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)

Ten of 136 consecutive adult patients with previously untreated acute leukemia had morphologically undifferentiated leukemia by light microscopy. Leukemic cells from these patients were characterized by agranular cytoplasm, negative histochemical staining with sudan black (SB) and nonspecific esterase, and absent lymphoid cell surface markers and therefore were not classifiable according to the French-American-British (FAB) system. Electron microscopy with myeloperoxidase (MPO) staining revealed the presence of peroxidase positive cytoplasmic granules and endoplasmic reticulum in eight of the nine patients studied. Cells from the patient who was negative for MPO were also negative for platelet peroxidase. A series of monoclonal antibodies to myeloid antigens also revealed myeloid features with all patients having at least one myeloid differentiation antigen present on the surface of their cells. Common acute lymphoblastic leukemia (ALL) antigen was absent in the nine patients tested. Cytogenetic analysis of blast cells was abnormal in seven patients on whom adequately banded chromosomes were obtained although there were no consistent abnormalities. No patient had a Ph1 chromosome. Only two of the ten patients achieved a complete remission. Morphologically undifferentiated leukemia may have myeloid features when studied by transmission electron microscopy or with monoclonal antibodies for cell surface markers. Such studies should be performed when the leukemia cannot be classified using either light microscopy or lymphoid cell surface markers. Such patients infrequently achieve remission with standard therapy and constitute a distinct entity.
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PMID:Minimally differentiated acute nonlymphocytic leukemia: a distinct entity. 366 39

The envelope protein (gp52) of Friend spleen focus-forming virus (F-SFFV) is defective in its intracellular transport and accumulates in the rough endoplasmic reticulum of F-SFFV-infected cells. This defect in transport has been attributed to the lack of a cytoplasmic domain, and possible loss of signals required for transport to the cell surface. The mature form of gp52, designated gp65, is also reported to be secreted from SFFV-infected cells. To determine the specific changes in the envelope protein which may lead to its lack of transport and to its lack of stability in associating with membranes, the 3' end of the F-SFFV envelope gene, which encodes the transmembrane domain, was inserted in place of the normal 3' end of the Friend murine leukemia virus genome. This chimeric envelope gene was expressed using the vaccinia virus expression system. The chimeric gp70/p15E glycoprotein molecule lacks the cytoplasmic tail residues and as a consequence is about 3300 daltons smaller. The chimeric PrEnv molecule was found to be cleaved efficiently as indicated by pulse-chase experiments. Immunofluorescence studies demonstrate that the chimeric molecule is efficiently transported to the surface of cells, unlike the SFFV gp52 glycoprotein. The chimeric molecule was found to be unstable in its membrane association and is released into the culture medium. These results indicate that the changes in the membrane spanning region and the lack of a cytoplasmic tail do not determine the defective transport of gp52, but may determine the stability of its association with membranes.
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PMID:Effects of deletion of the cytoplasmic domain upon surface expression and membrane stability of a viral envelope glycoprotein. 368 Feb 44

Newborn inbred CFW/D mice were inoculated intraperitoneally with ts1, a neurotropic temperature-sensitive mutant of Moloney murine leukemia virus TB (MoMuLV-TB), with the parental wild type (wt) MoMuLV-TB, or with culture medium. A progressive symmetric hindlimb paresis that progressed to paralysis was observed in ts1-infected mice. Wt-infected mice and control mice had no neurologic signs. The severity and progression of neurologic signs correlated with the location, development, and progression of lesions. Lesions consisted of neuronal and glial cell vacuolization in the brain and the anterior horn of the spinal cord, spongiform change in the associated neuropil, spongiform change in lateral and ventral funiculi, and late fibrillary gliosis in the brainstem. There was no inflammation. Lesions were symmetric, increased in severity with time, and consistently arose at specific times in specific nuclei and areas of the brain and spinal cord. Similar, but less severe, histologic lesions were observed in corresponding areas of the central nervous system from wt-infected mice. Ultrastructurally, neuronal and glial cell vacuolization in ts1-infected mice at 31 days after inoculation was caused by dilatation of the endoplasmic reticulum and Golgi complex. Virions were observed in extremely low numbers predominantly in extracellular space and budding from membranes of neurons and glial cells. Virions were not observed in the endoplasmic reticulum or Golgi complex of neurons, nor were there cytoplasmic vacuoles that contained abnormal virions.
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PMID:Noninflammatory spongiform polioencephalomyelopathy caused by a neurotropic temperature-sensitive mutant of Moloney murine leukemia virus TB. 376 4

A variety of lymphoid cell populations were examined in terms of their ability to replicate vesicular stomatitis virus (VSV), a lytic, RNA-containing virus maturing at the cell surface. The number of cells capable of producing VSV was estimated in terms of infectious centers by the virus plaque assay (VPA), and morphologically by electron microscopy (EM). The lymphoid cells examined in this study included: (a) lymph node cells from delayed hypersensitive guinea pigs stimulated by specific antigen, (b) mouse spleen cells activated by selective bone marrow-derived (B) cell and thymus derived (T) cell mitogens, and (c) cells of human and murine continuous lymphoblastoid or lymphoma lines. In unstimulated cultures of guinea pig lymph node cells there is a background of approximately 1 in 1,000 cells which produces VSV; in purified protein derivative (PPD)-stimulated cultures the number of cells producing virus was 1.6% in the VPA and 1.9% by EM. These cells were large lymphocytes with some morphological features of transformed lymphocytes but were not typical blast cells. A few macrophages were associated with virus in both stimulated and control cultures. These observations indicate that (a) cells responsive to antigens, as detected by a marker virus, were lymphocytes; (b) cells other than lymphocytes (macrophages) were capable of replicating VSV even without antigenic stimulation; and (c) the correlation of results obtained by VPA and morphologic examination was usually quite good. Of the total number of mouse spleen cells stimulated with concanavalin (Con A), a T cell mitogen, 4.5 (EM)-5.7% (VPA) were associated with VSV. These were characteristic transformed lymphocytes, similar to phytohemagglutinin (PHA)-stimulated human lymphocytes. In contrast Escherichia coli lipopolysaccharide (LPS)-treated mouse spleen cultures contained lower numbers of virus plaque-forming cells. The majority of such cells associated with virus displayed extensive rough endoplasmic reticulum. Two cultured murine lymphomas containing lymphocytes with the theta surface marker (L5178Y and EL-4) showed a 15-100-fold higher incidence of virus-producing cells than leukemias (L1210 and C57Bl/6) which did not carry this marker. Similarly, the L2C guinea pig leukemia, a known B cell leukemia, yielded a low percent of virus plaque-forming cells (<2%). However, MOPC-104, a plasma cell tumor presumed to be of B cell origin, was found to be an efficient virus producer. There was a wide variation in the efficiency of VSV replication among human lymphoblastoid lines. One line, Wil-2, produced 80% infectious centers after 24 h of exposure to VSV, and all cells were associated with virus at the EM level. The relationship between the virus-producing cells and different lymphocyte subpopulations as well as the efficiency of the two assays for studying virus-producing lymphocytes is discussed.
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PMID:The production of vesicular stomatitis virus by antigen- or mitogen-stimulated lymphocytes and continuous lymphoblastoid lines. 434 76

Quantitative and qualitative electron microscopic studies were performed on the leukemic cells of 3 patients with stem cell leukemia, 6 patients with acute lymphoblastic leukemia, 7 patients with acute monoblastic leukemia, 3 patients with acute myeloblastic leukemia and 7 patients with acute monomyeloblastic leukemia. Significant quantitative differences were noted between some of the leukemic cells in heterochromatin:euchromatin ratios, cell size, granules per cell, amount of endoplasmic reticulum and the number of polyribosomes. Qualitative abnormalities which were found in some cells of all the leukemic groups were observed. These abnormalities included nuclear pockets, deep nuclear indentations (usually not the stem cell), nucleosomes, dilated perinuclear spaces, centrioles located in nuclear pockets (not in the stem cell or lymphoblast), accumulation of microfibrils (greatest in the monoblast and myeloblast), disrupted mitochondria with virus-like particles (none in stem cells), smaller granules and mitochondrial DNA, glycogen, and myelin whorls. The presence of the smaller granules in disrupted mitochondria and the resulting clear areas is probably related to the deranged carbohydrate metabolism of these cells. The presence of virus-like particles within mitochondria may be extremely important, but requires much more investigation. Some of the above findings may offer clues to further investigation of the acute leukemic cell.
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PMID:Acute leukemic cells. Qualitative and quantitative electron microscopy. 451 24

This article describes three patients with megakaryoblastic leukemia, in whom the blast cells were identified as megakaryoblasts by the platelet peroxidase (PPO) reaction. More than 70% of the blasts in these patients were positive for the PPO reaction. Ultrastructurally, acid phosphatase activity in the megakaryoblasts was detected in the nuclear envelope, the endoplasmic reticulum, and in a few granules, but not in the Golgi cisternae. Some blast cells were identified by immunofluorescence or immunoalkaline phosphatase, using monoclonal antiplatelet glycoprotein IIb/IIIa antibody. In one patient, most of the blasts were positive for anti-HLA-DR monoclonal antibody. The possible order of the appearance of markers in the maturation of the megakaryocytic cell lineage is postulated, based on the data from the present cases and those previously reported. PPO activity appears in very immature cells, which retain Ia-like antigens. Platelet-specific glycoprotein IIb/IIIa is seen in immature cells that are only recognized by PPO activity.
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PMID:Megakaryoblastic leukemia: the characterization and identification of megakaryoblasts. 608 61

Simultaneous detection of specific surface markers by immunogold and intracellular peroxidase activity was determined ultrastructurally in normal and leukaemic progenitors of platelets, erythrocytes and granulocytes. A new method of fixation was employed to preserve platelet peroxidase activity. Monoclonal antibodies to platelet glycoproteins labelled exclusively platelet peroxidase (PPO) positive cells, i.e. platelets, megakaryocytes and promegakaryoblasts (PMKB). In acute megakaryoblastic leukaemia, most PMKB possessed both markers while a few PMKB identified by PPO did not bind monoclonal antibodies. This result suggests that PPO appears earlier in maturation than platelet glycoproteins. Although all glycoproteins (GP) displayed fewer sites in PMKB than platelets, GP Ib was often observed in more mature megakaryocytes. Surface (glycophorin A) and intracytoplasmic markers including ferritin, intra-mitrochondrial iron and diffuse peroxidase activity due to haemoglobin of erythroid progenitors, appeared simultaneously. The number of glycophorin A sites increased with maturation. In leukaemia involving PMKB and proerythroblasts, the surface markers were coincident with the localization of peroxidase activity; glycophorin A was always absent from blasts which exhibited PPO activity localized in endoplasmic reticulum. Platelet glycoproteins were never expressed in any other cell lineage. The myeloid surface antigen was present on normal late neutrophilic promyelocytes after the cessation of myeloperoxidase synthesis. In some cases of M1 and M2 AML (FAB classification), labelling was identical to normal cells while in others the antigen appeared earlier than normal. Our findings show that the surface phenotype of blasts from non-lymphoid leukaemia and the intracellular peroxidase activity of a given cell type can be simultaneously demonstrated and analysed by electron microscopy.
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PMID:Simultaneous detection of membrane markers with monoclonal antibodies and peroxidatic activities in leukaemia: ultrastructural analysis using a new method of fixation preserving the platelet peroxidase. 609 46

A new rapid assay for inorganic pyrophosphatase has been developed and the procedure optimised for measurement of the enzyme in human neutrophils. Kinetic studies showed that the activity was optimal at pH 8.0 and was activated by Mg2+. No neutral or acid pyrophosphatase was detected. Neutrophils were homogenised in isotonic sucrose and, after low speed centrifugation the intracellular localization of pyrophosphatase was determined by analytical subcellular fractionation with sucrose density gradient centrifugation. Pyrophosphatase was shown to have a dual localization to mitochondria and cytosol. No activity could be attributed to either the endoplasmic reticulum or alkaline phosphatase-containing granules (phosphasomes). Inhibitor studies clearly show that the cytosolic and mitochondrial pyrophosphatases are due to distinct enzymes. Neutrophils were isolated from control subjects, patients with chronic granulocytic leukaemia and subjects in the third trimester of pregnancy. The specific activity (mU/mg protein) of pyrophosphatase, in contrast to that of alkaline phosphatase was similar in the three groups. Levamisole, a potent inhibitor of alkaline phosphatase had no effect on pyrophosphatase activity, confirming that this activity is not attributable to neutrophil alkaline phosphatase.
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PMID:Subcellular localization and properties of alkaline inorganic pyrophosphatase in human polymorphonuclear leucocytes. 612 Jul 71

Immunological and ultrastructural morphometric evaluation of the cytoplasmic components of cells was performed in five cases of acute lymphoblastic leukaemia of the T-cell type. All cases were a uniform group as regards clinical and immunological evaluation. On the basis of the mean cell diameter, the volume fractions and true volumes of cell organelles, cells from various cases of acute lymphoblastic leukaemia were found to be no homogeneous group. The cases examined were most homogeneous as far as the volume fraction of the Golgi apparatus and the true volumes of the cell nucleus, mitochondria, lysosomes, smooth and rough endoplasmic reticulum and Golgi apparatus were concerned.
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PMID:Morphometrical ultrastructural evaluation of the cytoplasmic components in acute lymphoblastic leukaemias of T-cell type. 618 57

Light microscopic and electron microscopic findings in thymuses from 4-week old feline leukemia virus-infected and 4- and 9-week old noninfected kittens were evaluated and found to be morphologically similar to each other. Thymuses from 9-week old feline leukemia virusinfected kittens were markedly atrophied and individual lobules within each thymus varied in the severity of atrophy. Loubules having the least severe atrophy had a moderate thinning of the cortex and a heterogeneous thymuses included intense eosinopoiesis at the corticomedullary junction, increased prominence of vasculature, and enlarged Hassal's corpuscles. In addition to these changes lobules of thymus having the most severe atrophy had a marked cortical thymocyte depletion, lobule collapse, and increased numbers of mast cells. Degeneration of epithelial cells in most lobules was indicated by electronlucency of the cytoplasmic matrix and often greatly dilated rough endoplasmic reticulum.
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PMID:Light and electron microscopic evaluation of thymuses from feline leukemia virus-infected kittens. 624 86


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