating dural penetration in clival chordoma. 3253 22