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primary myelofibrosis/phosphatase

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Studies were done to test the neutrophil alkaline phosphatase (NAP) synthesizing capacity of the neutrophils of patients with chronic phase chronic myeloid leukemia (CML) and of patients with stable-phase myeloid metaplasia (MM) and to test the NAP synthesis-inducing capacity of monocytes (Mos) of

[Alkaline phosphatase activity of the granulocytes in polycythemia vera and myelofibrosis].

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Letter: Leukocyte alkaline phosphatase in agnogenic myeloid metaplasia.

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[Leukocyte alkaline phosphatase in polycythemia and osteomyelofibrosis].

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Platelet-derived growth factor receptor β activation and regulation in murine myelofibrosis.

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Prevailing evidence suggests a decisive role of platelet-derived growth factors (PDGFs) and their receptors in primary myelofibrosis. While PDGF receptor β (PDGFRβ) expression is increased in bone marrow stromal cells of patients correlating with the grade of myelofibrosis, knowledge on the precise
A 43-yr-old Japanese woman presented with mild anemia, leukocytosis and splenomegaly in May 1984. Splenomegaly and anemia gradually progressed. Sixteen years later, in October 2000, she developed inguinal lymphadenopathy. Biopsy of the lymph node revealed infiltration of blasts, megakaryocytes,
A young female patient presented with severe anemia and myelofibrosis. The spleen was not enlarged on clinical examination and no leukoerythroblastosis or tear-drop poikilocytosis was found. A bone marrow biopsy disclosed severe myelofibrosis and many megakaryocytes, which appeared morphologically
The patient was a 45-year-old male who had been diagnosed with pancytopenia in 1998 at another hospital, where he continued treatment for idiopathic thrombocytopenic purpura (ITP) as an outpatient. After atypical lymphocytes were detected in his peripheral blood, he was admitted to our hospital for

Transient myeloid metaplasia associated with an unusual hemoglobin in a newborn infant.

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A newborn infant presented with hepatosplenomegaly, rash, anemia, and leukocytosis at one day of age and manifested characteristic myeloid metaplasia by one mouth of life. Vitamin B12 and leukocyte alkaline phosphatase were elevated and platelet aggregation was impaired. Myelofibrosis was not
A systematic analysis of the blast cell population was carried out on samples from 50 patients suffering from blast transformation of chronic granulocytic leukaemia (CGL) (31) and of myelofibrosis (4), acute myelofibrosis (AM) (11) and undifferentiated acute leukaemia (4). Transmission electron
In 40 patients (17 male, 23 female, median age 57 years) with the presumptive diagnosis of primary (essential) thrombocythemia (PTH) according to the diagnostic requirements of the Polycythemia-Vera-Study-Group (PVSG) a follow-up study and a histological evaluation of initial trephine biopsies of
The clinical criteria for the diagnosis of essential thrombocythemia (ET) according to the polycythemia vera study group (PVSG) do not distinguish between ET and thrombocythemia associated with early stage PV and prefibrotic chronic idiopathic myelofibrosis (CIMF). The clinical criteria of the PVSG

[Myelofibrosis with marked subcapsular bleeding of the spleen--a case report].

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A 22-year old male was admitted to Ashikaga Red Cross Hospital because of the progressing abdominal distension in May 1988. The physical examinations disclosed marked hepato-splenomegaly, lymphadenopathy and cachexic state. In the laboratory examinations, anemia, leukocytosis with left shift of

Lymphoblastic leukemic transformation (lymphoblastic crisis) in myelofibrosis and myeloid metaplasia.

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Acute lymphoblastic leukemia (ALL) developing in myelofibrosis (MF) and myeloid metaplasia (MM) is reported in two patients. In both cases, the clinical course of the "blastic crisis" was rapidly progressive with little response to chemotherapy. The circulating cells were readily identified as

2-Chlorodeoxyadenosine treatment after splenectomy in patients who have myelofibrosis with myeloid metaplasia.

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2-Chlorodeoxyadenosine (2-CdA) is a purine nucleoside analogue with therapeutic activity in low-grade lymphoproliferative disorders. In addition, 2-CdA has a potent myelosuppressive effect, and it has been shown to be toxic to malignant myeloid cells both in vitro and in vivo. In this pilot study we
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