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)

Glomerulonephritis constitutes an important category of renal diseases in animals and has been recognized with increasing frequency in the last decade. We report here the comparative morphologic aspects of glomerulonephritis as a naturally occurring disease of animals. We briefly review the immunopathogenesis of glomerulonephritis. The morphology of renal lesions occurring in glomerulonephritis in dogs, cats, cattle, sheep, horses and swine has been reviewed with emphasis on the range and specificity of various glomerular lesions and on the comparison of lesions between various species. A distinction was made between glomerulonephritis as a primary disease entity and glomerulonephritis associated with other disease processes. Primary idiopathic glomerulonephritis occurred in all species but was most commonly recognized as a clinically important disease in dogs and cats. Glomerulonephritis also occurred in association with other diseases such as equine infectious anemia, chronic hog cholera, canine pyometra, dirofilariasis, feline leukemia virus infection and canine systemic lupus erythematosus.
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PMID:Comparative pathology of glomerulonephritis in animals. 44 47

Several case reports6-8 in the literature have pointed out that a clinical and morphologic picture resembling that of acute leukemia may be secondary to infection or use of toxic drugs or alcohol. In these cases, the leukemic picture spontaneously returns to normal when the precipitating factor is no longer present. This condition has been termed pseudoleukemia. Unless the history of a precipitating factor is clear, the patient may be wrongly treated for leukemia. In the case reported here, initial findings suggested acute promyelocytic leukemia and chemotherapy was planned, but further investigation indicated that the condition was essentially reactive and related to a presumed viral infection. Even though pseudoleukemia is sometimes described as a leukemoid reaction, we believe that the term "pseudoleukemia" should be reserved for more specific differentiation.
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PMID:Pseudoleukemia: when "leukemia" is not leukemia. 45 Aug 11

Mouse cells infected with Moloney murine leukemia virus (M-MuLV) were prepared by two methods, and the number of M-MuLV-specific DNA copies in the infected cells was measured. The number of M-MuLV-specific DNA copies detected varied from one to eight per infected cell in different cell lines. Cells in which multiple rounds of viral infection occurred during establishment had on the average more viral DNA copies than cells in which infection at low multiplicity was performed, followed by cloning of the cells. However, even in cells derived by the low multiplicity of infection method, most cell lines carried more than one copy of M-MuLV-specific DNA. Virus production per cell was also measured, and no strict correlation was observed between the number of M-MuLV DNA copies present and the amount of virus produced.
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PMID:Low-multiplicity infection of Moloney murine leukemia virus in mouse cells: effect on number of viral DNA copies and virus production in producer cells. 73 93

Numbers of B, T and total lymphocytes, monocytes, heterophils, eosinophils and basophils have been examined in the peripheral blood of chickens between 2 and 42 days after infection with Marek's disease virus. During the stage of the acute restrictively productive virus infection of lymphoid tissues at 2-9 days after infection, absolute numbers of B cells, T cells, total lymphocytes and heterophils were increased, those of monocytes and eosinophils were decreased, and those of basophils were unchanged. The lymphoproliferative phase of the disease, from 21-42 days after infection leading to lymphoma formation, was accompanied by an increase in T cells, total lymphocytes and possibly eosinophils, and a decrease in B cells, monocytes, heterophils and basophils. The T-cell increase following infection occurred only in female birds, and there were more lymphomas in females than in males. The increase in lymphocytes in the blood of six birds with leukemia was mainly due to an increase in T cells, but in one bird B cells were also increased. Blast cells and atypical lymphoid cells were increased in leukemic birds. Regression coefficients were calculated between different pairs of leukocytes in infected and uninfected birds at different stages of the disease. Particularly noteworthy were the associations between B and T cell numbers, which indicated constant proportions of these cells irrespective of total numbers, possibly due to a common control mechanism.
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PMID:Sequential changes in the numbers of B and T lymphocytes and other leukocytes in the blood in Marek's disease. 78 60

Purified gp71 of Friend murine leukemia virus (FLV) can interfere with virus infection, absorb neutralizing antibody, and in the presence of group-specific anti-gp71 antibody, hemagglutinate sheep erythrocytes. Interference by FLV gp71 with several murine leukemia viruses (MuLV) was tested in the XC and S + L- assay systems. Treatment of gp71 with trypsin or Pronase eliminated its interfering capacity. However, treatment with neuraminidase or a mixture of glycosidase enzymes, which left the major serological properties of gp71 intact, did not reduce the interference potential of gp71 for FLV or AKR MuLV. The capacity of gp71 to absorb type- or group-specific virus-neutralizing antibodies was similarly affected by the various enzyme treatments. In contrast, indirect hemagglutination by gp71 was abolished not only by proteases but also by treatment with glycosidase enzymes, although neuraminidase had no effect. Preliminary data indicate that infectivity of FLV or xenotropic MuLV was not affected by short treatment with glycosidase enzymes.
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PMID:Role of carbohydrate in biological functions of Friend murine leukemia virus gp71. 83 28

The correlation of murine leukemia virus (MuLV) infection and leukemogenesis was examined by XC plaque assay in W/F rats neonatally infected with the rat-adapted Gross virus (RAGV). Thymic lymphomas developed in 100% of infected rats, with a mean latent period of 64 days. The virus infectivity was first detected in the thymus as early as 15 days after the virus infection; the titer steadily increased thereafter until the development of thymic lymphoma. No other tissues of virus-infected rats showed virus infectivity until the development of localized thymic lymphoma, though sera of a few rats showed low infectivity titers. In rats with generalized leukemia, however, high titers were detected in the sera and leukemic tissues. In untreated controls, all tissues tested invariably showed negative titers for MuLV infectivity at any age up to 7 months after birth. The results indicated that those tissue sites were common to both RAGV infectivity and the leukemogenic process, with the primary involvement of the thymus, and that the appearance of RAGV infectivity in various tissues represented the expression of the oncogenic genome of RAGV.
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PMID:Type C RNA viruses and leukemogenesis: association of Gross strain of murine leukemia virus infection and leukemogenesis in rats. 99 3

In 50 necropsies on leukaemic children, the major cause of death was infection. In patients dying during therapy for induction or reinduction of remission, the most frequent infection was a distinctive neutropenic enterocolitis or typhlitis. This was seen in 46% of the whole series and was a major factor in the death in 38%. Other infections were predominantly bacterial pneumonia in patients in relapse, and viral disease, e.g. measles pneumonia, in those in remission. One patient treated for meningeal leukaemia showed an unusual linear calcification of the cortical grey matter.
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PMID:Necropsy findings in childhood leukaemia, emphasizing neutropenic enterocolitis and cerebral calcification. 100 50

Clinico-pathological report on a boy with cytostatically treated leukemia, dying with cerebral symptoms after passing clinical measles 10 weeks before death. At autopsy, numerous nuclear inclusion bodies in glial and nerve cells were found. By electron microscopy, nuclear inclusions appeared as loosely arranged smooth tubules, corresponding to paramyxovirus nucleocapsids. Frequently, cytoplasmic changes appeared too, consisting of incomplete tubular structures and an abundant dense "fuzzy" material. No regular tubuli of the coated granular type were present, as in common measles virus infection, nor any mature viral structures or differentiation of the surface membrane. The lack of maturation in cytoplasm together with a predominance of nuclear changes suggested a slow type of measles virus infection, while the particular cytoplasmic changes suggested a defect in synthesis of granular nucleocapsids, possibly a basic factor for the slow type of the viral infection. Possible pathogenetic factors are discussed.
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PMID:SSPE-like inclusion body disorder in treated childhood leukemia. 105 44

A statistically significant seasonality by month of birth, which differed for children diagnosed as having acute lymphatic leukemia in the under 2, 2-3 and 4-9-year age groups, was observed in urban counties of upstate New York. This suggested that the mothers of patients diagnosed in these three age groups might have been exposed to leukemogenic factors during different trimesters, but with each trimester consisting of the same specific group of months. Since a similar birth-month seasonality was not observed in rural regions, it seemed likely that leukemogenic factors might operate with a greater regularity in urban areas. Using these observations and reported trends for acute leukemia in the United States and New York State (excluding New York City), an effort was made to determine whether varicella, influenza, rubeola or rubella had similar epidemiologic features. Only varicella manifested both the urban-rural differences in seasonality and concomitant variations in time trends that were comparable to reported mortality trends for acute leukemia. Rank correlation coefficients for varicella and lymphatic leukemia incidence rates by month were also statistically significant when leukemia cases diagnosed in the three age groups and born in urban countries, were placed in the month of their appropriate trimesters. A retrospective search of varicella case records identified 63 instances of this viral disease complicating pregnancy. Three children resulting from these pregnancies subsequently developed acute lymphatic leukemia.
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PMID:Childhood lymphatic leukemia: prenatal seasonality and possible association with congenital varicella. 106 32

Premature chromosome condensation (PCC) has previously been observed in tissue culture and is believed to arise from asynchronous mitotic activity in multinucleated cells in which the affected nucleus is in interphase and at least one nucleus is in metaphase. Such cells have been noted following fusion induced by virus infection, spontaneously, and after treatment with cytochalasin B. The phenomenon has also been observed in malignant pleural effusions, but has not previously been described as a feature of hematologic disease. In this study, we report the observations of PCC in seven patients. Six of these patients had either acute myeloblastic leukemia or acute myelomonoblastic leukemia in association with the features of erythroleukemia, i.e., leukoerythroblastic reaction in the blood, and erythroid multinuclearity, "megaloblastoid" changes, and PAS-positive staining of erythroid precursor cells in the bone marrow. In all patients, erythroid multinuclearity has been noted. However, not all patients with erythroleukemia exhibit PCC. In this series, three additional patients have had similar bone marrow morphologic changes without PCC. The finding of PCC in erythroleukemia may have important implications as to etiology of this disorder.
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PMID:Premature chromosome condensation in human leukemia. 106 46


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