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burkitt lymphoma/phosphatase
L'enllaç es desa al porta-retalls
Pàgina 1 des de 28 resultats
Comparative genomic expression signatures of signal transduction pathways and targets in paediatric Burkitt lymphoma: a Children's Oncology Group report.
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Burkitt lymphoma (BL) is the most common histological subtype of non-Hodgkin lymphoma (NHL) in children and adolescents. Through the introduction of short intensive multi-agent chemoimmunotherapy, survival has improved significantly over the past 30 years. However, this successful approach is
T lymphoblastic leukaemia with an unusual Burkitt lymphoma morphology--a case report.
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Precursor T-cell acute lymphoblastic leukaemia (T-ALL)/lymphoma (T-LBL) is a neoplasm with cytological features that include blast cells of medium size, high nuclear cytoplasmic ratio and inconspicuous nucleoli, which are usually TdT (Terminal Deoxynucleotidyl Transferase) positive and variably
[A case of Burkitt lymphoma with multifocal bone invasion].
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A 12-year-old boy admitted to a local hospital with fever, migratory arthralgia, and periosteal reaction on X Ray. He was transferred to our hospital because magnetic resonance imaging scan of his whole body showed multiple abnormal signals in bones. Laboratory findings on admission showed the
Comparative study of alkaline phosphatase activity in lymphocytes, mitogen-induced blasts, lymphoblastoid cell lines, acute myeloid leukemia, and chronic lymphatic leukemia cells.
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Alkaline phosphatase [orthophosphoricmonoester phosphohydrolase (alkaline pH optimum), EC 3.1.3.1] purified from a Burkitt lymphoma cell line (Daudi) and Moloney-virus-induced murine leukemia (YAC) showed unique catalytic properties in substrate specificity and inhibition by cysteamine-S-phosphate.
Downregulated expression of SHP-1 in Burkitt lymphomas and germinal center B lymphocytes.
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We wish to identify developmental changes in germinal center B cells that may contribute to their rapid growth. SHP-1 is an SH2 domain-containing phosphotyrosine phosphatase that negatively regulates activation of B cells and other cells of hematopoietic lineages. We have found that in all 13
Alternative splicing of the human CDC25B tyrosine phosphatase. Possible implications for growth control?
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CDC25B2, a protein tyrosine phosphatase closely related to the putative CDC25B oncogene, was identified in a Burkitt lymphoma cDNA library. CDC25B2 differs from CDC25B by a 14 residue insertion and a 41 residue deletion, which are both located in the amino-terminal region of the protein, upstream of
SPAG6 promotes cell proliferation and inhibits apoptosis through the PTEN/PI3K/AKT pathway in Burkitt lymphoma
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The main purpose of the present study was to elucidate the role of sperm‑associated antigen 6 (SPAG6) in the occurrence and development of Burkitt lymphoma (BL) and explore the underlying molecular mechanisms. A correlation was observed between the expression of SPAG6 and the prognosis of patients
Differentiation of Burkitt lymphoma cells by hexamethylenbisacetamide.
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Hexamethylenbisacetamide (HMBA) can induce the Burkitt lymphoma Raji cells to enter the differentiation process as evidenced by the decrease of HLA-DR antigens. This event is preceded by a decrease of c-myc expression and of the phosphorylation of cellular proteins, due to either a decrease of
Cooperation between SHP-2, phosphatidyl inositol 3-kinase and phosphoinositol 5-phosphatase in the Fc gamma RIIb mediated B cell regulation.
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Co-clustering B cell receptors (BCR) and type II receptors binding the Fc part of IgG (Fc gamma RIIb) inhibits B cell activation and antibody production. Tyrosine phosphorylation of an intracellular motif of Fc gamma RIIb has been shown to be a prerequisite of the inhibition. After being
Rapid desensitization of B-cell receptor by a dithiol-reactive protein tyrosine phosphatase inhibitor: uncoupling of membrane IgM from syk inhibits signals leading to Ca2+ mobilization.
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B-cell antigen receptor (BCR)-mediated calcium response can be blocked by phenylarsine oxide (PAO), a dithiol group-reactive protein tyrosine phosphatase inhibitor. We have examined the mechanism of this inhibition in BL41 Burkitt lymphoma cells. PAO-dependent inhibition is not restricted to the
Myeloid cell leukemia 1 is phosphorylated through two distinct pathways, one associated with extracellular signal-regulated kinase activation and the other with G2/M accumulation or protein phosphatase 1/2A inhibition.
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Protein kinase C activators and microtubule-damaging drugs stimulate BCL2 phosphorylation, which has been associated with either enhancement or inhibition of cell viability. In a Burkitt lymphoma cell line, both types of agents likewise stimulated phosphorylation of myeloid cell leukemia 1 (MCL1),
Regulation of CD45-induced signaling by galectin-1 in Burkitt lymphoma B cells.
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It has been well established that Galectin-1 (GAL1), a beta-galactoside-binding protein, regulates the viability of lymphoid cells. However, the signaling pathway governed by the binding of GAL1 to the cell membrane is not understood. As a first step towards the elucidation of GAL1-initiated
Oncogenic mechanisms in Burkitt lymphoma.
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Burkitt lymphoma is a germinal center B-cell-derived cancer that was instrumental in the identification of MYC as an important human oncogene more than three decades ago. Recently, new genomics technologies have uncovered several additional oncogenic mechanisms that cooperate with MYC to create this
Protein phosphatase 2A activation as a therapeutic strategy for managing MYC-driven cancers.
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The tumor suppressor protein phosphatase 2A (PP2A) is a serine/threonine phosphatase whose activity is inhibited in most human cancers. One of the best characterized PP2A substrates is MYC proto-oncogene BHLH transcription factor (MYC), whose overexpression is commonly associated with aggressive
Inhibition of protein phosphatase 2A (PP2A) prevents Mcl-1 protein dephosphorylation at the Thr-163/Ser-159 phosphodegron, dramatically reducing expression in Mcl-1-amplified lymphoma cells.
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Abundant, sustained expression of prosurvival Mcl-1 is an important determinant of viability and drug resistance in cancer cells. The Mcl-1 protein contains PEST sequences (enriched in proline, glutamic acid, serine, and threonine) and is normally subject to rapid turnover via multiple different
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