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)

An organ-specific alkaline phosphatase (AIP) inhibitor, L-homoarginine at 44.5 mM concentration inhibited 3H-thymidine uptake by mouse C3H/He osteosarcoma (OS) cells, while L-arginine, L-phenylalanine and L-glycine had little effect on the uptake. This inhibitory effect by L-homoarginine persisted even after the cells were washed free of the amino acid with fresh media. L-homoarginine did not affect 3H-thymidine uptake by mouse myeloma MOPC 104E cells. In the long-term culture, 22.3 mM L-homoarginine inhibited proliferation of OS cells. L-Arginine at the same concentration inhibited the proliferation to a lesser extent. On the other hand, L-phenylalanine and L-glycine did not affect in vitro proliferation of OS cells. When similar numbers of viable OS cells were inoculated s. c. after culturing with 44.5 mM L-homoarginine or L-arginine for 24 hr, the tumor growth in mice injected with L-homoarginine (but not L-arginine) treated cells was delayed markedly. Electron microscopic studies indicated that the inhibitory effect on OS cell proliferation was associated with a marked increase in lysosomal granules and a decrease in virus-like structures. Similarly, a biochemical assay of acid phosphatase (AcP) of the cell homogenates demonstrated two-fold increase of the activity in L-homoarginine treated cells when compared to the controls and L-arginine treated cells. Thus, L-homoarginine inhibits proliferation and AIP activity of mouse OS cells and appears to promote cell differentiation as evidenced by the increased synthesis of cytoplasmic granules and acid phosphatase activity.
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PMID:[Inhibitory effect of L-homoarginine on murine osteosarcoma cell proliferation]. 619 5

The effect of the growth of the Walker 256 carcinoma on the level of 5'-nucleotidase and alkaline phosphatase in the whole liver and in an isolated hepatocyte membrane preparation of its host was investigated. Alkaline phosphatase activities of whole liver and plasma membrane were increased approximately 5-fold by tumor growth. A 50% decrease in whole liver 5'-nucleotidase activity was observed in tumor-bearing rats while the 5'-nucleotidase activity per milligram membrane protein was unaltered. Tumor growth would therefore appear to affect a pool of 5'-nucleotidase which is not associated with the plasma membrane.
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PMID:Alterations in hepatic 5'-nucleotidase in the tumor-bearing rat. 627 89

Walker carcinoma 256 (W256) was reported to induce hypercalcemia dependent on bone metastasis and/or parathyroid hormone-related protein (PTHrP) in the rat, providing a model of the humoral hypercalcemia of malignancy. In this study, after the subcutaneous inoculation of cells of the W256/S line, which is maintained in this laboratory, into young female Wistar Imamichi rats (6 weeks old), serum calcium and phosphorus levels changed only within the control range, whereas serum alkaline phosphatase activity and urinary calcium level significantly increased and urinary phosphorus decreased during the tumor growth, resulting in hypercalciuria and hypophosphaturia. W256/S did not express PTHrP-mRNA, whereas LLC-W256 cells did express it. Serum PTHrP level was not changed in W256/S-bearing rats. Osteoporosis-like changes, bone weight loss, low contents of bone calcium and phosphorus, and a decrease in the bone mineral density (BMD), were observed in the femur 14 days after the tumor inoculation. There was a pronounced decrease in the serum 17 beta-estradiol level during the tumor growth. The reduction of BMD of femurs in W256/S-bearing rats was significantly inhibited by treatment with salmon calcitonin or 17 beta-estradiol. On the basis of these results, W256/S carcinoma-bearing rats seem to be a useful model for osteoporosis of hypoovarianism.
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PMID:Osteoporosis-like changes in Walker carcinoma 256-bearing rats, not accompanied with hypercalcemia or parathyroid hormone-related protein production. 754 Jun 9

Very late activation (VLA) receptors mediate cell adhesion to extracellular matrix, mainly by acting as adhesion receptors to fibronectin, collagen, and laminin as well as to other cells. These interactions not only regulate normal cell-extracellular matrix contact, but also are thought to be involved in metastasis and invasive tumor growth. Using immunohistochemistry [the alkaline phosphatase-anti-alkaline phosphatase (APAAP) technique] we compared the expression and distribution of VLA receptors in normal pancreatic tissue, chronic pancreatitis, and ductal pancreatic adenocarcinoma. Immunohistochemically, VLA alpha 2 and VLA alpha 6 were moderately to strongly expressed on the basal surface of ductal and acinar cells in normal pancreatic tissue, whereas centroacinar cells predominantly expressed VLA alpha 3 and VLA alpha 5. Similarly, pancreatic carcinoma showed an intensive staining for VLA alpha 2 and VLA alpha 6 with a diffuse distribution on the cell surface. Expression of VLA alpha 3 and VLA alpha 5 in pancreatic carcinoma was heterogeneous, ranging from moderate to weak and lost in about 50% of the cells. As our results suggest, cell-basement membrane interaction in ductal and acinar pancreatic cells is primarily mediated through VLA alpha 2 and VLA alpha 6, whereas VLA alpha 3 and VLA alpha 5 are the major VLA receptors on centroacinar cells. In pancreatic carcinoma a loss (VLA alpha 5) or redistribution (VLA alpha 2, VLA alpha 6) of VLAs was observed. This redistribution of VLA alpha 2 and VLA alpha 6 may reflect a loss of spatial arrangement of tumor cells and their ability to randomly interact with extracellular matrix structures during invasion and metastasis.
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PMID:Expression and distribution of VLA receptors in the pancreas: an immunohistochemical study. 825 85

A neoplastic clonal cell line, which was prepared by 5-azacytidine treatment of a neoplastic human salivary intercalated duct cell line, was cultivated in the presence of 22-oxa-1alpha, 25-dihydroxyvitamin D3 and 3 mM beta-glycerophosphate. Major alterations, such as expression of type I collagen and alkaline phosphatase as well as of human osteopontin and osteonectin, were observed in these cells with a phenotype similar to osteoblasts. In addition, formation of bone nodule was observed in the cultured cells. The tumors produced by transplantation into nude mice of the clonal cells were treated with 22-oxa-1alpha, 25-dihydroxyvitamin D3 and examined for tumor growth and morphology. Consequently, growth of the treated tumor was significantly suppressed. Moreover, it was found that bone formation was induced in the treated tumor, in which the tumor cells around bone formation expressed human osteopontin and osteonectin mRNA as could be detected by in situ hybridization. The above findings indicate that the emergence of osteoblast-like cells in the human salivary cancer cells occurs in the presence of 22-oxa-1alpha, 25-dihydroxyvitamin D3 and beta-glycerophosphate.
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PMID:Emergence of osteoblast-like cells in a neoplastic human salivary cancer cell line after treatment with 22-oxa-1alpha, 25-dihydroxyvitamin D3. 914 18

In vivo cell growth inhibition of Ehrlich ascites carcinoma (EAC) has been evaluated with chloroacetohydroxamic acid, (CHA), having -CH2 Cl, for the -NH2 group of hydroxyurea (HU). The inhibitory character of CHA against EAC in mice model has been found to be comparable with that of HU. Cell growth inhibition by CHA is accompanied by inhibitions of DNA and protein synthesis of the treated cells. The transplantability of EAC cells treated with a single dose of (100 mg/kg) CHA is found to be reduced. Enhanced intraperitoneal macrophage is observed in normal mice following CHA (100 mg/kg) treatment. Deviations of hematological parameters and alkaline phosphatase (ALKP) activity consequent to tumor growth are found to be recovered in tumor bearing mice treated with CHA. All these studies suggest the importance of CHA for further trial as a potent antitumor agent.
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PMID:Chloroaceto hydroxamic acid as antitumor agent against Ehrlich ascites carcinoma in mice. 937 63

Vascular endothelial growth factor (VEGF) is a major angiogenic growth factor. Angiogenesis stimulated by VEGF occurs in several important clinical contexts, including myocardial ischemia, retinal disease, and tumor growth. The level of VEGF is increased in several skin disorders and is stimulated by ischemia. Tissue expansion has been shown to induce angiogenesis and ischemia on the overlying skin. We therefore investigated the hypothesis that VEGF was expressed in expanded tissue. Three samples of skin were obtained from five patients who sustained reconstruction with tissue expansion. One sample was taken on the implantation site of the expander before implantation. Two samples were taken at the time of removal, respectively, one on the nonexpanded skin adjacent to the expanded area and one on the expanded skin on the site of expansion. On these samples we performed immunolocalization of VEGF. Mouse monoclonal antibody was used, recognized with rabbit anti-mouse immunoglobulin alkaline phosphatase-anti-alkaline phosphatase (APAAP) complex conjugated and revealed with naphthol red. Our results showed clearly an increased number of cells that fixated VEGF antibody on the site of expansion. Cell counts revealed that the numbers of cells expressing VEGF were statistically higher in expanded tissue than in nonexpanded tissue. Before expansion skin specimens did not express VEGF. These findings are the first to show the presence of a growth factor in expanded tissue. They open a new field of research on the biological explanation of tissue-expanded angiogenesis.
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PMID:Vascular endothelial growth factor expression in expanded tissue: a possible mechanism of angiogenesis in tissue expansion. 946 72

The commencement of the complex process of carcinogenesis, and subsequent, rapid tumor growth and progression of mammalian neoplasms, including malignant melanomas, depends upon the continuous de novo formation of capillaries [i.e. neovascularization (NV)/neoplasm-related angiogenesis (NRA)]. The generation of a dedifferentiated, malignant, highly invasive cellular immunophenotype (CIP) and distant metastases, as aspects of constant neoplastic progression, are also NRA-dependent processes. Endothelial cells undergo rapid proliferation during malignant melanoma (MM) related angiogenesis. Human endoglin (CD105/EDG), is a homodimeric cell surface component of the transforming growth factor-beta (TGF-beta) type I receptor complex and is also a proliferation-associated antigen (PAA) expressed at high density on endothelial cells. Formalin fixed, paraffin-wax embedded, tissue sections (3-5 microns thick) of 25 MMs were employed for the assessment of EDG expression. An indirect, four-step, alkaline phosphatase (AP) (or diamino-benzidine [DAB]) conjugated, biotin-streptavidin based, antigen detection technique, employing the SN6h anti-EDG monoclonal antibody was conducted. Zymed's Histogold System was also utilized for immunocytological antigen detection. Strong expression (A; +3 to +4) of EDG on endothelial cells was demonstrated in all MM cases. The most striking feature of the newly formed neoplasm-related capillaries was the presence of an enlarged perivascular space. Blood vessels in several normal human tissues (cortex, cerebellum, thymus, tonsil, spleen, lymph node, skin) used as control tissues contained significantly lower levels of EDG (B and mostly C; +/- to +), in accordance with the extremely slow turnover rate of normal endothelial cells. Furthermore, a close apposition between the capillaries and the adjacent parenchyma was observed in these normal controls. MMs, like most mammalian neoplasms, are characterized by extensive neovascularization, and thus are candidates for anti-angiogenic therapy. Further studies should substantiate the importance of EDG expression in the earliest possible detection, diagnosis and NRA inhibition-based treatment of solid tumors, including MMs. The importance of TGF-beta in all of the various aspects of neoplastic transformation, as well as malignant disease progression should also be studied more extensively in the future.
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PMID:Immunocytochemical detection of endoglin is indicative of angiogenesis in malignant melanoma. 970 32

The commencement of the complex process of carcinogenesis, and subsequent, rapid tumor growth and progression of mammalian neoplasms, including breast carcinomas (BCs), depends upon the continuous de novo formation of capillaries [i.e. neovascularization (NV)/neoplasm-related angiogenesis (NRA)]. The generation of a malignant, invasive cellular immunophenotype (CIP) and distant metastases, as aspects of tumor progression, are also NRA-dependent processes. Endothelial cells undergo rapid proliferation during mammary carcinoma-related angiogenesis. Human endoglin (CD105/EDG), is a homodimeric cell surface component of the transforming growth factor-beta (TGF-beta) type I receptor complex and is also a proliferation-associated antigen (PM) expressed at high density on endothelial cells. Formalin fixed, paraffin-wax embedded, tissue sections (3-5 microns thick) of 15 BCs were employed for the assessment of EDG expression. An indirect, four-step, alkaline phosphatase (AP) (or diamino-benzidine [DAB]) conjugated, biotin-streptavidin based, antigen detection technique, employing the SN6h anti-EDG monoclonal antibody was conducted. Zymed's Histogold System was also utilized for immunocytological antigen detection. Strong expression (A; ++ + to ++ ++) of EDG on endothelial cells was demonstrated in all 15 BC cases. The most striking feature of the newly formed neoplasm-related capillaries was the presence of an enlarged perivascular space. Blood vessels in several normal human tissues (cortex, cerebellum, thymus, tonsil, spleen, lymph node, skin) used as control tissues contained significantly lower levels of EDG (B and mostly C; +/- to +), in accordance with the extremely slow turnover rate of normal endothelial cells. Furthermore, a close apposition between the capillaries and the adjacent parenchyma was observed in these normal controls. BCs, as most mammalian neoplasms, are characterized by extensive neovascularization and thus are candidates for anti-angiogenic therapy. Further studies should substantiate the importance of EDG expression in the earliest possible detection, diagnosis and NRA inhibition-based treatment of solid tumors, including BCs.
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PMID:Over-expression of endoglin (CD105): a marker of breast carcinoma-induced neo-vascularization. 985 49

Activities of some enzymes and content of medium-weight molecules in patients with colorectal cancer were studied in order to assess the diagnostic value of these parameters for detection of tumors in the large intestine and development of endogenous intoxication after surgery and for prediction of remote results of treatment. Increased activities of creatine phosphokinase and hexokinase is typical of tumor growth, whereas increased activities of alkaline phosphatase and gamma-glutamyl transpeptidase are observed only in metastases to the liver. The role of medium-weight molecules in the diagnosis of endogenous intoxication during the early postoperative period is shown. The content of these molecules in the sera increases 3 days before clinical manifestation of endotoxicosis, when the traditional parameters are virtually normal.
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PMID:[Diagnostic and prognostic significance of biochemical indicators in colorectal neoplasms]. 986 99


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