{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T14:15:55Z","timestamp":1791900955952,"version":"4.3.4"},"reference-count":319,"publisher":"Bioscientifica","issue":"3","content-domain":{"domain":["journals.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2005,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Calcium homeostasis is a tightly regulated process involving the co-ordinated efforts of the skeleton, kidney, parathyroid glands and intestine. Neoplasms can alter this homeostasis indirectly through the production of endocrine factors resulting in humoral hypercalcaemia of malignancy. Relatively common with breast and lung cancer, this paraneoplastic condition is most often due to tumour production of parathyroid hormone-related protein and ensuing increased osteoclastic bone resorption. Although control of hypercalcaemia is generally successful, the development of this complication is associated with a poor prognosis. The metastasis of tumour cells to bone represents another skeletal complication of malignancy. As explained in the \u2018seed and soil\u2019 hypothesis, bone represents a fertile ground for cancer cells to flourish. The molecular mechanisms of this mutually beneficial relationship between bone and cancer cells are beginning to be understood. In the case of osteolytic bone disease, tumour-produced parathyroid hormone-related protein stimulates osteoclasts that in turn secrete tumour-activating transforming growth factor-\u03b2 that further stimulates local cancer cells. This \u2018vicious cycle\u2019 of bone metastases represents reciprocal bone\/cancer cellular signals that likely modulate osteoblastic bone metastatic lesions as well. The development of targeted therapies to either block initial cancer cell chemotaxis, invasion and adhesion or to break the \u2018vicious cycle\u2019 is dependent on a more complete understanding of bone metastases. Although bisphosphonates delay progression of skeletal metastases, it is clear that more effective therapies are needed. Cancer-associated bone morbidity remains a major public health problem, and to improve therapy and prevention it is important to understand the pathophysiology of the effects of cancer on bone. This review will detail scientific advances regarding this area.<\/jats:p>","DOI":"10.1677\/erc.1.00543","type":"journal-article","created":{"date-parts":[[2005,9,19]],"date-time":"2005-09-19T12:42:55Z","timestamp":1127133775000},"page":"549-583","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-8","source":"Crossref","is-referenced-by-count":208,"title":["Hypercalcaemia of malignancy and basic research on mechanisms responsible for osteolytic and osteoblastic metastasis to bone"],"prefix":"10.1530","volume":"12","author":[{"given":"G A","family":"Clines","sequence":"first","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia, PO Box 801419, Charlottesville, Virginia 22908-1419, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T A","family":"Guise","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia, PO Box 801419, Charlottesville, Virginia 22908-1419, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"2026070905554005000_ABOU-SAMRA-ETAL-1992","doi-asserted-by":"crossref","unstructured":"Abou-Samra\n            AB\n          , Juppner H, Force T, Freeman MW, Kong XF, Schipani E, Urena P, Richards J, Bonventre JV, Potts JT Jr et al.1992 Expression cloning of a common receptor for parathyroid hormone and parathyroid hormone-related peptide from rat osteoblast-like cells: a single receptor stimulates intracellular accumulation of both cAMP and inositol trisphosphates and increases intracellular free calcium. 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