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

Bone marrow transplantation is a new concept in the treatment of leukemia and aplastic anemia. The problems seen in the transplanted patient are abundant and often life-threatening. Caring for these patients offers one of the most exciting challenges of nursing. The nurse not only acquires skill in caring for a patient with leukemia and aplastic anemia, but also becomes knowledgeable in infectious diseases, immunology, fluid and electrolyte balance, and cardiac, respiratory, and renal diseases. The complexity of these patients allows the nurse more direct, comsistent contact with them. As she becomes involved, she is given excellent opportunities for supporting the patient and family through this stressful time. Althoug bone marrow transplantation is an experimental procedure with problems still to be solved, results indicate its value in the treatment of refractory leukemia and aplastic anemia.
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PMID:Bone marrow transplantation in children. 0 69

A previously described type virus stock (designated PP-1R), isolated by cocultivating baboon cells with mink cells transformed by Kirsten sarcoma virus (64J1), has been further cloned and characterized. End point-diluted stocks of PP-1R have been obtained that are free of focus-forming activity and lack both Kirsten sarcoma and primate type C viral sequences. Nucleic acid hybridization experiments show that the cloned virus (MiLV) is an endogenous, genetically transmitted virus of the mink (Mustela vison). MiLV replicates in canine, feline, and 64J1 mink cells but not in an untransformed mink cell line. Multiple viral gene copies can be detected in the DNA of normal mink cells in culture and in normal mink tissues; related endogenous viral genes are also detected in several related Mustela species. The virus codes for a p30 protein very closely related antigenically to that of feline leukemia virus but contains p15 and p12 proteins that are antigenically distinct. The mink cell line, Mv1Lu, and its Kirsten sarcoma-transformed derivatives, 64J1, express relatively low levels of type C viral RNA related to MiLV and normally do not produce detectable levels of MiLV p30 protein or complete, infectious viral particles. Infection of sarcoma virus-transformed mink cells with baboon type C virus, however, can augment the level of expression of endogenous mink viral RNA and can result in the synthesis and packaging of mink viral RNA and p30 antigen in extracellular virions. Since the Mv1Lu cell line and its tranformed derivatives have become widely used in studies of retroviruses, the possibility of activating endogenous mink viral genes should be considered by investigators working with these cells.
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PMID:Endogenous mink (Mustela vison) type C virus isolated from sarcoma virus-transformed mink cells. 7 84

Infection with the Friend murine leukemia virus complex (F-MuLV) suppressed humoral antibody synthesis in vivo and lymphocyte mitogenesis in vitro. Both these effects of F-MuLV were under host genetic control. In vitro suppression of lymphocyte mitogenesis was regulated by a single autosomal gene called Fv-3 that is dominant for susceptibility. Genetic analyses, with the use of the susceptible DBA/2 and resistant B10.D2/n parents, their F1, intercross, and backcross progeny, indicated that a single autosomal gene dominant for susceptibility regulated the in vivo susceptibility to immunosuppression by F-MuLV. Individual [(DBA/2xB10.D2)F1xB10.D2] mice were typed both for susceptibility to F-MuLV-induced suppression of lymphocyte mitogenesis in vitro (an Fv-3 function) and susceptibility to immunosuppression by F-MuLV in vivo. Such an analysis indicated that the same mice that were susceptible or resistant to immunosuppression in vivo were susceptible or resistant to suppression of lymphocyte mitogenesis in vitro. Spearman's rank analysis of the data also indicated that the in vivo and in vitro immunosuppressive effects of F-MuLV were correlated with and not independent of each other. Thus Fv-3, which regulates the effect of F-MuLV on lymphocytes in vitro, also appears to regulate the effect of F-MuLV on antibody-forming cells in vivo.
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PMID:Mechanism of genetic resistance to Friend virus leukemia in mice. V. Relevance of Fv-3 gene in the regulation of in vivo immunosuppression. 10 Jun 4

Healthy feline leukemia virus (FeLV)-infected cats from leukemia cluster environments were followed for up to 23 months for development of disease and evidence of alteration in the hemogram. The incidence of disease development in FeLV-postive cats was more than fivefold higher than the incidence for FeLV-negative cats. Ten cases of leukemia developed in 69 infected cats, whereas one case of leukemia occurred in 59 uninfected cats. The incidence for development of diseases other than leukemia was 30.4 percent for FeLV-infected cats as opposed to 6.8 per cent for uninfected cats. This could be a result of the immunosuppressive effects of FeLV. Felv-infected cats had no evidence of subclinical anemia. Mean packed cell volumes and total leukocyte counts were about the same for infected and uninfected animals. The only variation seen in healthy FeLV-infected cats was a decreased mean lymphocyte count. The difference between mean lymphocyte count for FeLV-infected and uninfected animals was significant at the 0.999 level. These findings suggest that the incubation period for feline leukemia may be very prolonged under natural conditions and that an increased susceptibility to unrelated infectious diseases exists during this period. This increased susceptibility was apparently not associated with anemia or depressed total leukocyte counts.
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PMID:Naturally occurring persistent feline oncornavirus infections in the absence of disease. 16 93

Cats with naturally occurring leukemia and lymphoma had low or negative humoral antibody titers to the feline oncornavirus-associated cell membrane antigen (FOCMA). Geographic differences were seen in the relative frequencies of various forms of lymphoproliferative neoplasms. Lymphatic leukemia and thymic lymphoma were most common in Boston, whereas alimentary lymphoma was most frequent in Glasgow. No significant differences were found in geometric mean FOCMA antibody titers for the various forms of leukemia-lymphoma or for feline leukemia virus (FeLV)-positive as compared to FeLV-negative cats. Approximately 70% of 76 Boston cats with nonregenerative anemias were FeLV gs antigen (gsa) positive; this was similar to the percentage with leukemia-lymphoma from the same population that was positive. Fifty-five to 62% of the Boston cats with other infectious diseases, such as peritonitis and septicemia, were gsa positive. We postulate that this is due to a predisposition to infectious diseases by the immunosuppressive action of FeLV. Young cats from the Boston population that developed lymphoma, infectious peritonitis, and certain other diseases were more likely to be FeLV gsa positive than older cats with the same diseases.
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PMID:Feline oncornavirus-associated cell membrane antigen. IV. Antibody titers in cats with naturally occurring leukemia, lymphoma, and other diseases. 16 77

Feline leukemia is an infectious disease caused by a horizontally transmitted virus. Infection of animals or cultured cells with feline oncornaviruses results in the expression of a specific cell membrane antigen, feline oncornavirus-associated cell membrane antigen (FOCMA). The humoral antibody response to FOCMA is directly correlated with tumor progression. The measurement of this antibody is a useful tool for determining virus exposure. Using this procedure it was determined that cats living in leukemia "cluster" households as well as cats used as contact controls in virus injection experiments have a risk of infection of 90% or higher.
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PMID:Immune response of healthy and leukemic cats to the feline oncornavirus-associated cell membrane antigen. 16 20

Traditionally, cancer has not been considered an infectious disease although some multiple cases of leukemia in man and cattle have been reported. The discovery that feline lymphosarcoma was associated with an RNA virus (feline leukemia virus(FeLV)) meant that infectious transmission of the disease was a possibility. The critical question was whether the predominant method of transmission from one animal to another was 'vertical' (via the gametes) or 'horizontal' (via contagion or infection). A number of epidemiological studies have shown that the chances of healthy cats contracting lymphosarcoma are greatly increased when a cat with the disease lives in close proximity. It does not matter whether the healthy cats are related to the sick animal or not. It has also been established that viremic normal cats have an approximately 900 times greater chance of developing leukemia than cats whose FeLV status is unknown. Infectious FeLV is present in the excretions and blood of viremic animals. In the natural environment, feline lymphosarcoma occurs in clusters. The results in pet cats have been supported by experiments with cat colonies under controlled conditions and prove that horizontal transmission of FeLV occurs. This does not mean that epigenetic (infection in utero or via the milk) or vertical transmission cannot also occur. It should be possible to break the cycle of horizontal transmission of the virus by vaccination and thus control FeLV-related diseases.
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PMID:Horizontal transmission of feline leukemia virus in cats. 16 34

Infection of adult BALB/c mice with murine leukemia virus (MuLV) induces thymic lymphomas histologically indistinguishable from those caused by neonatal infection. X-irradiation permitted early and high levels of viral expression when given before or after MuLV administration and hastened the development of lymphomas. Expression of virus was assayed by using a radioimmune assay for murine p30, a virion core protein. Seventeen to 21 days after injection of MuLV into adult mice, there was 0.3 mug p30 per ml serum, approximately 5 times normal. Seventeen to 21 days after injection of MuLV into X-irradiated (600R) adult mice, there were 2.7 mug p30 per ml serum. The virus produced by infected adult mice was infectious and oncogenic when given to newborn mice.
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PMID:Enhancement of infectivity and oncogenicity of a murine leukemia virus in adult mice by X-irradiation. 17 43

Organ transplantation and the modern treatment of leukemia have created a new situation favouring bacterial infection under immunosuppressive drugs. Exceptionally, due to pathogenic bacteria, these infections are usually due to various germs normally considered as inoffensive saprophytes, which may thus reveal immune deficiency in the patient. This immune failure, which is very pronounced in treated leukemic patients and following transplantation, is on the contrary often localised at a precise level during common infections. Knowledge of these levels is thus essential for the clinician who, in all infected patients, should assess the state of the skin, mucosal and tissue and humoral defences whether specific or non-specific in the light of modern immunological data. Infection in the immunodepressed subject requires urget treatment. Antibiotics are not the only form of treatment, one should supervise, maintain and restore adequate immune levels. Furthermore, antibiotics alone, although they reduce the frequency, do not finally improve the mortality rate from gram-negative septicemia acquired in hospital.
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PMID:[Bacterial infections and immunosuppression]. 18 4

Pseudotypes of vesicular stomatitis virus (VSV) and Moloney murine leukemia virus (MuLV), defined by their resistance to neutralization by anti-VSV antiserum, are released preferentially at early times after infection of MuLV-producing cells with VSV. At later times, after synthesis of MuLV proteins has been inhibited by the VSV infection, neither MuLV virions nor the VSV (MuLV) pseudotypes are made. Infection of MuLV-producing cells with mutants of VSV having temperature-sensitive lesions in either G or M protein does not generate pseudotypes at nonpermissive temperature, indicating that both proteins are needed for pseudotypes to form. Although the pseudotypes resist neutralization by anti-VSV serum, they are inactivated by anti-VSV serum plus complement, and they can be precipitated by rabbit anti-VSV serum plus goat anti-rabbit IgG. These results, coupled with experiments using a temperature-sensitive mutant of VSV G protein grown at partly restrictive temperature, suggest that small numbers of VSV G protein are obligately incorporated into VSV(MuLV) pseudotypes. There appears to be a stringent requirement for recognition of the viral core by homologous envelope components as the nucleating step in the budding process. Only after such a nucleation can the envelope components of the second virus substitute into the membrane of the budding particle.
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PMID:Mechanism of formation of pseudotypes between vesicular stomatitis virus and murine leukemia virus. 19 40


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