Immunohistochemical analysis of low-grade and high-grade prostate carcinoma: relative changes of parathyroid hormone-related protein and its parathyroid hormone 1 receptor, osteoprotegerin and receptor activator of nuclear factor-kB ligand

Pérez-Martínez, Francisco C.; Alonso, V.; Sarasa, José Luis Andrès; Nam-Cha, Syonghyun; Vela-Navarrete, R.; Manzarbeitia, Félix; Calahorra, F.J.; Esbrit, Pedro

doi:10.1136/jcp.2006.037853

Cited by 29 publications

(22 citation statements)

References 33 publications

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“…The effects of PTHrP have been studied in tumor and normal tissues, including bone, prostate, skin, heart and lung [11,[20][21][22]. However, the exact role of the PTHrP in the urinary bladder is not fully understood.…”

Section: Discussionmentioning

confidence: 99%

Expression of parathyroid hormone-related protein in the partially obstructed and reversed rabbit bladder

et al. 2008

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Section: Discussionmentioning

confidence: 99%

Expression of parathyroid hormone-related protein in the partially obstructed and reversed rabbit bladder

et al. 2008

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“…However, other studies have failed to correlate serum RANKL or OPG levels with presence of bone disease or survival (reviewed in [42]). In prostate cancer, increased RANKL expression has been observed in primary and bone metastatic tumor cells, with increased expression in metastatic tumors compared with primary tumors [37,44,45]. In separate studies, levels of serum RANKL have not been observed to increase in prostate cancer patients [46,47].…”

Section: Regulation Of Rankl and Opg Expression In Cancermentioning

confidence: 95%

The RANK/RANKL/OPG triad in cancer-induced bone diseases

Dougall

Chaisson

2006

Cancer Metastasis Rev

169

114

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The maintenance of skeletal integrity in a healthy individual requires a balanced regulation of the processes of bone formation, mediated by osteoblasts, and bone resorption, mediated by osteoclasts. This balanced process of bone remodeling becomes co-opted in the skeleton by tumor cells and this dramatically accelerates the process of remodeling and disrupts the normal equilibrium resulting in a spectrum of osteolytic to osteoblastic bone lesions. Certain tumor types, such as breast and prostate, frequently metastasize to the bone. It is now widely understood that the molecular triad--receptor activator of NF-kappaB ligand (RANKL), its receptor RANK, and the endogenous soluble RANKL inhibitor, osteoprotegerin (OPG)--play direct and essential roles in the formation, function, and survival of osteoclasts. Osteoclastic bone resorption contributes to the majority of skeletal sequelae, or skeletal-related events (SREs), in patients with bone metastases. In addition, osteoclastic bone resorption also contributes to the establishment of tumors in the skeleton. Therefore, blocking osteoclast activity and differentiation via RANKL inhibition may not only provide a beneficial treatment for skeletal complications of malignancy, but may also prevent bone metastases. In this review, we will first describe the operative role of osteoclasts and the RANK/RANKL/OPG triad in the pathophysiology of cancer-induced bone diseases, specifically solid tumor metastases to the bone. Secondly, we will describe a therapeutic approach that specifically targets the RANKL molecule.

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“…An extensive review of the literature indicates that hypercalcemia is exceptionally rare in prostate cancer, occurring in <2% of cases (37,38). PTH and PTH-related protein are immunologically distinct proteins that bind with equal affinity to the PTH-IR, which is highly expressed on prostate cancer bony metastases (39 (41). This suggests that an increased sensitivity of prostate cancers to PTH also may contribute to the progression of metastases in bone.…”

Section: Pth Promotes the Proliferation And Migration Of Prostate Canmentioning

confidence: 99%

Prostate Cancer, Serum Parathyroid Hormone, and the Progression of Skeletal Metastases

Schwartz

2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Bony metastases from prostate cancer are a significant cause of morbidity and mortality. These metastases are predominantly blastic (bone-forming) and commonly cause increased serum levels of parathyroid hormone (PTH) as calcium ions are transferred from serum into blastic bone. The epidemiologic and clinical significance of secondary hyperparathyroidism in advanced prostate cancer have not been widely appreciated. Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone. Thus, blastic metastases appear to induce a ''vicious cycle'' in which PTH resorbs normal bone to support the growth of blastic bone. Recognition of the potential role of PTH in the progression of skeletal metastases suggests novel opportunities for prostate cancer secondary prevention. In particular, we propose that suppressing serum PTH in advanced prostate cancer may reduce morbidity by decreasing fractures and pain caused by bone resorption and may reduce mortality by retarding the progression of metastatic disease. (Cancer Epidemiol Biomarkers Prev 2008; 17(3):478 -83)

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Immunohistochemical analysis of low-grade and high-grade prostate carcinoma: relative changes of parathyroid hormone-related protein and its parathyroid hormone 1 receptor, osteoprotegerin and receptor activator of nuclear factor-kB ligand

Cited by 29 publications

References 33 publications

Expression of parathyroid hormone-related protein in the partially obstructed and reversed rabbit bladder

Expression of parathyroid hormone-related protein in the partially obstructed and reversed rabbit bladder

The RANK/RANKL/OPG triad in cancer-induced bone diseases

Prostate Cancer, Serum Parathyroid Hormone, and the Progression of Skeletal Metastases

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