Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The peripheral blood cells of a patient with acute plasma cell leukemia were examined with transmission (TEM) and scanning (SEM) electron microscopes. The TEM features of the immature plasma cells comprised lobulated and irregulary shaped nuclei, with scanty heterochromating and bizarre nucleoli, parallel arrays of endoplasmic reticulum, cytoplasmic fibrils and numerous polymorphic mitochondria. SEM examination of the cells showed long, thin irregular ruffles, or round blebs on the cell surface, with appearance different from this observed on other types of leukemia. A remarkable clinical and hematological remission was achieved with administration of melphalan and steroids.
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PMID:Transmission and scanning electron microscopy study on plasma cell leukemia. 89 Jan 42

Studies of peripheral blood, bone marrow, and spleen cells from three patients with hairy-cell leukemia were performed. Two of the three patients had well-organized cytoplasmic, ribosome-lamellar inclusions in their leukemic cells. Blast transformation and 3H-thymidine incorporation of lymphocytes seemed to fall within normal ranges when the findings were related to the absolute numbers of lymphocytes. The enzymatic markers demonstrated in hairy cells-strong acid phosphatase activity in endoplasmic reticulum and lysosomes, marked alpha-naphthyl acetate esterase reaction, and weak beta-glucuronidase activity-as well as their phagocytosis of latex particles, indicate a common origin with monocytes or histiocytes. No decisive results were obtained by immunofluorescence. Evaluation of the significance of the formation by hairy cells of mouse erythrocyte rosettes, as well as the presence of the typical hair-like projections, may require additional knowledge concerning the membrane of these cells.
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PMID:A study of the nature of "hairy" cells, with emphasis on enzymatic markers. 94 41

The ultrastructual and immunologic features of the initial Reed-Sternberg and Hodgkin cells are compared with the ultimate leukemic cell type in a child with Hodgkin's disease who subsequently developed acute myelomonocytic leukemia (AMML) following 29 months of chemotherapy. Hodgkin tumor cells contained cytoplasmic IgG and ultrastructurally resembled large immunoblasts, containing one or two round nuclei with large bizarre nucleoli, many polyribosomes, sparase endoplasmic reticulum, underdeveloped Golgi lamellae, and few cytoplasmic granules. The Hodgkin tumor cells displayed no evidence of phagocytosis. The leukemic monocytic cells did not contain cytoplasmic IgG and, ultrastrucally, exhibited and indented and irregular nuclear profile with less prominent nucleoli, numerous pleomorphic granules, a moderate number of free ribosomes, short segments of endoplasmic reticulum, and stacked Golgi lamellae. The cell surface was irregular and occasionally appeared involved in endocytic activity. These results indicate that the Hodgkin tumor cells originated from B lymphocytes rather than tissue macrophages, whereas the leukemic monocytes arose from the bone marrow-derived monocyte-macrophage series. The findings suggest further that AMML developing after Hodgkin's disease consitutes a second neoplasm rather than a leukemic transformation of Hodgkin tumor cells.
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PMID:Hodgkin's disease and myelomonocytic leukemia: an ultrastructural and immunocytochemical study. 106 81

Thirty adults with acute leukemia and greater than 20% bone marrow infiltrate by promyelocytes were studied. Eighteen patients had acute promyelocytic leukemia (APML) as defined by the presence of malignant promyelocytes, and the remaining 12 patients had acute myelocytic leukemia (AML) with an elevated percentage of normal promyelocytes. Malignant promyelocytes were characterized by abundant, abnormal, cytoplasmic granules, by Auer rods in meshwork pattern, and by splinter cytoplasmic granulations and dilatation of the cisternae of endoplasmic reticulum. Patients with APML had, in general, greater than 35% bone marrow infiltrate by promyelocytes. The degree of bone marrow infiltrate by these cells correlated with the clinical status of the patients. Diffuse intravascular coagulation with bleeding occurred in 61% of patients with APML, and the bone marrows of these patients had greater than 50% promyelocytes. No coagulation abnormalities were seen among patients with elevated bone marrow promyelocytes infiltrate and without APML. Coagulation abnormalities in patients with APML were only corrected by controlling the leukemia itself. When this occurred, patients with APML had an excellent rate of complete remission, and the duration of remission and survival were comparable to the results obtained in adults with AML.
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PMID:Clinical and morphological correlations in acute promyelocytic leukemia. 106 21

The Cas-Br-E strain of murine leukemia virus is a neurovirulent retrovirus that induces progressive noninflammatory degeneration of the central nervous system (CNS). The molecular clone pNE-8 retains pathogenic properties of Cas-Br-E. The neurotropic determinants are known; however, the mechanism of neuropathogenesis is unknown. We examined the temporal development of disease after infection of SWR/J mice with pNE-8 virus. Development of CNS lesions, cellular targets of viral replication, accumulation of ubiquitinated proteins and integrity of blood-brain barrier were determined in mice infected with pNE-8 virus; and compared with uninfected, sham-infected, and nonneuropathogenic virus-infected mice. During 24 weeks of pNE-8 infection, noninflammatory spongiform lesions developed initially in the lumbar spinal cord and progressed to involve the brainstem and deep cerebellar nuclei. Virions and viral antigens accumulated for 18 weeks postinfection and then declined. Major sites of viral infection outside the CNS were splenic megakaryocytes, and skeletal muscle. Cellular targets of viral replication in the CNS included neurons, oligodendrocytes, and capillary endothelium. No astrocytic infection was observed; however, a reactive gliosis marked the development of clinical symptoms and histopathology. Spongiform lesions began as swelling of perivascular astrocytic processes. Intramyelinic vacuoles with splitting of myelin at major dense lines were prominent around dystrophic axons at later time points. Dendritic processes showed vacuolization and local degeneration. Viral particles were most commonly observed in extracellular spaces and within rough endoplasmic reticulum of neurons, oligodendrocytes, and splenic megakaryocytes. Infected megakaryocytes and regions of spleen containing viral aggregates showed accumulation of ubiquitinated proteins. Areas of histopathology in the CNS showed accumulation of ubiquitinated proteins but unlike spleen, viral proteins were not highly ubiquitinated. Disruption of the blood brain barrier was only evident at late stages of infection. In conclusion, the neuropathogenic damage associated with pNE-8 infection appears to be tightly associated with direct viral infection of oligodendroglia and neurons.
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PMID:Development of spongiform encephalopathy in retroviral infected mice. 131 97

A mixture of 2,3,6-tri-O-benzoyl-4,5-di-O-benzyl-D-myo-inositol and 1,3,6-tri-O-benzoyl-4,5-di-O-benzyl-D-myo-inositol, obtained during our synthesis of D-myo-inositol 1,4,5-trisphosphate [C.E. Ballou and W. Tegge, Proc. Natl. Acad. Sci. U.S.A., 86 (1989) 94-98], was separated after tetrahydropyranylation of the free hydroxyl group in each. 2,3,6-Tri-O-benzoyl-4,5-di-O-benzyl-1-O- (tetrahydro-2-pyranyl)-D-myo-inositol was debenzylated and the two free hydroxyl groups were phosphorylated by a dibenzyl phosphoramidite procedure. The tetrahydropyranyl group was then removed, and phosphorylation at position 1 with benzyl 3-(benzyloxycarbonylamino)propyl di-N-isopropylphosphoramidite, followed by oxidation and deprotection, provided 1-[3-aminopropoxy(hydroxy)phosphinyl]-D-myo-inositol 4,5-bisphosphate. This compound was coupled to activated agarose to prepare an affinity matrix for the isolation of D-myo-inositol 1,4,5-trisphosphate-binding proteins, and it was coupled to 4-azido-2-hydroxybenzoic acid to give a product that was labeled with 125I to prepare a photoactivable derivatizing reagent. The new derivatives retain significant biological activity as assessed by their ability to stimulate the release of stored Ca2+ from the endoplasmic reticulum of permeabilized rat basophilic leukemia cells.
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PMID:Syntheses of D-myo-inositol 1,4,5-trisphosphate affinity ligands. 132 99

The histopathological changes in WEHI-3B leukemia cells were followed by light and electronmicroscopy at different time intervals following exposure to cytotoxin P4 from Naja nigricollis nigricollis venom. At 1 hr after exposure to the toxin (2.5 x 10(-7) M) deformation was detected, primarily in the mitochondria, followed by vacuolization in the cytoplasm and an increase in lysosome number at 2 hr post-intoxication. Thereafter, the endoplasmic reticulum assumed a microsomal-like appearance, the plasma membrane was disrupted and, finally, the cells released their content to the culture medium. It is postulated that cytotoxin P4 may affect mitochondria either indirectly, by stimulating intracellular processes after binding to the cell membrane, or directly by interaction with the mitochondria after penetrating into the cell.
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PMID:Histopathological changes in WEHI-3B leukemia cells following intoxication by cytotoxin P4 from Naja nigricollis nigricollis venom. 144 Jun 50

We have analyzed a series of Moloney murine leukemia (M-MuLV) envelope (env) protein fusions to the marker proteins invertase and placental alkaline phosphatase (PLAP), expressed in Psi2 retrovirus packaging cells. The yeast invertase protein, fused at its third amino acid residue to the amino-terminal signal sequence and 17 residues of the mature M-MuLV env protein, retained its enzymatic activity and was secreted from mammalian cells. However, env protein fusions to the C-terminal portion of invertase were inactive. In contrast, some, but not all, env protein fusions at the C-terminal region of PLAP were enzymatically active: PLAP fusions containing long C-terminal portions of env localized to the rough endoplasmic reticulum (RER) and possessed low enzyme activity levels, while fusion constructs containing relatively short portions of the M-MuLV env gene localized to the Golgi and had higher activity levels. Those proteins that localized to the Golgi also were processed, in part, to forms of 67 to 68 kDa, the size of the mature PLAP protein. Since PLAP ordinarily is transferred to a phosphatidyl-inositol glycan tail (PIG-tail) in the Golgi and then transported to the plasma membrane, it appears that Golgi-localized PLAP-env fusions are processed imperfectly. PLAP itself, when expressed in Psi2 cells, accumulated at the plasma membrane and, unlike the PIG-tailed Thy-1 protein, was not incorporated into virus particles. Thus, the reported incorporation of the Thy-1 protein into M-MuLV virions does not appear to be a consequence of its glycoprotein tail.
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PMID:Retroviral envelope protein fusions to secreted and membrane markers. 158 54

A 57-year-old male who had suffered from polycythemia vera (PV) and had been treated with pipobroman, carbazilquinon and busulfan for ten years presented with fever. CBC revealed anemia and thrombocytopenia without an increase of leukemic blasts (WBC, 7,700/microliters, RBC 294 x 10(4)/microliters, Hb 9.1 g/dl, Plt 1.5 x 10(4)/microliters). Bone marrow aspiration resulted in dry tap. Bone marrow biopsy showed hyperplastic marrow with fibrosis and no increase in leukemic blasts. Eleven days later the patient became leukemic and he died of DIC. Blast cells showed a high nucleo-cytoplasmic ratio, basophilic cytoplasm and cytoplasmic blebs. Cytochemical and immunophenotype analysis of the blast cells showed the following results; myeloperoxidase (-), chloroacetate esterase (-), Sudan black (-), acid phosphatase (+), acetate esterase (+), PAS (+), HLA-DR (+) and GPIIb/IIIa (+). Platelet peroxidase reaction on electron microscopy was positive in perinuclear spaces and endoplasmic reticulum. A diagnosis of megakaryoblastic transformation of PV was made. Although acute myelogenous leukemia has been shown to develop occasionally in the course of PV, acute megakaryoblastic leukemia with DIC following PV is a very rare condition.
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PMID:[Megakaryoblastic transformation associated with disseminated intravascular coagulation in the course of polycythemia vera: a case report]. 160 15

The hydrolysis of sphingomyelin (SM) is a key reaction in the "sphingomyelin cycle," which plays a role in the regulation of cell proliferation and differentiation (Okazaki, T., Bell, R. M., and Hannun, Y. A. (1989) J. Biol. Chem. 264, 19076-19080). SM is produced from endoplasmic reticulum-derived ceramide and is delivered to organelle membranes in a regulated manner, presumably through the same endomembrane trafficking system used for sorting and delivery of proteins. Since brefeldin A (BFA) interferes with this endomembrane trafficking system and thus alters normal membrane and organelle distribution, we investigated the effect of BFA on SM levels in HL-60 leukemia cells. BFA caused a dose-dependent decrease of 20-25% in cellular SM levels, with effects observed at concentrations of BFA as low as 0.10 microgram/ml. BFA effects on SM levels were noted as early as 5 min and were maximal by 20 min, with no further SM hydrolysis observed up to 60 min following treatment with BFA, suggesting the presence of a fixed SM-sensitive pool. BFA did not cause SM hydrolysis at 16 degrees C, a temperature that inhibits the effects of BFA on endomembrane mixing. The very early effects and temperature dependence of BFA-induced SM hydrolysis suggest that the mechanism of hydrolysis may be closely related to endomembrane mixing. These studies are beginning to define important interrelationships between membrane trafficking and topology, SM metabolism, and cell regulation.
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PMID:Brefeldin A promotes hydrolysis of sphingomyelin. 163 30


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