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splenomegaly/phosphatase
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 316 tuloksia
Hemopoietic Cell Kinase amplification with Protein Tyrosine Phosphatase Receptor T depletion leads to polycythemia, aberrant marrow erythoid maturation, and splenomegaly.
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Deletion of long arm of chromosome 20 [del(20q)] is the second most frequent recurrent chromosomal abnormality in hematological malignancies. It is detected in 10% of myeloproliferative neoplasms, 4-5% of myelodysplastic syndromes, and 1-2% of acute myeloid leukaemia. Recurrent, non-random
Splenomegaly, elevated alkaline phosphatase and mutations in the SRSF2/ASXL1/RUNX1 gene panel are strong adverse prognostic markers in patients with systemic mastocytosis.
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We evaluated the impact of clinical and molecular characteristics on overall survival (OS) in 108 patients with indolent (n=41) and advanced systemic mastocytosis (SM) (advSM, n=67). Organomegaly was measured by magnetic resonance imaging-based volumetry of the liver and spleen. In multivariate
[Splenomegaly, thrombopathy and increase of acid phosphatase].
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Clinical Sequelae Associated with Unresolved Tropical Splenomegaly in a Cohort of Recently Resettled Congolese Refugees in the United States-Multiple States, 2015-2018.
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Tropical splenomegaly is often associated with malaria and schistosomiasis. In 2014 and 2015, 145 Congolese refugees in western Uganda diagnosed with splenomegaly during predeparture medical examinations underwent enhanced screening for various etiologies. After anecdotal reports of unresolved
Oncogenic KIT-induced aggressive systemic mastocytosis requires SHP2/PTPN11 phosphatase for disease progression in mice.
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Acquired mutations in KIT are driver mutations in systemic mastocytosis (SM). Here, we tested the role of SHP2/PTPN11 phosphatase in oncogenic KIT signaling using an aggressive SM mouse model. Stable knock-down (KD) of SHP2 led to impaired growth, colony formation, and increased rates of apoptosis
The "pseudo-cholangiocarcinoma sign" in patients with cavernous transformation of the portal vein and its effect on the serum alkaline phosphatase and bilirubin levels.
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OBJECTIVE
The goal of this study was to identify the underlying disorder responsible for portal venous thrombosis and cavernous transformation of the portal vein (CTPV). All patients with this finding underwent a thorough medical examination with intent to determine the cause and biochemical
Perturbed myelo/erythropoiesis in Lyn-deficient mice is similar to that in mice lacking the inhibitory phosphatases SHP-1 and SHIP-1.
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The Lyn tyrosine kinase plays essential inhibitory signaling roles within hematopoietic cells by recruiting inhibitory phosphatases such as SH2-domain containing phosphatase-1 (SHP-1), SHP-2, and SH2-domain containing 5'-inositol phosphatase (SHIP-1) to the plasma membrane in response to specific
Alkaline and acid phosphatase activity in murine femoral bone marrow following X-irradiation, or X-irradiation and repopulation with syngenic or allogeneic bone marrow or marrow stroma cells.
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The activity of alkaline and acid phosphatases in the bone marrow from the femoral cavity was investigated in the following groups of mice: (1) normal (non-irradiated); (2) irradiated with 600 R; (3) irradiated and repopulated with syngeneic bone marrow; (4) irradiated and repopulated with syngeneic
[European-American-type hairy cell leukemia without splenomegaly, treated successfully with deoxycoformycin].
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A 55-year-old Japanese man was hospitalized on October 5, 1999, because of high fever. Physical examination revealed neither lymphadenopathy nor hepato-splenomegaly. Laboratory data on admission showed a white blood cell count of 1,580/microliter, a hemoglobin level of 9.1 g/dl, and a platelet count
Intrahepatocellular erythrocyte inclusions with hepatic sinusoidal infiltrates and splenomegaly.
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We describe two patients suffering from a prolonged fever, pancytopenia, and splenomegaly. The spleen of both patients was grossly enlarged and the liver was moderately enlarged. The blood pictures were characterized by anemia and leukopenia to a severe degree, with moderate thrombocytopenia and
Small lymphocytic lymphomas with predominant splenomegaly: a comparison of immunophenotypes with cases of predominant lymphadenopathy.
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In this study, we compared small lymphocytic lymphomas with predominant lymphadenopathy with those with predominant splenomegaly and found differences in morphology and immunophenotype as well as clinical features. Cases with lymphadenopathy were characterized by widespread disease, CLL type
Massive splenomegaly responsive to proguanil and with features of hairy cell leukaemia.
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A recent Ethiopian immigrant to Israel presented with pneumococcal sepsis, massive splenomegaly and lymph-adenopathy. Investigations revealed many features of both hairy cell leukaemia (HCL) and hyperreactive malarious splenomegaly (HMS). Proguanil therapy for HMS was followed by rapid, marked
[Malignant lymphoma with "hairy" lymphocytes in the blood and splenomegaly--a new variant of lymphoproliferative diseases].
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A total of 5 patients with a clinicohematological picture resembling hairy-cell leukemia (HCL) have been described. However, the morphological features of leukemic lymphocytes, the absence of acid phosphatase in them, the nodular character of the bone marrow lesion combined with an unusual phenotype
A possible mechanism of increase in serum alkaline phosphatase activity in rats given granulocyte colony-stimulating factor.
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Recombinant human granulocyte colony-stimulating factor (G-CSF) at a dose of 1 to 300 micrograms/kg/day was administered intravenously to rats daily for 13 weeks. Serum alkaline phosphatase (ALP) activity increased dose-dependently with leukocytosis. Most of the increased leukocytes were segmented
Absence of neutral protease and alkaline phosphatase in neutrophils of a case of hairy cell leukemia.
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Enzymaticaly homogeneous fractions of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from peripheral blood of a patient with hairy cell leukemia, or leukemic reticuloendotheliosis, LRE,(with leukopenia, neutropenia, lymphocytosis, and massive splenomegaly). To detect
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