polycythemia/tyrosine

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Erythropoietin hypersensitivity in primary familial and congenital polycythemia: role of tyrosines Y285 and Y344 in erythropoietin receptor cytoplasmic domain.

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Erythropoietin receptor (EPOR) gene mutations leading to truncations of the cytoplasmic, carboxy-terminal region of EPOR have been described in some patients with primary familial and congenital polycythemia (PFCP), a disorder characterized by isolated erythrocytosis and increased sensitivity of

Increased basal and induced tyrosine phosphorylation of the insulin-like growth factor I receptor beta subunit in circulating mononuclear cells of patients with polycythemia vera.

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We have previously shown that circulating progenitor cells in patients with polycythemia vera (PV) are hypersensitive to insulin-like growth factor I (IGF-I) with respect to erythroid burst formation in serum-free medium, and that this effect occurs through the IGF-I receptor. To investigate the

Src tyrosine kinase preactivation is associated with platelet hypersensitivity in essential thrombocythemia and polycythemia vera.

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Polycythemia vera (PV) and essential thrombocythemia (ET) are chronic myeloproliferative disorders characterized by an increased incidence of thrombo-hemorrhagic complications. The acquired somatic Janus kinase 2 (JAK2) V617F mutation is present in the majority of PV and ET patients. Because

Identification of increased protein tyrosine phosphatase activity in polycythemia vera erythroid progenitor cells.

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Polycythemia vera (PV) is a clonal hematologic disease characterized by hyperplasia of the three major bone marrow lineages. PV erythroid progenitor cells display hypersensitivity to several growth factors, which might be caused by an abnormality of tyrosine phosphorylation. In the present study, we

Role of tyrosine kinases and phosphatases in polycythemia vera.

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Protein tyrosine kinases (PTKs) and phosphatases (PTPs) play a crucial role in normal cell development, and dysfunction of these enzymes has been implicated in human cancers. Polycythemia vera (PV) is a clonal hematologic disease characterized by hypersensitivity of hematopoietic progenitor cells to

Study of two tyrosine kinase inhibitors on growth and signal transduction in polycythemia vera.

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OBJECTIVE An activating somatic mutation of Janus kinase 2 V617F (JAK2V617F) is present in most polycythemia vera (PV) patients. We studied efficacy of two potent tyrosine kinase inhibitors (TKI), AEE788 and AMN107, in vitro on cells bearing this mutation. METHODS We employed reporter cells

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

Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.

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Polycythemia vera (PV), essential thrombocythemia (ET), and myeloid metaplasia with myelofibrosis (MMM) are clonal disorders arising from hematopoietic progenitors. An internet-based protocol was used to collect clinical information and biological specimens from patients with these diseases.

Secondary erythrocytosis produced by the tyrosine kinase inhibitors sunitinib and sorafenib.

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[Tyrosine kinase inhibitors in the treatment of polycythemia vera and related conditions. Danish Society of Hematology].

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[Clinical study on relationship between protein tyrosine kinase JAK2 V617F mutation and high altitude polycythemia].

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JAK2 V617F patients with essential thrombocythemia present with clinical features of polycythemia vera.

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Recent studies have shown that Janus tyrosine kinase 2 (JAK2) V617F mutation is found in nearly all patients with polycythemia vera (PV) and underlie the basis of PV molecular pathogenesis. Moreover, JAK2 V617F patients with essential thrombocythemia (ET) have been found to have some clinical

Absence of polycythemia in a child with a unique erythropoietin receptor mutation in a family with autosomal dominant primary polycythemia.

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Primary familial and congenital polycythemia (PFCP or familial erythrocytosis) is a rare proliferative disorder of erythroid progenitor cells, characterized by elevated erythrocyte mass and hemoglobin concentration, hypersensitivity of erythroid progenitors to erythropoietin (EPO), and autosomal

Imatinib effect on growth and signal transduction in polycythemia vera.

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OBJECTIVE An activating mutation of Janus kinase 2 (JAK2) in majority of polycythemia vera (PV) and other myeloproliferative disorders was reported. As imatinib inhibits several tyrosine kinases, we studied its effect in PV. METHODS We employed FDCP reporter cells expressing wild-type JAK2 and

[A Case of Metastatic Clear Cell Renal Cell Carcinoma Showing Long-Term Complete Response after the Discontinuation of Tyrosine Kinase Inhibitor].

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Randomized phase III trials demonstrated superiority of targeted therapy with tyrosine kinase inhibitors over cytokine-based therapy as first-line therapy for metastatic renal cell carcinoma. However, the rate of complete response (CR) with targeted therapy is smaller than that with cytokine-based

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