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)

Mouse cells (line N cIA cl10) contain 1.2-2.5 ng murine leukaemia virus (MuLV) p30 antigen/mg of protein; this amount of antigen is measurable by competition radioimmunoassay (RIA) but is not detectable by indirect immunofluorescence (IF). Infection of N cIA cl10 cells with herpes simplex virus type 2 (HSV-2) induces expression of MuLV p30. Induction by HSV-2 does not require either cell or virus DNA synthesis and is optimal 8 h post infection when cells at 50-70% confluence are infected at a multiplicity of infection (MOI) of 5-8 PFU/cell. At an MOI of 2.5, 70-80% of the cells express HSV antigens while none of the cells express p30; at an MOI of 5.0, 70-80% of the cells express HSV antigens but 55% of the cells express p30. Using the conditions reported in this paper for preparation of competing antigen, induction of p30 by HSV-2 (strain 333) infection is not measurable by competition RIA.
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PMID:Conditions required for induction of murine p30 by herpes simplex virus. 21 Jan 28

Horizontally transmitted viruses have been etiologically linked to leukemia and lymphoma in several higher mammals (gibbons, cows, and cats). In the best-studied example, the cat, feline leukemia virus is a common community-acquired virus that infrequently produces cancer. However, the infection and its complications (cancer) are not typical of infectious diseases. Epidemilogically, serologically, and virologically, infections with this type of virus can contradict classic infectious disease dogma. Therefore, previous studies that failed to link characteristics of infectious diseases (epidemiologic, serologic, or virologic) to human cancer must be cautiously interpreted. A link between retroviruses and/or DNA viruses and human lympho-reticular malignancies is hypothesized, and it is suggested that systematized nation-wide studies of selected cancer patients and their contacts be executed with the most sensitive and specific laboratory probes available.
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PMID:Leukemia and lymphoma: infrequent manifestations of common viral infections? A review. 21 56

An in vitro hematopoietic microenvironment was established from explained fragments of bone marrow from adult noninbred NIH Swiss mice with the use of corticosteroid-reconstituted horse serum. Infection with Kirsten murine sarcoma virus (Ki-MuSV) with either a Rauscher murine leukemia virus (R-MuLV) or Balb:virus-1 helper virus coat reduced proliferation of granulocytic and pluripotent hematopoietic stem cells and produced neoplastic transformation of both macrophages and preadipocytes in the adherent cell population within a 4-week period. Ki-MuSV-transformed, virus-releasing macrophages formed clusters of 4-49 cells in 0.8% methylcellulose-containing medium in the absence of added colony-stimulating factor (CSF), synthesized lysozyme, ASD-chloroacetate substrate-specific esterase-M, and CSF, and produced tumors following inoculation iv into adult NIH Swiss mice or ip into newborn NIH Swiss mice. In cultures infected with helper leukemia viruses R-MuLV or Balb:virus-1, gradual transformation of a distinct cell phenotype was observed over a 9-week period with generation of increasing numbers of atypical myeloblasts and promyelocytes which showed dyssynchronous nuclear-cytoplasmic maturation, basophilic granulation, cytoplasmic vacuolation, and formation of incompletely maturing CSF-dependent granulocyte-macrophage colonies in vitro and small spleen colonies in vivo. These data demonstrated that rapid biologic expression of the murine sarcoma virus genome in specific adherent "stromal" marrow cells prevents detection of a more subtle helper-virus-induced dysmyelopoiesis in a distinct nonadherent cell population.
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PMID:Phenotypically distinct target cells for murine sarcoma virus and murine leukemia virus marrow transformation in vitro. 21 35

Clones of mouse myeloid leukemic cells that differ in their competence to be induced for normal cell differentiation by the protein inducer MGI produce type C virus. These viruses have been studied for their effect on the viability, multiplication, and differentiation of normal bone marrow cells either with or without the addition of MGI. Virus from leukemic clones that can differentiate normally to mature macrophages and granulocytes (MGI+D+ clones) induced some multiplication of myeloblasts in the bone marrow, but the cells did not differentiate without adding MGI. In the presence of MGI, this virus then induced an increased number of colonies whose cells differentiated to mature macrophages or granulocytes as in colonies of uninfected cells. Virus infection also resulted in a decrease in the amount of MGI and fetal calf serum that was required for colony formation. Virus from MGI+D+ clones, in the presence of MGI, was 500-fold more effective in increasing colony formation than virus from the differentiation-defective MGI-D- clones, although both types of virus replicated with equal efficiency in the normal bone marrow cells. No such increase was obtained after infection with the Friend leukemic virus complex or the Moloney murine leukemia virus. Infection with virus from a MGI+D+ clone that was differentiated by MGI mainly to macrophages induced a higher percentage of macrophage colonies than virus from MGI+D+ clones that were differentiated by MGI to granulocytes and macrophages. Studies with isolated myeloblast colony-forming cells from the bone marrow have indicated that these are the target cells for the virus. Infections of these isolated myeloblasts with virus from MGI+D+ clones induced some multiplication without differentiation in the absence of MGI, and increased the viability and multiplication of the myeloblasts without inhibiting their ability to differentiate in the presence of MGI. The results, therefore, indicate that virus from MGI+D+ cells can increase the viability and multiplication of normal myeloblasts in the bone marrow without blocking the ability of these cells to be induced to differentiate by MGI, and that this effect was directly related to the competence of the leukemic host cells to be induced for normal differentiation. It is suggested that the difference between the effect of virus from MGI+D+ and MGI-D- cells may be due to a difference in their integration sites in relation to the genes that control cell viability, multiplication, and differentiation.
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PMID:Increase of normal myeloblast viability and multiplication without blocking differentiation by type C RNA virus from myeloid leukemic cells. 22 69

Infection of C3H mice with live or UV-inactivated murine cytomegalovirus (MCMV) was able to generate population(s) of lymphocytes in the spleen (CTL) which could exert a lytic effect against L cells infected with MCMV but not against uninfected or those infected with HSV-1. The effector cells proved to be theta-bearing T cells and the lysis of target cells was H-2 restricted. Data presented show that early viral protein synthesis but not viral DNA synthesis was necessary for the appearance of relevant antigenic determinant(s) on target cells. The results of co-capping experiments suggest that H-2 molecules may have close association with MCMV induced product(s) as also with murine leukemia virus glycoprotein (gp70) which is carried by normal L cells. Despite this observation, anti-H-2 serum effectively blocked the cytolysis whereas anti-gp70 and anti-MCMV sera failed. Anti-MCMV serum was effective in blocking cytolysis, only if the L cells were infected for 24 hours and then used as targets. MCMV infected L cells which were coated externally with inactivated Sendai virus could be effectively recognised by MCMV as also by sendai specific CTL. That the cytotoxicity exerted on such targets was of specific nature was revealed by the results of competitive blocking experiments with unlabelled targets.
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PMID:Induction of virus specific and H-2 restricted cytotoxic T cells by UV inactivated murine cytomegalovirus. 22 35

In a cooperative study on the efficiency of isolation and decontamination in patients with acute leukaemia performed in seven hospitals in Europe, faecal samples and oral washings were collected twice weekly and shipped for culturing to a Central Bacteriological Laboratory. In this laboratory the Enterobacteriaceae species isolated from these samples were biotyped as well as those isolated from infections that occurred in these patients during treatment. Enterobacteriaceae biotypes isolated for the first time during the isolation phase of the patient indicated a leak in the isolation system. The "colonizing" (newly resident) biotypes of Enterobacteriaceae species were found to be more often involved in infections and to be more commonly distributed among the patients in the participating hospitals than the "contaminating" (transient) Enterobacteriaceae biotypes. Furthermore, a linear correlation was found between the incidence of gram-negative infections and the number of cases in which these Enterobacteriaceae biotypes colonized the gastro-intestinal tract of patients. The majority of the infections was caused by Enterobacteriaceae biotypes that had settled in the gastro-intestinal tract during treatment and consequently were of nosocomial origin.
Infection 1977
PMID:Infection by the distribution of biotypes of enterobacteriacease species in leukaemic patients treated under ward conditions and in units for protective isolation in seven hospitals in Europe. 26 42

Twenty-four consecutive deaths from a total of 70 children receiving treatment for acute lymphoblastic leukaemia (ALL) have been reviewed. An attempt has been made to ascribe the cause of death to either infection, haemorrhage, the leukaemia itself, or a combination of these factors. No child was free of infection at death. Infection, with or without haemorrhage, was responsible for the deaths of all 15 children whose leukaemia had not relapsed. Although infection was present at death in all 9 children whose leukaemia had relapsed, the leukaemia process itself was also a major contributing factor. Viruses were associated with death in many of the children and may be emerging as important pathogens in children with ALL. Familiarity with a protocol may be an important factor in the prevention of fatal infections in such children. Centralization of treatment is necessary if this expertise is to be acquired.
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PMID:Role of infection in the death of children with acute lymphoblastic leukaemia. 27 Sep 64

Infection of adult C57BL/6 mice with variants of the radiation leukemia virus resulted in variable leukemia incidence. One variant, designated D-RadLV, induced lymphatic leukemia in 0 to 25% of mice after virus inoculation directly into the thymus of young adult mice. The leukemia incidence could be increased to 80 to 100% by host exposure to x-rays. The second variant, A-RadLV, induced lymphatic leukemia in 80 to 100% of similarly inoculated mice without the need for additional radiation treatment. Adult mice were inoculated with D-radLV or A-RadLV. Both variants reduced the immune response to sheep erythrocytes whereas only D-RadLV had an immunosuppressive effect after immunization with a thymus-independent immunogen polyvinyl-pyrrolidone (PVP). Results of transfer experiments indicated that the immunosuppressive effects were expressed at the immunocompetent cell level. Thymus-derived cells were affected by A-RadLV since their immunocompetent function was impaired, whereas D-RadLV affected the marrow cell population of immunocytes. Exposure of D-RadLV-inoculated mice to x-rays induced functional impairment of both thymus and marrow cells. Since the radiation leukemia virus induces "T" lymphatic leukemia it could be proposed that the initial tropism of the virus to thymocytes would lead to high leukemia induction potential, whereas virus tropism to bone marrow cells would yield a low leukemia incidence. The coleukemogenic effect of x-rays could perhaps be related with its capacity to alter and introduce a change in virus-lymphoid cells interaction.
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PMID:Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. I. Cellular analysis of immunosuppression. 32 Feb 61

Thirty-six febrile neutropenic episodes were treated by granulocyte transfusions in 33 children. Septicemia and mucous membrane ulcerations were most commonly associated with the fever. Infection cleared in 81% of the episodes, eight per cent ended in death from bacterial infections, 11% from nonbacterial infections or hemorrhage. The median number of polymorphonuclear leukocytes given was 1.1 X 10(10)/m2/transfusion. Two to twenty-eight (median 8.5) transfusions were given over 3--34 days (median 10.5). The source of cells (parental or random) and the method of collection did not seem to affect the outcome. None of the 23 patients whose marrow recovered during the transfusions died of bacterial infections. Infection cleared even without marrow recovery in 62% of the patients, but then only 25% lived for more than two months after clearing of sepsis. In a subgroup of patients with nonlymphoblastic leukemia on the same chemotherapy and antibiotic treatment protocol, 8/11 (73%) survived bacteremia when white cell support was available; only 2/11 (18%) of a historical control group survived when such support was not available. Granulocyte support appears to be a valuable tool in helping neutropenic patients overcome their infections or, at the very least, helping them survive long enough for normal marrow recovery to occur.
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PMID:Granulocyte transfusions in infected neutropenic children with malignancies. 44 Feb 6

Infection of BALB/c mice with Rauscher leukemia virus (RLV) gives rise to pronounced erythrocytopoiesis manifesting in splenomegaly and is associated with progressive development of anemia. In the spleen erythroid colony forming units (CFU-E) increase exponentially up to 800-fold that of normal levels by the third week of infection. In vitro these CFU-E are dependent on erythropoietin for colony formation, their erythropoietin requirements being higher than that of CFU-E from normal mice. Numbers of CFU-E in spleen and degree of splenomegaly in anemic RLV infected mice were also shown to be modified by red blood cell transfusion, but progression of the disease was not stopped. Erythroid burst forming units (BFU-E) were also responsive to erythropoietin. However, a small proportion of cells also formed BFU-E colonies at concentrations which did not support growth of normal marrow BFU-E. When compared to normal, CFU-E found in RLV-infected spleen have similar velocity sedimentation rates. However, buoyant density separation of leukemic spleen cells indicated that CFU-E were more homogeneous (modal density 1.0695 g/cm3) than CFU-E from normal spleen. Analysis of physical properties of CFU-E and the nonhemoglobinized erythroblast-like cells, which accumulate in the spleen showed that they differed mainly in their distribution of cell diameter. Our findings show that erythroid progenitor cells in RLV infected mice are responsive to erythropoietin in vitro. Also in vivo erythropoiesis appears to be under control of erythropoietin but other factors which lead to progression of RLV disease apparently exist. Most proerythroblast-like cells, which are characteristic of this disease, apparently lack the potential to form colonies and may be more mature than CFU-E.
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PMID:Erythropoietin responses and physical characterization of erythroid progenitor cells in Rauscher virus infected BALB/c mice. 46 21


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