polycythemia vera/tyrosine

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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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Ingia / Ingia

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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Ingia / Ingia

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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Ingia / Ingia

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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Ingia / Ingia

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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Ingia / Ingia

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

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

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Ingia / Ingia

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.

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

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

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Ingia / Ingia

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

Imatinib effect on growth and signal transduction in polycythemia vera.

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Ingia / Ingia

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

Identification of a novel inhibitor of JAK2 tyrosine kinase by structure-based virtual screening.

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Ingia / Ingia

Janus kinase 2 (JAK2) plays a crucial role in the pathomechanism of myeloproliferative disorders and hematologic malignancies. A somatic mutation of JAK2 (Val617Phe) was previously shown to occur in 98% of patients with polycythemia vera and 50% of patients with essential thrombocythemia and primary

Effective quantification of 11 tyrosine kinase inhibitors and caffeine in human plasma by validated LC-MS/MS method with potent phospholipids clean-up procedure. Application to therapeutic drug monitoring.

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Ingia / Ingia

Therapeutic drug monitoring (TDM) help to improve treatment efficacy and safety. Therefore, a simple and sensitive liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed and validated for the simultaneous monitoring of 11 tyrosine kinase inhibitors (TKIs) in human plasma.

Abnormal adhesion of red blood cells in polycythemia vera: a prothrombotic effect?

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Ingia / Ingia

Polycythemia vera (PV) is a myeloproliferative neoplasm (MPN) characterised by the V617F activating mutation in the tyrosine kinase JAK2. PV patients exhibit increased haemoglobin levels and red cell mass because of uncontrolled proliferation of the erythroid lineage. Thrombosis and transformation

Imatinib mesylate therapy for polycythemia vera: final result of a phase II study initiated in 2001.

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Ingia / Ingia

Polycythemia vera (PV) is a chronic myeloproliferative neoplasm (MPN) characterized by excessive production of red blood cells. Patients with PV are at a risk of thrombosis, bleeding, and transformation to myelofibrosis or acute myeloid leukemia. Therapy for PV is based on the use of phlebotomy,

[Abnormal activation of tyrosine kinases and its role in the pathogenesis of hematological malignancies - review].

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Ingia / Ingia

Protein tyrosine kinases are key participants in signal transduction pathways that regulate cellular growth, activation and differentiation. Aberrant PTK activity resulting from gene mutation (often accompanying chromosome translocation) or overexpression of these enzymes plays an etiologic role in

Application of tyrosine kinase inhibitors as a promising targeting treatment for myeloproliferative neoplasms --- review.

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Ingia / Ingia

As well as playing vital roles in main cellular processes, such as abnormal proliferation, differentiation, survival, apoptosis, and a lot of tyrosine kinases (TK) are involved in oncogenesis. TK or components of their signal pathways have been found abnormal in many hematological malignancies.

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