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

Herpesvirus saimiri induces leukemia and/or malignant lymphoma when inoculated into different species of nonhuman primates including marmosets and owl monkeys. No malignant disease, however, has been recognized in the natural host for this virus, the squirrel monkey, although a high percentage of these monkeys are chronically infected with H. saimiri. Furthermore, one species of marmosets, as well as capuchin and some owl monkeys, fail to develop lymphoma following experimental virus infection but developed a chronic infection similar to that noted in the natural host. The availability of susceptible and resistant species made it possible to attempt to delineate those humoral and cellular immune parameters that might correlate both with tumor induction and resistance. The findings from these investigations are reviewed and discussed in relation to vaccine studies in this system as a model for a human herpesvirus vaccine.
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PMID:Immune response of monkeys to lymphotrophic herpesvirus antigens. 17 27

Thymocytes from preleukemic mice persistently infected with Moloney murine leukemia virus (MuLV-M-carriers) were vigorously autoaggressive toward normal syngeneic target cells; they exhibited a graded response to allogeneic cells, but they spared xenogeneic cells or syngeneic cells infected with MuLV-M or MuLV-G (Gross). Syngeneic target cells infected with nononcogenic lymphocytic choriomeningitis virus (LCMV), or transformed by the chemical carcinogen 3-methylcholanthrene were not similarly spared. This phenomenon, apparently induced by MuLV-M, is not associated with all persistent virus carrier states. Thymocytes from mice persistently infected with LCMV or with the lactic dehydrogenase virus (LDHV) failed to demonstrate an autoaggressive behavior. That transplantable lymphoma cells (derived from MuLV-M-carriers) were autoreactive in a pattern similar to thymocytes from preleukemic mice suggests a unique role for MuLV in the events leading from altered recognition of "self" to lymphoma.
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PMID:Immunologic mechanisms in the pathogenesis of virus-induced murine leukemia. III. Target cell specificity of autoreactive thymocytes. 18 Jan 78

A consideration of the world-wide incidences of childhood cancer and of hereditary subgroups leads to the conclusion that two successive mutations can initiate cancer cells and that such cells usually proceed to develop into detectable cancers in a period of time which is short compared with the time required for most adult cancers. Environmental carcinogens could hypothetically increase the rates at which these mutations occur, but they probably, in fact, contribute little to the incidences. Certain exceptions, notably leukemia and lymphoma, are noteworthy, and a viral origin for them has been widely hypothesized. If most solid tumors of childhood are indeed correctly attributable to mutations in germ and/or somatic cells, then the prospect for the prevention of childhood cancer becomes very dim. In fact, the incidence of the germinal forms may increase as treatment improves (18). In theory, one might be able to identify individuals harboring cancer genes germinally and even to identify them prenatally. But even if the burden of cancer attributable to the hereditary subgroups were elimanted, there would still remain the larger nonhereditary group resulting from somatic mutations. If this hypothesis is correct, then childhood cancer cannot be prevented. With this conclusion goes the admonition, however, that environmental mutagens might significantly increase the burden of childhood cancer. One such mutagen, therapeutic radiation, is known to increase the prospect that second tumors will occur in patients who carry a germinal cancer mutation. The major effort to reduce the incidence of childhood cancer by prevention should be spent in examining the possibility that leukemia and lymphoma are viral in origin. If the arguments presented are correct, then the main effort against childhood cancer must be that of early diagnosis and treatment. I realize that many have already argued for that strategy in the approach to cancer generally, but I now believe that it is particularly relevant to any program against cancer in children.
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PMID:Genetics and the etiology of childhood cancer. 18 Apr 83

The nephrotic syndrome complicating malignancy in the absence of renal vein thrombosis, amyloid or neoplastic infiltration of the kidney is an unusual occurrence. A case of diffuse, well differentiated, lymphocytic lymphoma and lipoid nephrosis documented by light microscopy, electron microscopy and immunofluorescent studies is reported. A review of the literature revealed 76 case reports in which the nephrotic syndrome was associated with neoplasia. The most frequently associated neoplasms are Hodgkin's disease, various carcinomas, nonHodgkin's lymphoma and leukemia in descending order. The most frequent renal lesion in patients with the nephrotic syndrome associated with various carcinomas is membranous glomerulonephritis (81 per cent) as opposed to patients with lymphomas or leukemias who have predominantly lipoid nephrosis (60 per cent). The evidence is reviewed suggesting that the lesions in membranous nephropathy are immunologically mediated by tumor or viral antigen-antibody complexes and in lipoid nephrosis perhaps by a defect in t-lymphocyte function.
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PMID:The nephrotic syndrome associated with neoplasia: an unusual paraneoplastic syndrome. Report of a case and review of the literature. 18 Aug 1

Various facts are now known about the relative lymphoma resistance of a group of tetraparental AKR reversible CBA/H-T6 chimaeras derived by early embryo aggregation. Firstly, their tumour resistance is not due to the lack of the lymphomaprone AKR cells. Secondly, results showing titres of MuLV-gs antigen comparable with, and occasionally in excess of, those in the AKR suggest that the tumour resistance of the chimaeras is unlikely to be due to a lack of oncogenic leukaemia virus. However, in marked contrast to the AKR, antibody-viral antigen renal complexes in the chimaeras were minimal. Lack of viral antigens could not explain the relative lack of renal complexes. Absence of the corresponding anti-viral antibody is the most likely explanation and this has to be attributed to the CBA component of the tetraparental AKR reversible CBA/H-T6 chimaeras. We suggest that with tolerance to the leukaemia virus being maintained and in the absence of anti-viral antigenic complexes, tumour-specific sites can be recognized and thus tumours are eliminated. This hypothesis remains to be proven.
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PMID:Murine leukaemia virus group-specific antigen in tumor-resistant tetraparental AKR reversible CBA/H-T6 chimaeras. 18 91

The incidence of lymphomata in CBA mice is low and furthermore is unaltered by transplantation at the early blastocyst stage and being born from the lymphoma-prone AKR. The number of C-type murine leukaemia virus particles in CBA derived in this manner and milk-fostered by AKR mice in no way differs from normal CBA. The results suggest that the oncogenic Gross virus does not pass through either the transplacental or transmammary routes, or alternatively that viral replication in the CBA was in some way inhibited. Both possibilities have still to be distinguished.
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PMID:The innate resistance of CBA mice to endogenous murine leukaemia virus infection. 18 92

Fluorescent antibodies prepared against extracellular particles from a continuous culture of cells derived from a monocytic leukemia stained JIII cells but not cells infected with Rauscher leukemia virus or simian sarcoma virus. These antibodies reacted with 38% of bone marrow preparations from patients with lymphoma, 26% of preparations from patients with nonmalignant blood disorders and 6% of preparations from patients with leukemia. Bone marrow films from patients with lymphoma over the age of 50 stained less frequently than those from patients under 50. These particles released from JIII cells are not antigenically related to two of the commonly studied oncornaviruses, but may be indicative of the etiology or disease process of lymphoma in young patients.
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PMID:Occurrence in human bone marrows of an antigen released from continuous cell cultures derived from human leukemia. 18 76

Cytologic examination of cerebrospinal fluid was performed in 1,021 patients, using Nuclepore and Millipore filter techniques. Positive findings were obtained in 89 cases, including 40 with primary central nervous system tumors, 24 with metastatic tumors and 25 with leukemic or lymphomatous involvement. When correlated with histologic findings, the overall detection rate was 32.2 per cent for primary tumors, 53.3 per cent for metastatic tumors and 65.8 per cent for leukemia and lymphoma. Highest degree of accuracy in the primary tumor group was achieved with medulloblastoma (61.9 per cent). Among metastatic tumors, those originating in the lung (70 per cent) and breast (83 per cent) were the one most often detected. Comparison of the two filter techniques indicated a slightly higher detection rate when the Millipore filter was used. The reasons for this are not entirely clear, but increased cellular yield with the Millipore filter may be an important factor. The cytocentrifuge method was found to be generally inferior to either of the filter techniques in quality of cell preservation. Our findings indicate that diagnostic usefulness of cerebrospinal cytology depends on collection and preparation methods as well as the anatomic distribution and biologic behavior of the lesions.
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PMID:Cerebrospinal fluid cytology: diagnostic accuracy and comparison of different techniques. 18 97

Correlation between infectivity of type-C RNA virus) murine leukemia virus, MLV) and development of leukemia was tested in female ICR/JCL mice treated with either 1-ethyl-1-nitrosourea (ENU) or 1-butyl-1-nitrosourea (BNU). Continuous administration of either chemicals resulted in the occurrence of thymic lymphoma in every mouse with a short latent period. The time of appearance and distribution pattern of MLV infectivity in various tissues were examined by the XC plaque assay technique at fixed intervals during the leukemogenic treatment. In ENU- or BNU-treated mice, only a few samples of the thymus showed MLV infectivity with rather low titers during incubation period and the presence of MLV was not consistent even in leukemic cases though the thymus was almost invariably the target of leukemogenesis. On the other hand, many samples of the uterus, spleen, and mesenteric node from non-leukemic and leukemic mice harbored a good quantity of MLV. In tissues such as the liver, kidney, bone marrow, and muscle, positive cases occurred only sporadically. Observations on the MLV infectivity in untreated controls were almost comparable with those in leukemogen-treated mice. These results indicate that the infectivity of MLV, detected by the XC plaque assay technique, is not necessarily related to the induction of leukemia in mice by exogenous agents.
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PMID:Type-C RNA viruses and leukemogenesis: relation of type-C virus infectivity and leukemogenesis induced by nitrosourea compounds in mice. 18 21

Transmission of murine leukemia virus (MuLV) from parent to progeny C3H/St and C57BL/St mice was examined by four assay systems: 1) recovery of infectious NB-tropic MuLV from spleen cultures, 2) the radioimmunoassay for p30 antigenemia, 3) morphologic examination for lymphoma development, and 4) the indirect fluorescent antibody technique for antinuclear antibodies (ANA). Transmission of MuLV (Scripps) occurred in 90-100% of C3H/St and C57BL/St progeny nursed by mothers with p30 antigenemia. All assays except ANA were equally sensitive for the determination of MuLV transmission in C3H/St mice, but the incidence of transmission in C57BL/St mice was determined only by assays of their cultured spleens for MuLV. Incidences of ANA were increased in all generations of C57BL/St mice compared with controls; the route of transmission of MuLV (Scripps) was not a factor. Only C3H/St mice infected by virus transmitted from parent to progeny developed ANA. Infectious MuLV was invariably recovered from spleens cultured from mice with p30 antigenemia, which was present in all mice that developed lymphoma. NB-tropic MuLV was also recovered after prolonged cultivation from spleens of 75% of C57BL/St progeny mice that did not develop p30 antigenemia. These suggested that MuLV (Scripps) could exist either as a productive persistent or nonproductive latent infection in C57BL/St mice.
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PMID:Transmission of murine leukemia virus (Scripps) from parent to progeny mice: a comparison of assay systems. 18 73


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