hemoglobinuria/neoplasms

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Management of acquired thrombophilic disorders in 2011: focus on heparin-induced thrombocytopenia, antiphospholipid syndrome, myeloproliferative neoplasms and paroxysmal nocturnal hemoglobinuria.

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Arterial and venous thrombosis are interrelated disorders at the interplay of platelets and fibrin. Arterial thrombi are platelet-rich and occur at sites vulnerable to atherosclerotic plaque rupture where blood shear rates are high; on the contrary, venous thrombi occur in association with slow

The role of Wilms' tumor gene peptide-specific cytotoxic T lymphocytes in immunologic selection of a paroxysmal nocturnal hemoglobinuria clone.

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OBJECTIVE To clarify an expansion mechanism of a paroxysmal nocturnal hemoglobinuria (PNH) clone with the Wilms' tumor gene (WT1). METHODS In PNH patients with the HLA-A*2402 allele, frequencies of peripheral blood (PB) WT1 peptide-specific and HLA-A*2402-restricted CD8+ cells and WT1

Increased resistance of PIG-A- bone marrow progenitors to tumor necrosis factor a and interferon gamma: possible implications for the in vivo dominance of paroxysmal nocturnal hemoglobinuria clones.

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OBJECTIVE Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal disorder due to a PIG-A gene mutation, resulting in deficient expression of GPI-anchored-proteins. Both immune-mediated suppression of hematopoiesis and cytokine alterations have been reported in aplastic anemia, a disease closely

Prevalence of Paroxysmal Nocturnal Hemoglobinuria Clones in Myeloproliferative Neoplasm Patients: A Cross-Sectional Study.

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The myeloproliferative neoplasms (MPN) are clonal diseases that confer an increased risk of thrombohemorrhagic complications. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare clonal disease associated with an increased thrombotic risk. Small PNH clones are prevalent in aplastic

[Proliferation and anti-tumor activity of lymphocytes and their effect on normal phenotype of autologous bone marrow hematopoietic cells in patients with paroxysmal nocturnal hemoglobinuria].

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There is a hypothesis that paroxysmal nocturnal hemoglobinuria (PNH) hematopoitic stem cells are resistant to the cytotoxic effect of T cells because they lack glycosylphosphatidylinositol (GPI)-linked proteins. The aim of this study is to investigate proliferation and anti-tumor activity of

Development of paroxysmal nocturnal hemoglobinuria in CALR-positive myeloproliferative neoplasm.

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Paroxysmal nocturnal hemoglobinuria (PNH), a disease characterized by intravascular hemolysis, thrombosis, and bone marrow failure, is associated with mutations in the PIG-A gene, resulting in a deficiency of glycosylphosphatidylinositol-anchored proteins. Many hypotheses have been posed as to

Clonal variation, autoimmunity, and neoplasia: an ecology lesson from paroxysmal nocturnal hemoglobinuria.

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[Paroxysmal hemoglobinuria following trimethoprim-sulphamethoxazole in a lung cancer case treated by radiation therapy].

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Monoclonal antibodies in rare acquired thrombotic disorders: the paradigms of paroxysmal nocturnal hemoglobinuria, thrombotic thrombocytopenic purpura and central retinal vein occlusion.

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Monoclonal antibodies have been developed to optimize treatment effects in various malignant and nonmalignant conditions, by selectively targeting key components of the underlying pathophysiologic processes. Rituximab, a chimeric anti-CD20 antibody has revolutionized treatment of malignant

Viscous resistance to blood flow in solid tumors: effect of hematocrit on intratumor blood viscosity.

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Blood flow rate in a vascular network is proportional to the arteriovenous pressure difference and inversely proportional to the geometric and viscous resistances. We have recently shown that the geometric resistance to blood flow increases with increasing tumor size and/or decreasing arterial

[Treatment of paroxysmal nocturnal hemoglobinuria with danazol].

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Glucocorticoid and androgen therapy have been used with moderate success in paroxysmal nocturnal hemoglobinuria (PNH). However, both are poorly tolerated, especially in women, although the side effects of glucocorticoid can be diminished by alternate day therapy. We have treated two patients with

Impaired phagocyte responses to lipopolysaccharide in paroxysmal nocturnal hemoglobinuria.

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Bone marrow-derived cells from patients suffering from paroxysmal nocturnal hemoglobinuria (PNH) show a defect in the expression of phosphatidylinositol-anchored membrane proteins, including the CD14 molecule. Blocking experiments with anti-CD14 monoclonal antibodies have shown that

Markedly high plasma erythropoietin and granulocyte-colony stimulating factor levels in patients with paroxysmal nocturnal hemoglobinuria.

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In patients with paroxysmal nocturnal hemoglobinuria (PNH), we measured plasma concentrations of endogenous hematopoiesis-regulatory cytokines to characterize bone marrow (BM) hypoplasia which is a major cause of death. Contrary to 10 healthy individuals, all 14 patients with PNH showed increases of

Hematopoietic Cell Transplantation for Paroxysmal Nocturnal Hemoglobinuria in the Age of Eculizumab.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired clonal hematopoietic cell disease characterized by the destruction of hematopoietic cells through activation of the complement system with manifestations that can be life-threatening including hemolysis, thrombosis, and marrow failure.

Clonal populations of hematopoietic cells with paroxysmal nocturnal hemoglobinuria phenotype in patients with splanchnic vein thrombosis.

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BACKGROUND Splanchnic vein thrombosis (SVT) is a serious complication in patients with paroxysmal nocturnal hemoglobinuria (PNH). Mutant PNH clones can be associated with an increased risk of SVT even in the absence of overt disease, but their prevalence in non-selected SVT patients remains

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