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adenoma/phosphatase
Veza se sprema u međuspremnik
Page 1 od 473 rezultati
[High serum alkaline phosphatase level revealing a liver adenoma].
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A 25-year-old woman had a high serum level of alkaline phosphatase activity (2571 UI/L). Serum levels of transaminases, gamma glutamyl transferase and bilirubin were normal. Abdominal ultrasonography revealed a tumor nodule in the right liver lobe. There was no evidence of biliary obstruction. The
Phosphatase enzymes. Cytochemical study of pleomorphic adenoma and normal human salivary glands.
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Human parotid glands, submandibular glands, and pleomorphic adenomas were examined by electron microscopic histochemistry. All epithelial cells of the normal salivary glands showed plasma membrane adenosine triphosphatase (ATPase) and inosine diphosphatase (IDPase) activity. However, myoepithelial
[Citrate and acid phosphatase in the ejaculate in prostatic carcinoma and adenoma].
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The simultaneous determination of acid phosphatase and citrate concentration in the seminal fluid obtained from 16 patients with prostatic adenoma showed normal values, 6 patiients with prostatic carcinoma (cytologically and histologically verified) however extremely low values. The difference
Ultrastructural cytochemistry of phosphatases in the ductal component of pleomorphic adenoma of human parotid and submandibular salivary glands.
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Some ductal cells of pleomorphic adenomas showed evidence of secretory activity, with apical secretory granules, thiamine pyrophosphatase activity in the Golgi apparatus, and acid phosphatase activity in GERL-like structures and in immature secretory granules. Alkaline phosphatase activity was
Butyrate- but not TGFbeta1-induced apoptosis of colorectal adenoma cells is associated with increased expression of the differentiation markers E-cadherin and alkaline phosphatase.
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Sodium butyrate and transforming growth factor beta (TGFbeta1) are growth inhibitory to colonic adenoma cell lines. Butyrate induces apoptosis, whereas in some adenoma cell lines, TGFbeta1 can be growth inhibitory without apoptosis. In this report, we show that the adenoma cell line PC/BH/C1
Immunohistochemical and Western blot analysis of two protein tyrosine phosphatase receptors, R and Z1, in colorectal carcinoma, colon adenoma and normal colon tissues.
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Two classes of proteins, namely tyrosine kinases (PTK) and phosphatases (PTP), play an important role in cell proliferation and differentiation, thus leading to an acceleration or inhibition of tumour growth. The role of the above proteins in colorectal carcinoma (CRC) growth is a well-known event.
Polynucleotide kinase 3' phosphatase variant, dietary variables and risk of adenoma recurrence in the Polyp Prevention Trial.
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Polymorphisms in a number of genes encoding for DNA repair enzymes have been associated with altering the function of these enzymes and increasing risk of a number of cancers, including colon cancer. We have investigated the association between a common variant in polynucleotide kinase 3'
Targeted deletion of liver glucose-6 phosphatase mimics glycogen storage disease type 1a including development of multiple adenomas.
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OBJECTIVE
Glycogen storage disease type 1a (GSD1a) is an inherited disease caused by a deficiency in the catalytic subunit of the glucose-6 phosphatase enzyme (G6Pase). GSD1a is characterized by hypoglycaemia, hyperlipidemia, and lactic acidosis with associated hepatic (including hepatocellular
Induction of the adenoma-carcinoma progression and Cdc25A-B phosphatases by the trefoil factor TFF1 in human colon epithelial cells.
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TFF1 is overexpressed in inflammatory diseases and human cancers of the digestive and urogenital systems. To examine the transforming potential of TFF1 in human colon epithelial cells, premalignant PC/AA/C1 adenoma cells (PC) derived from a patient with familial adenomatous polyposis (FAP) were
Minimal hepatic glucose-6-phosphatase-α activity required to sustain survival and prevent hepatocellular adenoma formation in murine glycogen storage disease type Ia.
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Glycogen storage disease type Ia (GSD-Ia), characterized by impaired glucose homeostasis and chronic risk of hepatocellular adenoma (HCA), is caused by a deficiency in glucose-6-phosphatase-α (G6Pase-α or G6PC) activity. In a previous 70-90 week-study, we showed that a recombinant adeno-associated
Phosphatase and tensin homologue and pituitary tumor-transforming gene in pituitary adenomas. Clinical-pathologic and immunohistochemical analysis.
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Pituitary tumor-transforming gene (PTTG) is also known to induce angiogenesis during pituitary tumorigenesis. It has not been clarified whether PTTG functions as a cytoplasmic or a nuclear protein. Pituitary tumor-transforming gene-1 is usually expressed in most pituitary tumors, and little is known
Orthotopic liver transplantation in glucose-6-phosphatase deficiency--Von Gierke disease--with multiple hepatic adenomas and concomitant focal nodular hyperplasia.
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Von Gierke disease is occasionally complicated by hepatic adenomas (HAs) causing great concern owing to the current difficulties in monitoring them regarding malignant transformation. Orthotopic liver transplantation (OLT) is proposed as a therapeutic tool when multiple HAs and poor metabolic
[Diagnostic value of prostatic specific antigen (PSA) in comparison to prostatic acid phosphatase (PAP) in prostatic cancer and adenoma].
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The diagnostic value of the tumour markers: PSA, PAP and AcP was studied before treatment in 379 men (47 with prostatic cancer--PC, 306 with benign hyperplasia--PBH, and 26 healthy subjects--control group CG). PSA was determined by the enzymoimmune method, and the phosphatases were evaluated by the
A case of glycogen storage disease type Ia with multiple hepatic adenomas and G727T mutation in the glucose-6-phosphatase gene, and a comparison with other mutations previously reported.
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We report a case of 23-yr-old man with glycogen storage disease (GSD) type Ia complicated by multiple hepatic adenomas. Analysis of the G-6-Pase gene using peripheral blood sample showed this patient to be homozygous for a G-to-T transversion at nucleotide 727 in exon 5. This mutation is prevalent
[The activity of nonspecific phosphatases of the thyroid gland in diffuse toxic goiter and thyrotoxic adenoma].
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