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[Bone metastases: pathogenesis and treatment with diphosphonates].
Bull Mem Acad R Med Belg. 1997; 152(3):169-74; discussion 174-6.BM

Abstract

Tumor-induced osteolysis is essentially mediated by the osteoclasts whose number and activity appear to be stimulated under the influence of tumor secretory products. In cases of hypercalcemia, there is also a variable inhibition of the bone formation rate leading to a characteristic "uncoupling" in bone turnover. An analog of parathyroid hormone--"parathyroid hormone-related protein (PTHrP)"--plays an essential role in the pathogenesis of neoplastic hypercalcemia. PTHrP concentrations are not regulated by calcium levels which is in marked contrast for PTH. We have also shown that osteoblasts could be essential target cells in the process of tumor-induced osteolysis leading to an increase in osteoclast function and number. From a therapeutic point of view, we have contributed to the optimalization of the therapeutic schemes for tumor-induced hypercalcemia and tumor-induced osteolysis for which the dose of 90 mg of pamidronate appears to be optimal.

Authors+Show Affiliations

Body JJ
Clinique des soins supportifs et Clinique des maladies osseuses, Institut J. Bordet, Université libre de Bruxelles.

MeSH

Antineoplastic AgentsBone NeoplasmsDiphosphonatesHumansHypercalcemiaNeoplasm ProteinsOsteoclastsOsteolysisPamidronateParathyroid HormoneParathyroid Hormone-Related ProteinProteins

Pub Type(s)

Journal Article

Language

fre

PubMed ID

9491638

Citation

Body, J J.. "[Bone Metastases: Pathogenesis and Treatment With Diphosphonates]." Bulletin Et Memoires De l'Academie Royale De Medecine De Belgique, vol. 152, no. 3, 1997, pp. 169-74; discussion 174-6.
Body JJ. [Bone metastases: pathogenesis and treatment with diphosphonates]. Bull Mem Acad R Med Belg. 1997;152(3):169-74; discussion 174-6.
Body, J. J. (1997). [Bone metastases: pathogenesis and treatment with diphosphonates]. Bulletin Et Memoires De l'Academie Royale De Medecine De Belgique, 152(3), 169-74; discussion 174-6.
Body JJ. [Bone Metastases: Pathogenesis and Treatment With Diphosphonates]. Bull Mem Acad R Med Belg. 1997;152(3):169-74; discussion 174-6. PubMed PMID: 9491638.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Bone metastases: pathogenesis and treatment with diphosphonates]. A1 - Body,J J, PY - 1997/1/1/pubmed PY - 1998/3/10/medline PY - 1997/1/1/entrez SP - 169-74; discussion 174-6 JF - Bulletin et memoires de l'Academie royale de medecine de Belgique JO - Bull Mem Acad R Med Belg VL - 152 IS - 3 N2 - Tumor-induced osteolysis is essentially mediated by the osteoclasts whose number and activity appear to be stimulated under the influence of tumor secretory products. In cases of hypercalcemia, there is also a variable inhibition of the bone formation rate leading to a characteristic "uncoupling" in bone turnover. An analog of parathyroid hormone--"parathyroid hormone-related protein (PTHrP)"--plays an essential role in the pathogenesis of neoplastic hypercalcemia. PTHrP concentrations are not regulated by calcium levels which is in marked contrast for PTH. We have also shown that osteoblasts could be essential target cells in the process of tumor-induced osteolysis leading to an increase in osteoclast function and number. From a therapeutic point of view, we have contributed to the optimalization of the therapeutic schemes for tumor-induced hypercalcemia and tumor-induced osteolysis for which the dose of 90 mg of pamidronate appears to be optimal. SN - 0377-8231 UR - https://www.unboundmedicine.com/medline/citation/9491638/[Bone_metastases:_pathogenesis_and_treatment_with_diphosphonates]_ L2 - https://medlineplus.gov/bonecancer.html DB - PRIME DP - Unbound Medicine ER -