Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of Regan isoenzyme (the heat stable fraction of alkaline phosphatase) in serum of patients with osteosarcoma has been proposed as a prognostic factor indicating the metastatic evolution of the disease. This work reports on 9 patients with osteosarcoma. In 4 of them Regan isoenzyme was present 4, 6, 12, and 16 months before clinical-instrumental evidence of lung metastases. These results further support the significance of this isoenzyme as a marker of relapse in an early subclinical stage.
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PMID:[Role of alkaline phosphatase Regan isoenzyme in prognosis of patients with osteosarcoma]. 227 51

Animal models of osteosarcoma with spontaneous pulmonary metastasis which retain metastatic capacity and osteoid formation after serial passages have been reported infrequently. In this communication we describe some biological features of a transplantable osteosarcoma, Os515, induced by BK-virus in Syrian golden hamsters. The subcutaneously transplanted tumours in 2-week-old animals grew progressively until death, with a mean survival time of 32 days. Distant metastases occurred only in the lungs in all animals. The histological appearance was osteosarcoma of osteoblastic type. Enzyme-histochemical staining showed alkaline phosphatase activity in many cells and beta-glucuronidase activity in few cells. Tumours transplanted intramuscularly in the hind limbs were amputated radically at 5 or 11 days. A small number of animals died from lung metastases without local relapse during the observation period of 140 days after grafting. All the control hamsters bearing unamputated tumours died much earlier. Necropsy revealed large metastatic nodules in the lungs of limb-amputated animals and small diffuse nodules in the lungs of untreated control animals. The development of lung metastases was monitored by soft X-ray without sacrificing the animals. This model will be useful in studies of mechanisms of metastasis and for the experimental treatment of osteosarcoma.
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PMID:An experimental transplantable osteosarcoma with spontaneous pulmonary metastasis in hamsters. 814 74

Pulmonary metastasis is a major cause of death and a major obstacle to the successful treatment of canine osteosarcoma. However, the residual capacity of the neoplasia for differentiation and its susceptibility to undergo apoptosis may be used to suppress its growth and metastatic properties. The highly metastasizing POS (HMPOS) canine osteosarcoma cell line which preferentially metastasize to the lungs was used to test the possible efficacy of 22-oxa-calcitriol (OCT) and all- trans retinoic acid (ATRA) to inhibit growth and pulmonary metastasis of the subcutaneously grown osteosarcoma in nude mice. Treatments in vitro, morphologically elongated and increased alkaline phosphatase activity and staining of cells. Tumour growth in vivo was inhibited significantly and the combination treatment of OCT and ATRA (OCT + ATRA) exerted a synergistic and stronger suppression at concentration of 1.0 microg kg(-1)body weight when given subcutaneously three times a week for 5 weeks. The subcutaneous tumours of the control mice consisted of osteoblast-like cells and isolated chondroblast-like cells, but formed several areas of osteoid and increased amount of collagen tissue in all treated mice. Pinpoint macrometastatic nodules developed only in all control mice. Micrometastatic nodule developed only in two of six mice treated with ATRA. However, nodule size and number, and lung wet weight were all reduced significantly. Metastasis were not seen in the mice treated with OCT or OCT + ATRA. This study demonstrated that inhibition of growth and pulmonary metastasis was induced by subcutaneous treatment with these drugs and suggest that both its differentiating and apoptotic inducing activities may be responsible for the antitumour effects. These drugs may be useful in the clinic as an adjunct for the treatment of canine osteosarcoma.
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PMID:Inhibitory effects of 22-oxa-calcitriol and all- trans retinoic acid on the growth of a canine osteosarcoma derived cell-line in vivo and its pulmonary metastasis in vivo. 1068 63

Satisfactory experimental models for preclinical cancer studies must follow several criteria: (1) reproducibility of the method used to induce the tumor and (2) clinical, pathological and kinetic similarity with the corresponding human tumors. We developed a model of osteosarcoma locally induced by the intrafemoral injection of osteosarcoma (OSR) cells in Sprague-Dawley rats. This method yields nearly 80% of bone tumors at the injection site. These tumors double their volume fairly slowly (in approximately 20 days) and lung metastases occur in 96% of the animals. The OSR cell-induced tumor is characterized by a direct production of mineralized matrix by the tumor cells themselves, as revealed by histochemical analysis. The microarchitectural parameters which were quantified by a microscanner show an increased trabecular bone volume (+238%) when OSR cells were injected in the femur, as compared to controls injected with vehicle. Osteoblastic markers such as alkaline phosphatase, osteopontin, osteocalcin and bone sialoprotein were expressed by the tumor in vivo, whereas the initially injected OSR cells did not express some of these markers, suggesting that OSR cells reacquired an osteoblastic phenotype in a favorable environment. The clinical, radiological and histological data show that this model shares high similarities with the osteocondensing forms of osteosarcoma in humans.
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PMID:A new experimental rat model of osteosarcoma established by intrafemoral tumor cell inoculation, useful for biology and therapy investigations. 1597 Jun 46

Zoledronic acid (ZOL) has been shown to reduce osteolysis in bone metastasis. Its efficacy in osteosarcoma has not been convincingly proved in a clinically relevant model for the disease. In vitro, ZOL decreased osteosarcoma cell proliferation, mainly due to an increase in apoptosis in a dose-dependent fashion. There was a decrease in cell migration at >or=10 micromol/L concentrations, but invasion was inhibited at a much lower dose of 0.1 micromol/L. Reverse transcription-PCR showed that ZOL overall caused an increased expression of osteocalcin and decreased expression of alkaline phosphatase, osteopontin, osteonectin, and vascular endothelial growth factor, with no change in expression of osteoprotegerin. ZOL administration s.c. twice weekly at 0.12 mg/kg to SaOS-2 tumor-bearing mice resulted in primary tumor growth inhibition, reduction in lung metastases, and dramatic decrease in osteolysis. Furthermore, in the ZOL cohort, there was a clear reduction in the number of osteoclasts in bone exposed to tumor and a lower tumor vessel density. These data point to the adjuvant potential of ZOL in the management of osteosarcoma not only for its antiosteolytic properties but also for its ability to directly halt tumor cell growth and metastasis via its effects on viability, invasion, differentiation, and angiogenesis.
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PMID:Zoledronic acid inhibits osteosarcoma growth in an orthotopic model. 1808 20

Paget's disease of the bone, which is characterized by a focal region of highly exaggerated bone remodeling, is very rare in Asia. Most patients with Paget's disease are asymptomatic; they are normocalcemic and show elevated alkaline phosphatase levels. Hypercalcemia in patients with Paget's disease has rarely been reported. We report one Chinese patient with Paget's disease involving the maxilla bone with an initial presentation of facial cellulitis. Asymptomatic hypercalcemia with a low-normal intact parathyroid hormone level developed 9 years later. After clodronate treatment, the level of alkaline phosphatase normalized, but the hypercalcemia did not respond adequately. After analysis of tumor markers and imaging studies, a clinical diagnosis of pancreatic adenocarcinoma with multiple hepatic and lung metastases with pleural effusion was made. We suggest that malignancy-associated hypercalcemia should be considered as one of the causes of hypercalcemia in patients with Paget's disease.
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PMID:Tumor-associated Hypercalcemia in a patient with Paget's disease. 1836 76