Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten clinical observations concerning six families with familial myeloproliferative disorders are reported. Family no. 1 : two brothers, RES with myelosclerosis and ROS with chronic myeloid leukemia. Family no. 2 : PG atypical myeloproliferative syndrome and his brother polycythemia vera. Family no. 3 : DF myelosclerosis and her son (DR) polycythemia vera. Family no. 4 : DM, polycythemia vera, the mother and a sister with splenomegaly. The brother died with myelofibrosis. Family no. 5 : GA and ML, cousins with polycythemia vera. Family no. 6 : MB and ZG, a brother and sister with polycythemia vera. No consanguinity and no toxic, infections or malignant etiology were found in these families. The literature reviewed emphasises the rarity of the familial incidence of myeloproliferative disorders.
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PMID:[Familial myeloproliferative syndromes. Study of 6 families and review of literature]. 35 25

Since the discovery of a very high blood histamine level in chronic myelocytic leukemia (CML) 1936, the author could ascertain that this parameter is very useful in the differential diagnosis between CML and various "leukemoid" reactions; in the early diagnosis of CML and in the differential diagnosis between CML and other myeloproliferative disorders. Recent researches proved that no correlation exists between blood histamine level and basophil count in the peripheral blood. Further investigations in this field have to clear up the questions whether it is possible by means of repeated controls of the blood histamine level to predict the development of a polycythemia vera into CML or to establish in a case of osteomyelosclerosis that this disease has been Preceeded by A CML.
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PMID:[Blood histamine level in chronic myeloproliferative diseases; a review]. 39 72

Two additional cases of myeloproliferative disorders are described showing as the only chromosome abnormality a loss of the Y chromosome. Comparing these cases with cases reviewed from the literature indicates that a loss of the Y chromosome in Ph1-positive and Ph1-negative CML may cause only a somewhat longer life expectancy following diagnosis. The exact role of the Y chromosome, however, in the initiation or progression of a malignant disorder cannot be stated at this time.
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PMID:Loss of the Y chromosome from bone marrow cells of males with myeloproliferative disorders. Report of two cases and review of the literature. 40 35

Reports of heterogeneity of IgG receptor activity of normal circulating neutrophils prompted measurements in myeloproliferative disease to determine if dysplasia of the hematic stem cell resulted in an abnormality of this membrane property. IgG receptors were assayed by rosette formation in suspension with human Rh-positive erythrocytes sensitized with high-titer Rh antiserum. IgG receptors were detected on 19 +/- 1.6% (mean +/- SEM) of neutrophils from 45 normal subjects. A significant increase in IgG-receptor-bearing neutrophils was found in polycythemia vera (PV) and myeloid metaplasia (MyM), with values of 70 +/- 3.6% and 69.7 +/- 4.3%, respectively. Normal values were observed in polycythemic states not due to myeloproliferative disease and in chronic myelocytic leukemia. Rosette-forming neutrophils were increased to 52.3 +/- 3.7% in infection and inflammatory disease, but this value was significantly lower than those in PV and MyM. Increased IgG receptors in PV and MyM may be related to the activated state of the neutrophil and may result from an intrinsic cellular abnormality of the proliferating clone or from altered bone marrow release. Quantitation of neutrophil IgG receptors may be of value in the differential diagnosis of PV and MyM and may offer insights into the derangement of hematopoiesis that underlies these myeloproliferative disorders.
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PMID:Increased circulating neutrophils with surface receptor activity for immunoglobulin G in polycythemia vera and myeloid metaplasia. 44 52

Epidural myeloblastoma, which compressed the spinal cord, was the first evidence for chronic granulocytic leukemia, eosinophilic type, Ph chromosome negative. This manifestation was preceded by 3 years follow-up of a patient with persistent eosinophilia of 60% mature eosinophils. The only clues for the diagnosis of leukemia were splenomegaly and high serum vitamin B12, most of which was bound to transcobalamin I. The latter finding presents a useful diagnostic criterium in myeloproliferative disorders.
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PMID:Chronic eosinophilic leukemia complicated by epidural myeloblastoma. 80 41

Platelet function tests were done to ascertain whether they might have discriminatory significance in the differentiation of a myeloproliferative disorder from secondary thrombocytosis in a patient with an elevated platelet count. Amongst 14 subjects with polycythaemia vera and essential thrombocythaemia, significant abnormalities of platelet aggregation were the rule, while defective aggregation was unusual in 16 subjects with secondary thrombocytosis. Measurements of the bleeding time and of platelet factor 3 activity were of some value, but significant overlap was noted. Platelet function in four of five subjects with chronic myeloid leukaemia was essentially normal.
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PMID:Platelet function in patients with high platelet counts. 105 37

The technique described in the preceding paper was applied to 12 abnormal sera selected for their increase in one or more B12-binding proteins. Even in the presence of large amounts of R-type binder, the ammonium sulfate technique gave a reliable separation of R binding proteins from TC II. Measurement of the TC II in abnormal sera gave results identical to those obtained by the more standard gel filtration. The R binders of four subjects with myeloproliferative disease were further separated into alpha2-R and alpha1-R. The pattern of B12 binding of polycythemia vera (PV) was an exaggeration of the normal pattern. Binding to alpha2-R was three to four times that to alpha1-R, although the total amounts bound to both were increased. In chronic myelogenous leukemia (CML), both alpha2-R and alpha1-R were also increased, but in contrast to binding in normal sera, alpha1-R predominated. In order to interpret the findings, either whole serum R or alpha1-R and alpha2-R from patients with myeloproliferative disease were subject to isoelectric focusing. Alpha2-R consisted pricipally of components isoelectric at pH 2.9, 3.0, and 3.1. These components were present in only minor amounts in normal serum and were somewhat increased in the serum of PV. These components were very much increased in the serum of CML and predominated. Alpha2-R consisted of those components isoelectric at pH 3.4,3.6, and 4.0. These components predominated in the unsaturated binding capacity of normal sera and that of PV. It was concluded that the division of plasma R binders into alpha1-R and alpha1-R by the technique described provided information useful in the study of myeloproliferative diseases.
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PMID:Measurement of vitamin B12-binding proteins of plasma. II. Interpretation of patterns in disease. 105 10

Forty-three operative procedures were performed on a population of 250 patients with myeloproliferative disorders, including polycythemia vera, myeloid metaplasia (MM) and chronic myelogenous leukemia (CML). The overall operative mortality was approximately 7% and the incidence of excessive bleeding which could be related to coagulopathy was 5%. Twenty-one patients with MM or CML underwent splenectomy for palliation of symptoms related to the enlarged spleen or hematologic problems. Eighty-four percent of the latter group were improved. Adverse hematologic effects which could be attributed to splenectomy in these patients were confined to two patients who developed marked thrombocytosis. Among the 23 patients with MM, 9 had portal hypertension. Three underwent portacaval shunt and one a splenorenal shunt for bleeding varices. One of the patients died of hepatic necrosis. Estimated hepatic blood flow determinations (EHBF) in 4 patients with portal hypertension demonstrated a marked absolute increase and an increase in the ratio of EHBF/Cardiac Index. Absence of any evidence of intrahepatic or extrahepatic obstruction in these patients and the demonstration that splenectomy relieved portal hypertension defined at surgery in 4 patients, suggests that augmented adhepatic flow contributes to portal hypertension in some cases. The review leads to the conclusions that: 1) Operative procedures in prepared patients with myeloproliferative disorders are not associated with prohibitive mortality and morbidity rates. 2) Splenectomy is indicated for patients with increasing transfusion requirements and symptomatic splenomegaly or hypersplenism and should be performed early in the course of disease. 3) When associated portal hypertension and bleeding varices are present, hemodynamic studies should be carried out to define if splenectomy alone, or a portal systemic decompressive procedure is indicated.
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PMID:Myeloproliferative disorders. 105 48

Polycythemia rubra vera and chronic myelogenous leukemia are both myeloproliferative disorders and, as such, share certain clinical features. Although some myeloproliferative disorders may transform into others, conversion of polycythemia rubra vera to chronic myelogenous leukemia has been denied. We report here an elderly man with polycythemia rubra vera and a normal leukocyte alkaline phosphatase who developed chronic myelogenous leukemia with a low leukocyte alkaline phosphatase and a marrow karyotype of 45, X, Ph1-positive. In addition, we have collected evidence of two similar cases and thus conclude that, although uncommon, polycythemia rubra vera may on occasion progress to chronic myelogenous leukemia.
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PMID:Polycythemia rubra vera progressing to Ph1-positive chronic myelogenous leukemia. 106 Mar 94

Ultrastructural histochemical evaluation of the surface of normal human blood and bone marrow cells exposed to the pyroantimonate-osmium (PAO) reaction indicated the selective binding of pyroantimonate to certain cations (calcium, magnesium, and possibly sodium) associated with the plasma membrane of neutrophilic leukocytes and their developmental forms. Other leukocytes and their precursors did not exhibit plasma membrane PAO reactivity. The extent of surface binding was related to cell maturity, with maximal labeling evident in the mid and late promyelocytes; decreased binding occurred with subsequent maturation while myeloblasts were nonreactive. This study was initiated to ascertain if histochemical surface modifications of neutrophilic cells occur in certain myeloproliferative disorders. In this regard, we have been able to demonstrate a distinctive defect in the plasma membrane PAO binding characteristics of the leukemic cells in chronic myelocytic leukemia (CML). Limited binding of pyroantimonate to the plasma membrane of the leukemic cell series in four patients with CML contrasted with that of the normal granulocytic cell series and the neutrophilic cells seen in myelomonocytic leukemia (two patients), myelofibrosis (one patient), and acute myelocytic leukemia (three patients). Comparison of surface PAO reactivity of neutrophilic cells in all stages of maturation in two patients with CML in blast crisis revealed that, in the patient with 30% circulating blast cells, PAO reactivity was identical to that noted in CML, while in the patient with 80% circulating blast forms, the PAO reactivity of the maturing neutrophilic cells more nearly resembled that observed in neutrophilic cells from normal individuals. Many neutrophilic cells from patients with myelofibrosis and myelomonocytic leukemia and from one patient in severe blast crisis had large surface deposits of pyroantimonate considered to reflect increased membrane-associated reactive cation.
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PMID:Ultrastructural histochemical alteration of the plasma membrane in chronic myelocytic leukemia. 106 Apr 72


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