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lymphoma/phosphatase
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Prostatic acid phosphatase: a possible diagnostic marker of intravascular large B-cell lymphoma.
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OBJECTIVE
Intravascular large B-cell lymphoma (IVL) has been treated as fever of unknown origin (FUO), and many patients have been treated inadequately based on incorrect diagnoses. We previously cares for a patient with IVL who tested positive for prostatic acid phosphatase (PAP), a marker of
Alkaline phosphatase positive lymphomas: a morphologic, immunologic, and enzymehistochemical study.
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Among 87 cases of different non-Hodgkin lymphomas studied with morphologic, enzymehistochemical, and immunologic techniques, ten were found with a positive alkaline phosphatase staining reaction of the cell membranes. The ages of the seven adult patients included in this report varied between 48-85
Prostatic acid phosphatase is a possible tumor marker for intravascular large B-cell lymphoma.
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Intravascular large B-cell lymphoma (LBCL) is a rare and aggressive subtype of diffuse LBCL characterized by disseminated intravascular proliferation of neoplastic lymphocytes. Obstruction of blood flow by tumor cells in a variety of organs can cause an array of clinical changes, including
Fever of unknown origin (FUO) due to large B-cell lymphoma: the diagnostic significance of highly elevated alkaline phosphatase and serum ferritin levels.
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BACKGROUND
Determining the cause of fever of unknown origin (FUO) is often a vexing and difficult diagnostic process. In most cases, the signs and symptoms in adult FUOs suggest a malignant, infectious, or rheumatic/inflammatory etiology. The diagnosis of FUO may be narrowed if specific findings are
Plumbagin induces apoptosis in lymphoma cells via oxidative stress mediated glutathionylation and inhibition of mitogen-activated protein kinase phosphatases (MKP1/2).
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Maintaining cellular redox homeostasis is imperative for the survival and normal functioning of cells. This study describes the role and regulation of MAPKinases in oxidative stress mediated apoptosis. Plumbagin, a vitamin K3 analog and a pro-oxidant, was employed and it induced apoptosis in both
Assessment of corticosteroid-induced alkaline phosphatase as a prognostic indicator in canine lymphoma.
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OBJECTIVE
To examine the incidence of elevated corticosteroid-induced alkaline phosphatase (sALP) in dogs with lymphoma and to determine if sALP is a reliable prognostic indicator in canine lymphoma.
METHODS
The medical records of 62 canine lymphoma patients treated with a combination chemotherapy
Phosphatase inhibition augments anti-CD22-mediated signaling and cytotoxicity in non-hodgkin's lymphoma cells.
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CD22 is a cell-surface molecule found on most B-cell lymphomas (NHL). HB22.7 is an anti-CD22 antibody that blocks CD22 ligand binding, initiates signaling, and kills NHL cells. The SHP-1 tyrosine phosphatase is disproportionately associated with the cytoplasmic domain of CD22. Sodium orthovanadate
Treatment of non-Hodgkin's lymphoma xenografts with the HB22.7 anti-CD22 monoclonal antibody and phosphatase inhibitors improves efficacy.
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OBJECTIVE
To examine the role of phosphatase inhibition on anti-CD22, HB22.7-mediated lymphomacidal effects.
METHODS
CD22 is a cell-surface molecule expressed on most B cell lymphomas (NHL). HB22.7 is an anti-CD22 monoclonal antibody that binds a unique CD22-epitope, blocks ligand binding, initiates
Inhibition of constitutive serine phosphatase activity in T lymphoma cells results in phosphorylation of pp19/cofilin and induces apoptosis.
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In untransformed T lymphocytes, pp19/cofilin, a cytoplasmic actin-binding protein, undergoes dephosphorylation and nuclear translocation in response to costimulation through accessory receptors (e.g., CD2), but not following TCR/CD3 triggering. In malignant T lymphoma cells, dephosphorylation and
Characterization of the alkaline phosphatase expressed on the surface of a Hodgkin's lymphoma cell line.
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Alkaline phosphatase solubilized from a human Hodgkin's lymphoma cell line (L428) was compared with purified amphiphilic and hydrophilic forms of the enzyme from human liver, and with the enzyme solubilized from a cultured osteosarcoma cell line (Saos-2). Purified hydrophilic alkaline phosphatases
Alkaline phosphatase-positive B cell lymphomas.
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Alkaline phosphatase (ALP) activity of 70 cases of non-Hodgkin's lymphomas of the B-cell type was studied. ALP activity was found in malignant lymphoma (ML), follicular, small cleaved cell (1/5 cases); ML, diffuse, small cleaved cell (3/13 cases); and mantle zone lymphoma (intermediate lymphocytic
Cytochemical examination of acid phosphatase and beta-glucuronidase enzymes in low-grade B cell non-Hodgkin's lymphomas.
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The differential diagnostic significance of acid phosphatase and beta-glucuronidase were studied in 77 cases of low-grade B cell non-Hodgkin's lymphomas. In most cases the results of cytochemical enzyme studies performed on malignant cells of the bone marrow were evaluated. B cell chronic
Transcriptional regulation of a receptor protein tyrosine phosphatase gene hPTP-J by PKC-mediated signaling pathways in Jurkat and Molt-4 T lymphoma cells.
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The recently cloned type II receptor protein tyrosine phosphatase (RPTP) gene hPTP-J is a new member of the MAM (meprin, A5, PTPmicro) domain subfamily. We previously reported that hPTP-J mRNA was detected significantly in Jurkat T lymphoma cells and its expression was completely down-regulated by
The tyrosine 343 residue of nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) is important for its interaction with SHP1, a cytoplasmic tyrosine phosphatase with tumor suppressor functions.
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The cytoplasmic tyrosine phosphatase SHP1 has been shown to inhibit the oncogenic fusion protein nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK), and loss of SHP1 contributes to NPM-ALK-mediated tumorigenesis. In this study, we aimed to further understand how SHP1 interacts and regulates
Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation.
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Here, we demonstrate that the expression of the dual specificity phosphatase CDC25A, a key regulator of cell cycle progression, is deregulated in Ba/F3 cells expressing the oncogenic protein NPM/ALK and in human cell lines derived from NPM/ALK-positive anaplastic large cell lymphomas (ALCL). Both
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