wilms tumor/phosphatase

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Aberrant expression and mechanism of miR-130b-3p/phosphatase and tensin homolog in nephroblastoma in children.

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Nephroblastoma is the most common renal tumor in children. Abnormal expression of microRNAs (miRs) has been reported to be involved in the progression of various types of cancers. However, the role and underlying mechanism of miR-130b-3p in nephroblastoma remains unknown. Therefore, the present

Expression of phosphatase of regenerating liver-3 is associated with prognosis of Wilms' tumor.

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OBJECTIVE The current study was undertaken to explore the clinical and prognostic value of phosphatase of regenerating liver-3 (PRL-3) expression in Wilms' tumor. METHODS Seventy-six patients with Wilms' tumor in Qilu Hospital from January 2003 to July 2009 were enrolled in the study. Protein

Expression of SET, an inhibitor of protein phosphatase 2A, in renal development and Wilms' tumor.

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The human gene set was originally identified as a component of the set-can fusion gene produced by a somatic translocation event in a case of acute undifferentiated leukemia. In the developing kidney, set was highly expressed in the zone of nephron morphogenesis. Recently, SET was shown to be a

Nephroblastoma overexpressed (Nov) inhibits osteoblastogenesis and causes osteopenia.

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Nephroblastoma overexpressed (Nov), a member of the Cyr 61, connective tissue growth factor, Nov (CCN) family of proteins, is expressed by osteoblasts, but its function in cells of the osteoblastic lineage is not known. We investigated the effects of Nov overexpression by transducing murine ST-2

Calcineurin a-binding protein, a novel modulator of the calcineurin-nuclear factor of activated T-cell signaling pathway, is overexpressed in wilms' tumors and promotes cell migration.

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Current therapeutic strategies against Wilms' tumor (WT) reach 80% to 85% success rate. In spite of this, a remaining 15% to 20% of tumors relapse and are associated with increased metastasis and poor prognosis. To identify new regulators of WT progression, we screened for developmental target genes

Wilms tumor 1/cytokeratin dual-color immunostaining reveals distinctive staining patterns in metastatic melanoma, metastatic carcinoma, and mesothelial cells in pleural fluids: an effective first-line test for the workup of malignant effusions.

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BACKGROUND The workup of a malignant effusion usually requires immunostaining with a panel of markers. Although nuclear Wilms tumor 1 (WT1) expression is widely used to detect tumors of ovarian and mesothelial origin, it is less well known that WT1 is also expressed in the cytoplasm of melanomas and

Establishment and characterization of an immature epithelial cell line (ENU-T-1) derived from a rat nephroblastoma.

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A new cell line designated ENU-T-1 has been established from a xenotransplanted experimental rat nephroblastoma. The cultured cells are spindle-shaped or polygonal and are arranged in a wavy fashion morphologically similar to cultured embryonal renal epithelial cells. The cells exhibit a number of

Characterization of a Wilms' tumor model.

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Growth characteristics, survival time, sex differences and hormonal effects, and various biochemical parameters were evaluated in a transplantable Furth/Wistar rat Wilms' tumor model. Survival time was dependent on site of tumor transplant and ranged from a mean of 28 days for intrarenal

Immunohistochemical profiling of Wilms tumor: a tissue microarray study.

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OBJECTIVE Wilms tumor (WT) usually shows a bi-phasic or tri-phasic morphology comprised of blastemal, stromal, and epithelial cells. Other biphasic renal tumors that can mimic WT may pose diagnostic dilemmas especially in preoperative needle biopsy samples. This tissue microarray study was designed

Nephroblastoma overexpressed (Nov) inactivation sensitizes osteoblasts to bone morphogenetic protein-2, but nov is dispensable for skeletal homeostasis.

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Overexpression of nephroblastoma overexpressed (Nov), a member of the Cyr 61, connective tissue growth factor, Nov family of proteins, inhibits osteoblastogenesis and causes osteopenia. The consequences of Nov inactivation on osteoblastogenesis and the postnatal skeleton are not known. To study the

Absence of PPP2R1A mutations in Wilms tumor.

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Evidence from genetic linkage analysis indicates that a gene located at 19q13.4, FWT2, is responsible for predisposition to Wilms tumor in many Wilms tumor families. This region has also been implicated in the etiology of sporadic Wilms tumor through loss of heterozygosity analyses. The PPP2R1A

Loss of PTEN/MMAC1 activity is a rare and late event in the pathogenesis of nephroblastomas.

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Recent genetic investigations of nephroblastomas point to an activation of the Wnt pathway. Data indicate however that activation might be partly due to cross talk of different signaling pathways including the tumor suppressor gene PTEN (phosphatase and tensin homolog on chromosome 10). Therefore,

Histochemical and immunohistochemical characterization of surgically resected and heterotransplanted Wilms' tumor.

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Nine surgically resected Wilms' tumors (WIT) and nude mouse heterotransplants from one WIT were studied by histochemistry and immunohistochemistry. Histochemistry showed acid phosphatase in all cells, while alkaline phosphatase and gamma-glutamyl transpeptidase were present in only some tubules.

Wilms' tumor gene (WT1) is predominantly expressed in clonal hematopoietic cells in myelodysplastic syndromes.

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To determine the expression of Wilms' tumor gene (WT1) in clonal hematopoietic cells in patients with myelodysplastic syndromes (MDS), immunochemistry labelling (alkaline phosphatase anti-alkaline phosphatase) and fluorescence in situ hybridization (FISH) were coperformed on bone marrow cytospins

Unique utilization of a phosphoprotein phosphatase fold by a mammalian phosphodiesterase associated with WAGR syndrome.

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Metallophosphoesterase-domain-containing protein 2 (MPPED2) is a highly evolutionarily conserved protein with orthologs found from worms to humans. The human MPPED2 gene is found in a region of chromosome 11 that is deleted in patients with WAGR (Wilms tumor, aniridia, genitourinary anomalies, and

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