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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The amphotropic murine leukemia virus (MLV) has been shown to infect mammalian species other than mice. If this virus infects and expresses genes in cells of livestock species (cattle, sheep, and pigs) it has potential for use as a vector to produce transgenic livestock. Because the gene-injection technique for producing transgenic animals is inherently inefficient, our laboratory was interested in identifying or constructing retroviral vectors capable of infecting livestock embryos. The infectivity of an amphotropic MLV-based vector for ovine, bovine, and porcine cells was tested. Experiments were also conducted to test the ability of the amphotropic MLV promoter, compared with known strong promoters, to express genes in cells from these species. Results indicated that amphotropic MLV infects and expresses genes efficiently in porcine cells and is, therefore, a potential vector for producing transgenic pigs. Infection was not detected in cells from adult bovine and ovine species; however, low levels of infection, with subsequent gene expression, were detected in cells derived from bovine embryos.
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PMID:In vitro testing of a potential retroviral vector for producing transgenic livestock. 255 Dec 3

Transmission of the human immunodeficiency virus (HIV) and other blood-borne viruses in hospitals is discussed, and the infection control system and worker protection and education plan at San Francisco General Hospital (SFGH) are described. The acquired immunodeficiency syndrome (AIDS) epidemic has led to increased concern about occupationally acquired infections in health-care workers. As the number of HIV-infected persons increases, so does the risk of infection. Occupationally acquired HIV infection of health-care workers occurs principally in nurses, phlebotomists, and laboratory technicians through accidental subcutaneous injection of contaminated blood; splashing of blood onto open skin lesions, the eyes, and mucous membranes represents another route of exposure. The risk of infection from a single needle-stick exposure to HIV-infected blood is about 0.4%. Other blood-borne viruses to which employees are vulnerable include hepatitis B virus and human T-cell lymphotropic viruses, which may cause leukemia and lymphoma. SFGH has a comprehensive infection control system. Specimen containers are enclosed in transparent secondary containers, the worker is encouraged to wear protective clothing when necessary, and specific needle-stick precautions are promoted. There is also a health-care worker protection and education plan. The employee health services department provides immunizations, keeps records on accidental exposures, and operates a hot line. The education committee disseminates educational materials and arranges lectures. Infection control and education provide simple but effective measures for protecting hospital employees against HIV and other occupationally acquired infections.
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PMID:Infection of the health-care worker by HIV and other blood-borne viruses: risks, protection, and education. 261 Feb 20

Ten patients with plasma cell leukaemia (PCL), out of 259 cases of multiple myeloma diagnosed in the Haematology Service of the University Hospital of Barcelona in the last 18 years, are presented. Of the 10 PCL cases, 5 were primary and 5 were secondary. Anaemia and thrombocytopenia, along with massive plasma cell infiltration of the bone marrow, were the most striking findings. Osteolytic lesions were present in 9 of the cases and liver involvement in two. Chemotherapy including vincristine and prednisone was administered to eight patients, associated to alkylating agents (melphalan and/or cyclophosphamide) in six of them. Four of these patients received also adriamycin and BCNU. Two objective responses were achieved, lasting for 10 and 3 months, the remaining six patients failed to respond. The median survival for all the PCL patients was less than one month (ranging between 0.2 and 14 months). None of the secondary PCL patients survived for 2 months after diagnosis. Infection (3 cases of septicaemia and 3 of pneumonia), renal failure (2 cases) and liver insufficiency (1 case) were the causes of death in the nine deceased patients. The therapeutic possibilities for this severe haemopathy are discussed.
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PMID:[Plasma cell leukemia. Study of 10 cases]. 265 43

Enterobacter cloacae, sensitive to third-generation cephalosporins (cefotaxime and ceftazidime), was isolated from the stoma of a patient with leukaemia. One month later, he developed a fatal septicaemia, caused by an identical strain isolated from blood cultures. He had been treated with several antibacterial agents, including cefotaxime. The blood culture strain seemed to be a mixture of four variants with different resistance patterns to cefotaxime and ceftazidime. One variant was extremely sensitive to third-generation cephalosporins, one was completely resistant, and two showed variations in zone diameter within sensitivity group 2, both for cefotaxime and ceftazidime. Minimal inhibitory concentration (MIC) studies also showed different resistance patterns between the four variants. Similar variants were found when the stoma isolate was further investigated.
Infection
PMID:Septicaemia caused by an Enterobacter cloacae strain varying in resistance against cephalosporins. 273 58

Infection of mice with Moloney murine leukaemia virus (MuLV) induces T-cell lymphomas after an average latency period of 150 days. In these lymphomas the MuLV DNA is frequently integrated into the mouse chromosomal DNA in the vicinity of the pim-1 oncogene. Transgenic mice overexpressing the pim-1 oncogene are predisposed to develop T-cell lymphomas, but only to the extent that approximately 10% of the mice develop a lymphoma within 240 days. When these mice are infected with MuLV, lymphomas develop in all mice in only 50-60 days. In these lymphomas MuLV DNA is integrated near either the c-myc or N-myc gene, suggesting that pim-1 and myc synergize in lymphomagenesis. To determine whether this system has a more general application, we have now tested the susceptibility of pim-1 transgenic mice to N-ethyl-N-nitrosourea (ENU), a chemical carcinogen. With a single low dose of ENU, nearly all pim-1 transgenic mice, but only 15% of non-transgenic mice, develop T-cell lymphomas within 200 days. All ENU-induced lymphomas in both pim-1 transgenic and non-transgenic mice express high levels of c-myc messenger RNA, supporting the notion that pim-1 and c-myc synergize in lymphoma induction. We propose that pim-1 transgenic mice could be used to test the oncogenic potential of other chemical compounds.
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PMID:Very high frequency of lymphoma induction by a chemical carcinogen in pim-1 transgenic mice. 278 94

The hematopoietic disregulation in adult mice induced by the malignant histiocytosis sarcoma virus (MHSV) and the Harvey murine sarcoma virus (Ha-MuSV), which both possess c-Ha-ras-related oncogenic sequences, was investigated. Spleen focus formation induced by MHSV and Ha-MuSV was not restricted by the Fv-2 resistance locus in congenic DDD and C57BL/6 mice, unlike leukemogenesis induced by Friend virus, Rauscher virus, and the myeloproliferative sarcoma virus (MPSV). C57BL/6 mice were much more resistant to MHSV and Ha-MuSV-induced spleen focus formation than DDD mice regardless of their Fv-2 state. Infection of DDD mice with MHSV caused a systemic histiocytic neoplasia, best described as murine malignant histiocytosis. Transformed histiocytic cells proliferated excessively in the bone marrow, spleen, and lymph nodes and, in the final stages of the disease, in all major parenchymal organs. The Ha-MuSV caused a strikingly different benign histiocytic tumor in DDD mice and, unlike MHSV, did not induce a rapid, progressive splenomegaly in C57BL/6 mice. Infection of DDD mice with MHSV induced a rapid and synchronized depletion of early and late erythroid precursor cell pools. In MHSV-infected C57BL/6 mice comparable changes were observed with dissimilar kinetics. Macrophage colony-forming cells of MHSV-infected mice were increased in number and proliferated independently of stimulating growth factors. The disease induced by MHSV in mice can thus serve as a model for malignant histiocytosis in humans.
Leukemia 1987 Jan
PMID:Murine retrovirus-induced malignant histiocytosis, an experimental model for the disease in humans. 282 12

The occurrence of potential leukemia cells (PLC) among bone marrow, spleen, and thymus of AKR mice during the preleukemic period was tested by an in vivo transplantation bioassay. The presence of PLC in 30- and 75-day-old AKR mice was demonstrated mostly among bone marrow cells, less in spleen, and was lacking in thymus. Occurrence of PLC in young AKR mice was shown to be thymus independent. However, progression of PLC from young donors (14-80 days old) into overt leukemia following transplantation into F1 recipients was shown to be dependent on specific host conditions including an intact thymus and an Fv-1nn allele. In contrast, PLC from 7-9-month-old AKR mice or frank leukemic cells when transplanted grew in any intact or thymectomized histocompatible host, thereby indicating their autonomous growth state. Infection of 2-week-old AKR mice with the dual-tropic virus DTV-70 induced characteristic changes in the thymus and accelerated leukemia development. DTV-70 inoculation into 14-day-old AKR mice did not change the spontaneous PLC distribution pattern in the tested host organs within 30 days postinfection, nor did it change PLC-specific host requirements for further progression into leukemic cells; however, it enhanced PLC transition to autonomous leukemic cells. The preferential cell tropism of DTV-70 for target cells (prothymocytes) among bone marrow and young spleen cells rather than for thymocytes was also demonstrated in an in vitro-in vivo test. The dual tropic virus may act as a promoter on preexisting PLC (present mostly among bone marrow cells) by enhancing their ability to progress into autonomous leukemic cells.
Leukemia 1987 May
PMID:Enhanced AKR leukemogenesis by the dual tropic viruses. I. The time and site of origin of potential leukemic cells. 282 20

The effect of infecting fibroblasts with Kirsten murine sarcoma virus/murine leukemia virus (Ki-MSV/MLV) on constitutive and IFN-gamma-induced H-2 antigen expression was investigated. The fibroblasts used were two established cell lines (C3H10T1/2 and BALB/c3T3) and fresh embryo fibroblasts from C3H mice. Class I antigens were expressed constitutively by BALB/c3T3; infection with MLV, MSV or the two together had little effect on this constitutive expression. Class I antigens (H-2K, H-2D) were strongly induced on all three types of fibroblast by rIFN-gamma, and infection had little effect on this. None of the fibroblasts expressed constitutively detectable levels of class II antigen; however, C3H10T1/2 fibroblasts could be induced for both H-2A and H-2E by IFN-gamma. Infection of C3H10T1/2 with helper-free Ki-MSV, or MSV together with MLV, completely abolished this induction of class II antigens, while infection with MLV alone had little effect, implying that the abolition of class II induction was due to genomic regions of Ki-MSV not shared with Ki-MLV, probably the v-Ki-ras gene.
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PMID:Kirsten murine sarcoma virus abolishes interferon gamma-induced class II but not class I major histocompatibility antigen expression in a murine fibroblast line. 283 Dec 93

Infection by LP-BM5 murine leukemia virus (MuLV) suppressed significantly the percentage of peripheral blood cells showing surface markers for macrophages, lymphocytes and activated lymphoid cells. Chronic administration of a 7% (36% calories) ethanol diet or injection of 1.9 mg/mouse/day of morphine for a 7 day period were followed by 3 week periods of abstinence and then 1 week periods of consumption of 5% ethanol diets or morphine injection to female C57BL/6 mice resulted in changes in the numbers of macrophages and lymphocyte subsets. The number of lymphocytes of various subsets were not significantly changed by the ethanol exposure except those showing activation markers which were reduced. The percentage of peripheral blood cells showing markers for macrophage functions and their activation were significantly reduced after "binge" use of ethanol. Ethanol retarded suppression of cells by retroviral infection. However by 25 weeks of infection there was a 8.6% survival in the ethanol fed mice infected with retrovirus which was much less than virally infected controls (45.0%). Morphine treatment also increased the percentage of cells with markers for macrophages and activated macrophages in virally infected mice, while suppressing them in uninfected mice. The second and third morphine injection series suppressed lymphocyte T-helper and T-suppressor cells, but not total T cells. However, suppression by morphine was significantly less during retroviral disease than suppression caused by the virus only. At 25 weeks of infection 44.8% of morphine treated, infected mice survived. Morphine treatment also caused deaths such that the survival in morphine treated, retrovirally infected was higher than would have been expected if the death rate in virally infected, and morphine injected animals were combined during combined treatment. Thus these drugs of abuse can modulate peripheral blood lymphoid subsets, suppression caused by retroviral infection, and survival.
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PMID:Changes in lymphocyte and macrophage subsets due to morphine and ethanol treatment during a retrovirus infection causing murine AIDS. 284 47

Infection by LP-BM5 murine leukemia virus (MuLV) produces an AIDS-like condition in mice. The viral infection suppressed the percentage of peripheral blood cells showing surface markers for macrophages, activated macrophages, T lymphocytes and activated lymphoid cells. High dietary vitamin A (retinyl palmitate) caused increased numbers of activated macrophages. It also increased the percentage of cells with markers for Ia+ cells and macrophages in the retrovirally infected mice compared to infected controls. In uninfected mice retinyl palmitate stimulated the percentage of cells with activated lymphocytes bearing IL-2R, and T cytotoxic cells. These were associated with a retarded death rate during infection with LP-BM5 murine leukemia in C57BL/6 mice. By 25 weeks of infection and 20 weeks of retinyl palmitate supplementation 71.3% survived, while 45.0% virally infected controls survived. The mice also had elevated numbers of B cells measured in the blood after 4 and 8 weeks of dietary treatment. Vitamin A stimulation may play a role in the slower death rate for retrovirally infected mice.
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PMID:Enhanced survival by vitamin A supplementation during a retrovirus infection causing murine AIDS. 284 48


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