Neutrophil 5-nucleotidase reaction in chronic myelogenous leukemia, myelofibrosis with myeloid metaplasia, and polycythemia vera

1998 ◽  
Vol 76 (1) ◽  
pp. 1-5 ◽  
Author(s):  
N. B. Tsavaris ◽  
G. A. Pangalis
Keyword(s):  
Polycythemia Vera ◽  
Chronic Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
Myeloid Metaplasia ◽  
Myelofibrosis With Myeloid Metaplasia

scholarly journals The Plasma Disappearance of Radioactive Vitamin B12 in Myeloproliferative Diseases and Other Blood Disorders

Blood ◽  
1961 ◽  
Vol 18 (6) ◽  
pp. 717-726 ◽  
Author(s):  
CHARLES A. HALL ◽  
Alexander E. Finkler ◽  
Edward S. Allen ◽  
Booker T. Moore
Keyword(s):  
Vitamin B12 ◽  
Polycythemia Vera ◽  
Chronic Myelogenous Leukemia ◽  
Intravenous Dose ◽  
Myelogenous Leukemia ◽  
Blood Disorders ◽  
Myeloid Metaplasia ◽  
Myeloproliferative Diseases ◽  
Close Relationship ◽  
Secondary Polycythemia

Abstract 1. The plasma disappearance of a small intravenous dose of radioactive vitamin B12 was determined in control subjects and in patients with various blood disorders. 2. A delayed, sometimes irregular, disappearance was observed in the majority of patients with acute and chronic myelogenous leukemia, myeloid metaplasia, and polycythemia vera. 3. Disappearance was normal in the lymphogenous leukemias, secondary polycythemia and relative polycythemia. 4. The abnormalities observed are believed to indicate an abnormality of vitamin B12 metabolism common to the diseases of the myeloproliferative group and are further evidence of the close relationship between these diseases.

scholarly journals Neutrophil alkaline phosphatase: comparison of enzymes from normal subjects and patients with polycythemia vera and chronic myelogenous leukemia

Blood ◽  
1975 ◽  
Vol 45 (3) ◽  
pp. 335-343
Author(s):  
D Rosenblum ◽  
SJ Petzold
Keyword(s):  
Alkaline Phosphatase ◽  
Polycythemia Vera ◽  
Phosphatase Activity ◽  
Chronic Myelogenous Leukemia ◽  
Alkaline Phosphatase Activity ◽  
Normal Subjects ◽  
Myelogenous Leukemia ◽  
Precipitin Line ◽  
Neutrophil Alkaline Phosphatase ◽  
Sepharose 4B

To determine whether decreased alkaline phosphatase activity in the granules from neutrophils of patients with chronic myelogenous leukemia (CML) was due to an absence of enzyme or the production of defective enzyme, we compared the immunologic properties of granule alkaline phosphatase derived from patients with CML with that of normal subjects and patients with polycythemia vera (PRV). Antisera prepared in rabbits against granule alkaline phosphatase purified from the neutrophils of a patient with PRV produced a single precipitin line of antigenic identity when reacted with extracts of normal, PRV, and CML neutrophil granules. A histochemical stain for alkaline phosphatase activity (alpha-naphthyl acid phosphate coupled with Fast Blue RR) specifically stained the precipitin line. A variety of quantitative precipitin techniques failed to produce satisfactory precipitation of alkaline phosphatase activity. Comparative analyses were therefore performed by affinity chromatography using goat antirabbit-gammaglobulin linked to Sepharose 4B to adsorb alkaline phosphatase complexed with rabbit gamma globulin. With this method, 100% of CML, normal, and PRV alkaline phosphatase could be adsorbed. Using limiting concentrations of antibody, a proportionally smaller fraction of enzyme activity was absorbed as the concentration of PRV alkaline phosphatase or normal alkaline phosphatase was increased. Extracts of CML granules containing comparable amounts of protein but 200-fold less alkaline phosphatase activity per milligram did not specifically reduce adsorption. Thus, in CML, we found no evidence that the granulocytes contained a large amount of antigenically normal but enzymatically defective alkaline phosphatase. Examination of electron micrographs revealed no significant differences in the number or distribution of granules in the granulocytes of normal subjects or patients with PRV or CML. This suggests that the low level of neutrophil alkaline phosphatase in CML granulocytes is the result of decreased enzyme content and not a consequence of synthesis of catalytically defective enzyme.

scholarly journals Neutrophil alkaline phosphatase: comparison of enzymes from normal subjects and patients with polycythemia vera and chronic myelogenous leukemia

Blood ◽  
1975 ◽  
Vol 45 (3) ◽  
pp. 335-343 ◽  
Author(s):  
D Rosenblum ◽  
SJ Petzold
Keyword(s):  
Alkaline Phosphatase ◽  
Polycythemia Vera ◽  
Phosphatase Activity ◽  
Chronic Myelogenous Leukemia ◽  
Alkaline Phosphatase Activity ◽  
Normal Subjects ◽  
Myelogenous Leukemia ◽  
Precipitin Line ◽  
Neutrophil Alkaline Phosphatase ◽  
Sepharose 4B

Abstract To determine whether decreased alkaline phosphatase activity in the granules from neutrophils of patients with chronic myelogenous leukemia (CML) was due to an absence of enzyme or the production of defective enzyme, we compared the immunologic properties of granule alkaline phosphatase derived from patients with CML with that of normal subjects and patients with polycythemia vera (PRV). Antisera prepared in rabbits against granule alkaline phosphatase purified from the neutrophils of a patient with PRV produced a single precipitin line of antigenic identity when reacted with extracts of normal, PRV, and CML neutrophil granules. A histochemical stain for alkaline phosphatase activity (alpha-naphthyl acid phosphate coupled with Fast Blue RR) specifically stained the precipitin line. A variety of quantitative precipitin techniques failed to produce satisfactory precipitation of alkaline phosphatase activity. Comparative analyses were therefore performed by affinity chromatography using goat antirabbit-gammaglobulin linked to Sepharose 4B to adsorb alkaline phosphatase complexed with rabbit gamma globulin. With this method, 100% of CML, normal, and PRV alkaline phosphatase could be adsorbed. Using limiting concentrations of antibody, a proportionally smaller fraction of enzyme activity was absorbed as the concentration of PRV alkaline phosphatase or normal alkaline phosphatase was increased. Extracts of CML granules containing comparable amounts of protein but 200-fold less alkaline phosphatase activity per milligram did not specifically reduce adsorption. Thus, in CML, we found no evidence that the granulocytes contained a large amount of antigenically normal but enzymatically defective alkaline phosphatase. Examination of electron micrographs revealed no significant differences in the number or distribution of granules in the granulocytes of normal subjects or patients with PRV or CML. This suggests that the low level of neutrophil alkaline phosphatase in CML granulocytes is the result of decreased enzyme content and not a consequence of synthesis of catalytically defective enzyme.

Evaluation and clinical correlations of bone marrow angiogenesis in myelofibrosis with myeloid metaplasia

Blood ◽  
2000 ◽  
Vol 96 (10) ◽  
pp. 3374-3380 ◽  
Author(s):  
Ruben A. Mesa ◽  
Curtis A. Hanson ◽  
S. Vincent Rajkumar ◽  
Georgene Schroeder ◽  
Ayalew Tefferi
Keyword(s):  
Bone Marrow ◽  
Polycythemia Vera ◽  
Essential Thrombocythemia ◽  
Quantitative Methods ◽  
Prognostic Significance ◽  
Control Group ◽  
Prognostic Information ◽  
Myeloid Metaplasia ◽  
Bone Marrow Disease ◽  
Myelofibrosis With Myeloid Metaplasia

Abstract Recent observations have underscored the biologic relevance of intratumoral angiogenesis and its potential impact on prognosis. Increased bone marrow angiogenesis has been demonstrated in a variety of hematologic disorders, including multiple myeloma. The extent and prognostic significance of bone marrow angiogenesis in 114 patients with myelofibrosis with myeloid metaplasia (MMM) was investigated. A control group of 44 patients without bone marrow disease, 15 patients with polycythemia vera, and 17 patients with essential thrombocythemia was also studied. Bone marrow microvessel density was assessed by a semiquantitative method, visual microvessel grading, and 2 separate quantitative methods, visual count and computerized image analysis. Angiogenesis estimation by all 3 methods was highly comparable. On visual microvessel grading, a grade 3 or 4 increase in bone marrow angiogenesis was demonstrated in 70% of patients with MMM, 33% of patients with polycythemia vera, 12% of patients with essential thrombocythemia, and 0% of normal controls. In a multivariate analysis, increased angiogenesis in MMM correlated significantly with increased spleen size and was found to be a significant and independent risk factor for overall survival. Increases in marrow angiogenesis correlated with hypercellularity and megakaryocyte clumping. In contrast, these 2 features were inversely proportional to reticulin fibrosis, whereas increases in marrow angiogenesis were independent of reticulin fibrosis. These preliminary findings suggest that neo-angiogenesis is an integral component of the bone marrow stromal reaction in MMM and may provide useful prognostic information and a rationale for the therapeutic investigation of anti-angiogenic agents.

Abnormalities of Epinephrine-Induced Platelet Aggregation and Adenine Nucleotides in Myeloproliferative Disorders

1984 ◽  
Vol 52 (03) ◽  
pp. 292-296 ◽  
Author(s):  
Koichiro Yamamoto ◽  
Eisuke Sekiguchi ◽  
Osamu Takatani
Keyword(s):  
Platelet Aggregation ◽  
Polycythemia Vera ◽  
Chronic Myelogenous Leukemia ◽  
Platelet Function ◽  
Adenine Nucleotides ◽  
Myeloproliferative Disorders ◽  
Myelogenous Leukemia ◽  
Control Group ◽  
Storage Pool ◽  
Percentage Release

SummaryPlatelet aggregation was studied in 18 patients with myeloproliferative disorders, including 14 patients with chronic myelogenous leukemia, 2 with polycythemia vera, 1 with myelofibrosis and 1 with thrombocythemia. Fourteen patients (78%) were abnormal in epinephrine-induced platelet aggregation, while 3 (17%) and 4 (22%) cases showed impaired ADP or collagen induced platelet aggregation, respectively. A significant decrease of total ADP content in resting unstimulated platelets and of the amount released to the medium after aggregation was found in all six patients who were evaluated. ATP and AMP in resting platelets tended to be slightly higher in patients compared with the control group. Released ATP was also significantly less, and the percentage release of ADP and ATP was significantly decreased in patients. A storage pool deficiency of adenine nucleotides was considered to be responsible for abnormal platelet function in patients with myeloproliferative disorders.

MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients

Blood ◽  
2006 ◽  
Vol 108 (10) ◽  
pp. 3472-3476 ◽  
Author(s):  
Animesh D. Pardanani ◽  
Ross L. Levine ◽  
Terra Lasho ◽  
Yana Pikman ◽  
Ruben A. Mesa ◽  
...  
Keyword(s):  
Polycythemia Vera ◽  
De Novo ◽  
Blast Crisis ◽  
Molecular Testing ◽  
Myeloproliferative Disease ◽  
Myeloid Metaplasia ◽  
Mutational Frequency ◽  
Mutational Status ◽  
Myelofibrosis With Myeloid Metaplasia ◽  
Myelomonocytic Leukemia

Abstract Recently, a gain-of-function MPL mutation, MPLW515L, was described in patients with JAK2V617F-negative myelofibrosis with myeloid metaplasia (MMM). To gain more information on mutational frequency, disease specificity, and clinical correlates, genomic DNA from 1182 patients with myeloproliferative and other myeloid disorders and 64 healthy controls was screened for MPL515 mutations, regardless of JAK2V617F mutational status: 290 with MMM, 242 with polycythemia vera, 318 with essential thrombocythemia (ET), 88 with myelodysplastic syndrome, 118 with chronic myelomonocytic leukemia, and 126 with acute myeloid leukemia (AML). MPL515 mutations, either MPLW515L (n = 17) or a previously undescribed MPLW515K (n = 5), were detected in 20 patients. The diagnosis of patients with mutant MPL alleles at the time of molecular testing was de novo MMM in 12 patients, ET in 4, post-ET MMM in 1, and MMM in blast crisis in 3. Six patients carried the MPLW515L and JAK2V617F alleles concurrently. We conclude that MPLW515L or MPLW515K mutations are present in patients with MMM or ET at a frequency of approximately 5% and 1%, respectively, but are not observed in patients with polycythemia vera (PV) or other myeloid disorders. Furthermore, MPL mutations may occur concurrently with the JAK2V617F mutation, suggesting that these alleles may have functional complementation in myeloproliferative disease.

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