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 diagnosis and successful control of systemic Aspergillus niger infection in 2 adult patients with acute leukemia is reported. During induction therapy, the first patient developed pulmonary infiltrates, skin lesions and abnormal liver function tests. Aspergillus niger was found on skin and liver biopsy. This patient was successfully treated with Amphotericin B and granulocyte transfusions and he remains in remission. The second patient developed a pneumonitis and adynamic ileus with positive sputum and stool cultures for Aspergillus niger. The infection only responded to Amphotericin B and granulocyte transfusions and the leukemia to cytoreductive chemotherapy. The patient later relapsed and died after a febrile illness. Fungi morpholocially consistent with Aspergillus were found in the liver at autopsy. Infection with A. niger is rare even in this patient population; however fungal infections have become an increasing problem. The need for a high index of suspicion, especially when an infection is unresponsive to antibacterial antibiotics, the various diagnostic tools, and the need for aggressive therapy are stressed. Amphotericin B is the chemotherapy of choice but may be insufficient in a severely neutropenic host where the simultaneous use of granulocyte transfusions might be lifesaving.
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PMID:Successful control of systemic Aspergillus niger infections in two patients with acute leukemia. 106 May 8

Infection of Swiss mouse 3T3FL cells with a clonal isolate of Moloney leukemia virus (MLV-IC) resulted in virus progeny composed of at least three different murine helper oncornaviruses. Each entity was purified in appropriate cells by several sequential terminal dilution isolations and was grouwn to high titers. Besides ecotropic MLV-IC there was a pure xenotropic virus and a third novel virus with properties of both eco- and xenotropic viruses. The purified xenotropic virus had a wide host range, was restricted in mouse cells, and was inactivated by normal mouse sera like other xenotropic isolates. The purified virus with hybrid properties (HIX) could infect a wide range of mammalian cells, which included both N and B mouse cells. HIX gave single-hit titrations with equal titers on both mouse and cat indicator cells. Envelope properties of HIX were examined by virus preinfection interference, by interference involving viral glycoprotein, and by neutralization with specific antisera. Both xenotropic and MLV-IC type ecotropic determinants were found on the virus coat. The origins of HIX and the xenotropic virus were investigated in detail. The original MLV-IC stock had HIX type virus in low titer but no detectable pure xenotropic virus. Infection of mouse cells with a single infectious unit of the ecotropic virus from the MLV-IC virus stocks could at times give rise to HIX type virus. HIX type virus, passed once through heterologous rat cells, was subjected to long-term passage either in infected mouse or cat cells. After several months HIX type virus disappeared from some mouse and cat cell systems. The possible hybrid nature of HIX and the origins of newly appearing xenotropic viruses are discussed.
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PMID:A novel murine oncornavirus with dual eco- and xenotropic properties. 106 Nov

Investigations were carried out on 261 patients with chronic lymphatic leukaemia with survival over 4 years. The following problems were discussed: age and sex of patients, presenting symptoms, organ changes, laboratory investigations, infectious complications, coexistence of malignant tumours. Correlations were established between various parameters and the length of survival. It was demonstrated that patients without palpable lymph nodes and spleen at the beginning of the diseases and with leucocyte counts ranging from 10,000 to 100,000/1 mm-3 have a better prognosis, while thrombocytopenia even without haemorrhagic diathesis is a poor prognostic sign. Infections were observed in 50 percent of cases, more frequently in patients with hypogammaglobulinaemia. Coexistence of malignant tumours was found in 5.4 percent of cases. Pathological examinations including organ biopsy and autopsy failed to demonstrate characteristic features of lymphatic system proliferation as compared with patients with short survival.
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PMID:[Clinical and pathological analysis of patients with chronic lymphatic leukemia and long survival]. 112 36

Infection of adult CBA mice with Rauscher or Moloney leukaemia virus concomitantly with caseination significantly accelerated spleen amyloid development in irradiated, bone-marrow protected mice, but had no effect on untreated, adult thymectomized or thymectomized irradiated mice. Spleen tissue of mice infected with Moloney virus had the highest titre in the mice with accelerated amyloid development.
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PMID:The effect of Rauscher and Moloney leukaemia virus on amyloid development in casein-treated CBA mice. 116 70

We report on two patients with acute leukemia and prolonged granulocytopenia after cytotoxic therapy in whom the diagnosis hepatosplenic candidiasis was made. Both patients developed upper abdominal discomfort with elevated alkaline phosphatase after resolution of granulocytopenia. The diagnosis was established by demonstration of multiple abscesses in liver and spleen on ultrasound and computed tomography. Both patients were initially treated with amphotericin B i.v., one of them received liposomal amphotericin B (cumulative dose of 2,530 mg and 570 mg, respectively). Thereafter, therapy was continued for months with oral fluconazole. The treatment of hepatosplenic candidiasis was successful, however, the patients died from relapse and progression of leukemia.
Infection
PMID:Hepatosplenic candidiasis, a fatal disease? 129 53

Infection by exogenous avian leukosis viruses (ALVs) causes economic loss from neoplastic mortality and from impaired performance of subclinically infected chickens. This paper reviews progress in research related to natural infection and its control. Subgroup A ALVs causing lymphoid leukosis are the most common viruses in the field, but variant viruses can arise and cause losses. In Israel in recent years, epidemic outbreaks of haemangiosarcomas caused by a virus of unusual cytopathogenicity have occurred. In the UK, an ALV belonging to a new subgroup for chickens has been recently isolated; this virus is able to cause myeloid leukosis and nephromas. ALV infection of commercial stock is controlled by virus eradication schemes that prevent vertical transmission of ALV from one generation to the next. In this regard, endogenous leukosis viruses and ev loci, notably ev21 linked to the K slow-feathering gene, have been shown to have a detrimental influence on responses to infection by exogenous ALVs, and on the success of eradication schemes. Tolerogenic properties of the ev loci are involved. Attention has also been directed to whether ev loci have any direct influence on performance traits. Although eradication provides the main means of controlling ALV, the development of transgenic techniques in chickens has renewed interest in genetic resistance, and some progress has also been made in developing recombinant vaccines.
Leukemia 1992
PMID:Developments in avian leukosis research. 131 66

Infection with helper-free, defective MAIDS murine leukemia virus (MuLV) caused a rapid polyclonal activation of B cells in 0.75-, 2-, and 6-month-old C57L/J mice (H-2b, Fv-1n/n), similar to that in C57BL/6 mice (H-2b, Fv-1b/b), which was recognized by elevated plasma immunoglobulin concentrations. However, changes in plasma immunoglobulin levels differed in C57BL/J and C57BL/6 mice. In C57L/J mice, infection resulted in a rapid increase in plasma IgM and IgG2a, and the elevation of IgG2a persisted undiminished for 21 weeks. Levels of IgG2b also became slightly elevated, but those of IgG1 and IgG3 were not significantly affected. Plasma of 6 to 7-month-old C57BL/6 mice contained already high levels of IgM (30-40 mg/ml), which persisted undiminished in uninfected mice but decreased progressively in infected mice to 10% of the original concentration during 25 weeks of observation. In C57BL/6 mice, plasma IgG1 and IgG2b as well as IgG2a became similarly elevated after infection but also only transiently. Their levels began to decrease progressively about 10 weeks after infection and fell to far below the maximum concentration observed. The drastic loss of plasma IgM and IgGs observed in C57BL/6 mice during the later stages of MAIDS MuLV infection did not seem to be a consequence of the polyclonal activation of B cells per se but seemed to reflect additional immunological abnormalities arising in infected C57BL/6 but not C57L/J mice. In both mouse strains these changes in plasma Ig levels correlated with the formation of Ig-containing immune complexes that bound to high-affinity, protein-binding ELISA plates in the absence of antigen coating, which may represent unusual forms of self-antigen-antibody complexes.
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PMID:Correlation between levels of immunoglobulins and immune complexes in plasma of C57BL/6 and C57L/J mice infected with MAIDS retrovirus. 131 70

Infection with cytomegalovirus (CMV) is a major feature of acquired immunodeficiency syndrome (AIDS). Gastrointestinal involvement is being seen more frequently. Our collective experience involves nine patients with stomach involvement. Seven patients were intravenous drug abusers or homosexuals with AIDS. One developed CMV gastritis as a complication of leukemia and one patient was a West African with lymphoma and human immunodeficiency virus (HIV) infection. All our patients had biopsy-proven CMV inclusion bodies. The radiographic appearances varied widely. The findings included markedly thickened edematous folds, erosive gastritis with aphthous ulceration, and superficial and deep ulceration. One patient had deep ulceration with fistula formation. Computed tomographic (CT) scans confirmed the greatly thickened gastric wall and coarsened folds in two patients. Associated gastrointestinal infections included candida and herpes, and, in addition, pneumocystis carinii pneumonia (PCP) was present in two patients. CMV gastritis may mimic several other conditions including erosive gastritis, peptic ulceration, lymphoma, and carcinoma. It should be strongly considered in immunosuppressed patients.
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PMID:Cytomegalovirus gastritis: protean radiologic features. 131 63

Marrow stromal fibroblasts (FBs) likely play an important role in the regulation of hematopoiesis within the marrow microenvironment. Infection of these cells by feline leukemia virus (FeLV) might not only contribute to the pathogenesis of FeLV-induced hematologic diseases, but could provide a reservoir for virus in the infected cat. To determine the frequency of FeLV infection among marrow FB precursor cells (fibroblast colony-forming units, CFU-F) of cats viremic with FeLV-C/Sarma and FeLV-A/61E, marrow FBs and FB cell clones were isolated and assayed for expression of FeLV gag protein. From 30% to 86% and 64% to 88% of marrow FB precursors were infected with FeLV-C/Sarma and FeLV-A/61E, respectively. CFU-F from a cat viremic with FeLV-A/61E were not affected by exposure to antibody against FeLV envelope glycoprotein gp70 and heterologous complement, whereas similarly treated hematopoietic progenitors (erythroid colony-forming units, CFU-E; erythroid burst-forming units, BFU-E; and granulocyte-macrophage colony-forming units, CFU-GM) and culture-propagated, FeLV-infected marrow FBs were effectively lysed, suggesting that infected CFU-F within the marrow microenvironment do not express a significant amount of gp70 on their cell membranes. Thus, marrow FB precursor cells appear to be a major target for FeLV in vivo. Furthermore, the low level of gp70 antigen expression on the surface of these cells in vivo may allow them to escape immune surveillance and provide a reservoir of virus during active or latent infection.
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PMID:In vivo infection of marrow stromal fibroblasts by feline leukemia virus. 132 84

LP-BM5 murine leukemia virus (MuLV) infection induces an immunodeficient state in susceptible strains of mice. It has been previously characterized at the level of spleen and peripheral lymph nodes. We recently demonstrated that LP-BM5 MuLV-infected mice lost intestinal host resistance to common opportunistic pathogens. In this article we investigated how murine retroviral infection alters the differentiation of IgA B cell precursors in Peyer's patches (PP), mesenteric lymph nodes (MLN), and the intestinal lamina propria (ILP). After 4 months of LP-BM5 MuLV infection, there was a significant decrease in the absolute numbers of Thy1+, CD4+, and CD8+ cells in PP with a concomitant decrease in the percentage and in the absolute numbers of surface IgA+--(sIgA+) and surface IgM+--bearing (sIgM+) cells. Infection also produced an enlarged MLN with a six-fold increase in cell numbers and a decrease in the relative percentage of sIgA+, cytoplasmic IgA+, and cytoplasmic IgM+ cells. However, murine retrovirus infection caused no significant changes in the percentages of Thyl+, CD4+, CD8+, and CD5+ cells in the MLN. After 4 months of murine retrovirus infection cIgA+ cells from MLN were not able to populate the intestinal lamina propria as the number of IgA plasma cells was significantly decreased. Moreover, there was a concomitant decrease in the number of CD4+ cells per field in the ILP. These results suggest that murine retrovirus infection favors the expansion of IgA B cell precursors at the level of MLN, while simultaneously interfering with the terminal differentiation step and thus preventing IgA plasma cell precursors from seeding the ILP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suppressed mucosal lymphocyte populations by LP-BM5 murine leukemia virus infection producing murine AIDS. 133 92


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