Osteocalcin as a Biological Marker in the Therapeutic Management of Breast Cancer Bone Metastases

Neri, B; Cecchettin, M; Pacini, P; Bartalucci, S; Gemelli, M T; Giorgi, Francesca

doi:10.3109/07357908909017529

Cited by 8 publications

(3 citation statements)

References 13 publications

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“…Metastatic bone involvement in prostate and breast carcinomas as well as metabolic bone disease cause a significant rise in BALP (6,20). BGP is related to bone metastases in breast carcinoma and thyroid hormone metabolism (21,22).…”

Section: Discussionmentioning

confidence: 99%

Diagnostic Value of Biochemical Markers of Bone Turnover and Postmenopausal Osteoporosis

Yılmaz

Bayram²,

Erbağcı³

et al. 1999

CCLM

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We studied 77 women divided into postmenopausal osteoporotic and premenopausal and postmenopausal non-osteoporotic groups in order to evaluate bone metabolism and diagnostic value of biochemical markers of bone turnover in postmenopausal osteoporosis. Postmenopausal osteoporotic (n: 40), postmenopausal non-osteoporotic (n: 24) and premenopausal non-osteoporotic (n: 13) groups were defined according to bone mineral density (BMD) scores obtained with dual energy X-ray absorptiometry (DEXA). Urinary deoxy-pyridinoline (Dpd), pyridinoline (Pyd), serum total alkaline phosphatase (ALP), bone specific alkaline phosphatase (BALP), osteocalcin (BGP), total calcium, phosphorus, and creatinine levels were determined. Urinary Dpd and Pyd levels of postmenopausal osteoporotic group (8.7 and 18.7 mumol/mg creatinine) were significantly higher than postmenopausal control (5.1 and 11.7 mumol/mg creatinine, p < 0.0001) and premenopausal control (6.0 and 13.0 mumol/mg creatinine, p < 0.0005 and p < 0.001) groups. Bone formation markers were not significantly different between groups, although BGP correlated with Dpd and Pyd (r: 0.26 and r: 0.31, p < 0.05) in osteoporotic subjects. From receiver operating curve (ROC) analysis Dpd had the best diagnostic value (0.846), followed by Pyd (0.802) in evaluation of osteoporosis, whereas BALP (0.570) and BGP (0.528) were relatively inefficient in the discrimination of postmenopausal osteoporosis. This study suggests that bone resorption markers are more efficient than bone formation markers in the diagnosis of postmenopausal osteoporosis. Urinary Dpd/creatinine ratio has the highest diagnostic value.

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Section: Discussionmentioning

confidence: 99%

Diagnostic Value of Biochemical Markers of Bone Turnover and Postmenopausal Osteoporosis

Yılmaz

Bayram²,

Erbağcı³

et al. 1999

CCLM

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“…A similar mechanism of restoration of bone coupling has been proposed to explain the reparative bone formation in bone metastasis by solid cancers as an effect of anti-cancer therapy [33], [36], [50].…”

Section: Discussionmentioning

confidence: 84%

The Role of the BMP Signaling Antagonist Noggin in the Development of Prostate Cancer Osteolytic Bone Metastasis

et al. 2011

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Members of the BMP and Wnt protein families play a relevant role in physiologic and pathologic bone turnover. Extracellular antagonists are crucial for the modulation of their activity. Lack of expression of the BMP antagonist noggin by osteoinductive, carcinoma-derived cell lines is a determinant of the osteoblast response induced by their bone metastases. In contrast, osteolytic, carcinoma-derived cell lines express noggin constitutively. We hypothesized that cancer cell-derived noggin may contribute to the pathogenesis of osteolytic bone metastasis of solid cancers by repressing bone formation. Intra-osseous xenografts of PC-3 prostate cancer cells induced osteolytic lesions characterized not only by enhanced osteoclast-mediated bone resorption, but also by decreased osteoblast-mediated bone formation. Therefore, in this model, uncoupling of the bone remodeling process contributes to osteolysis. Bone formation was preserved in the osteolytic lesions induced by noggin-silenced PC-3 cells, suggesting that cancer cell-derived noggin interferes with physiologic bone coupling. Furthermore, intra-osseous tumor growth of noggin-silenced PC-3 cells was limited, most probably as a result of the persisting osteoblast activity. This investigation provides new evidence for a model of osteolytic bone metastasis where constitutive secretion of noggin by cancer cells mediates inhibition of bone formation, thereby preventing repair of osteolytic lesions generated by an excess of osteoclast-mediated bone resorption. Therefore, noggin suppression may be a novel strategy for the treatment of osteolytic bone metastases.

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“…This was accompanied by bone pain remission and regression of bone lesions in these patients. Therefore OSC appears to act as a biological marker of recovered osteoblast activity [223]. Despite this research, OSC has never been examined in the breast microenvironment or in relation to mammary microcalcifications.…”

Section: Osteocalcinmentioning

confidence: 99%

Microcalcifications in breast cancer: Lessons from physiological mineralization

Cox¹,

Morgan²

2013

Bone

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Osteocalcin as a Biological Marker in the Therapeutic Management of Breast Cancer Bone Metastases

Cited by 8 publications

References 13 publications

Diagnostic Value of Biochemical Markers of Bone Turnover and Postmenopausal Osteoporosis

Diagnostic Value of Biochemical Markers of Bone Turnover and Postmenopausal Osteoporosis

The Role of the BMP Signaling Antagonist Noggin in the Development of Prostate Cancer Osteolytic Bone Metastasis

Microcalcifications in breast cancer: Lessons from physiological mineralization

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