Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0023418 (
leukemia
)
93,477
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The studies were undertaken to determine whether the cat, a mammalian species that carries xenotropic endogenous C-type virus(es) and in addition undergoes horizontally transmitted oncogenic C-type RNA tumor virus infections, responds immunologically to the mammalian C-type virus interspecies antigens. Sera from normal cats and from cats with spontaneous or virus-induced neoplasms were examined for antibodies to interspecies antigen antigen by complement-fixation inhibition, by inhibition of the paired radioiodine-labeled antibody technique (PRILAT inhibition), and by two-step radioimmunoelectrophoresis. Using three separate complement-fixation inhibition systems designed to detect antibodies to interspecies antigen(s), 23 of 23 sera from tumor-bearing cats and 24 of 31 sera from normal cats were positive in both systems. The negative sera were from germ-free cats. Among the 49 positive sera, 47 yielded titers of 1:16 or greater by one or more complement-fixation inhibition tests. Of these 47 sera, 42 were positive by the paired radioiodine-labeled antibody technique inhibition test; the 5 paired radioiodine-labeled antibody technique-negative sera were from normal specific-pathogen-free cats. Direct reaction with the interspecies determinant on the p30 protein from Rauscher murine
leukemia
virus by immunoglobulin from cats immunized with feline
leukemia
virus was shown by two-step radioimmunoelectrophoresis. The feline antibody was also identified as an immunoglobulin by column chromatography and two-step radioimmunoelectrophoresis. These antibodies did not fix guinea pig complement during reaction with the interspecies antigen. That other mammals may produce similar noncomplement-fixing (guinea pig) antibodies to RNA tumor virus antigens is likely.
Cancer
Res 1975 Sep
PMID:Antibody in cats to mammalian RNA tumor virus interspecies antigens. 5 Jan 33
Antigenic determinants of p30, the most abundant internal virion protein of C type RNA viruses, were detected on the surface of spleen cells from mice bearing Moloney
leukaemia
and on an in vitro line of Moloney sarcoma, MSC. On both cell types, these determinants on the p30 molecules served as cytotoxic targets in a xenogenic complement dependent antibody mediated 51Cr release assay. Two antisera were used: a rat anti MLV -M induced lymphoma serum, and an antiserum raised in goats to either disrupted FeLV. The cytotoxic target antigens of these antisera were analysed by inhibition of cytotoxicity with viral and cellular proteins.
Br J
Cancer
1975 May
PMID:Studies on mouse Moloney virus induced tumours: I. The detection of p30 as a cytotoxic target on murine Moloney leukaemic spleen cells, and on an in vitro Moloney sarcoma line by antibody mediated cytotoxicity. 5 Aug 52
Sera from Balb/c mice bearing Moloney
leukaemia
block complement dependent antibody mediated cytotoxicity of an antiserum prepared in rats against syngeneic Moloney virus induced lymphomata when either spleen cells from mice bearing Moloney
leukaemia
(M) or an in vitro line of Moloney virus transformed cells (MSC) are used as targets. This antiserum has been shown to recognize p30, the major internal virion protein, as a cytotoxic target on these cells. Viral particles were identified by electron microscopic examination of pelleted material obtained from leukaemic sera after high speed centrifugation. However, removal of virus did not affect the capacity of the leukaemic sera to absorb cytotoxicity of rat ILR-3 for MSC targets, and only depressed somewhat its ability to absorb activity of the same antisera against M targets. Virus-free leukaemic sera also blocks complement dependent antibody mediated cytotoxicity of an antiserum prepared in goats against the gs3 determinant of p30. This indicates that the material in leukaemic sera responsible for the in vitro block of antibody mediated cytotoxicity was p30. A lesser degree of block was observed with sera obtained from normal Balb/c mice, but the nature of material responsible is as yet undefined.
Br J
Cancer
1975 May
PMID:Studies on mouse Moloney virus induced tumours: II. Detection of p30 in the serum of mice with Moloney leukaemia by in vitro blocking of complement dependent antibody mediated cytotoxicity. 5 Aug 53
Carbaryl(N-methyl-1-naphthylcarbamate) and its nitrosated product, N-nitrosocarbaryl, were tested for their effects of BALB/3T3 (clone A31) cells in culture. Nitrosocarbaryl, but not carbaryl, caused transformation of the BALB/3T3 fibroblasts, but neither chemical induced the complete expression of endogenous murine
leukemia
virus. Transformed cells differed from the parental control cells by loss of contact inhibition, change in morphology, growth in soft agar, growth to higher saturation densities, and tumorigenicity in normal newborn and irradiated weanling mice and athymic (nude) mice. Transformed clones were found to be negative for expression of RNA tumor virus antigens, viral reverse transcriptase, and infectious virus. Thus, it appears that nitrosocarbaryl can transform BALB/3T3 cells to tumorigenic cells with altered biological properties but without complete activation of RNA tumor viruses in the transformed cells. Expression of viral antigen in the transformed cells was inducible by iododeoxyuridine, indicating that the endogenous viral genome was retained in an unexpressed state.
Cancer
Res 1975 Oct
PMID:Effects of nitrosocarbaryl on BALB/3T3 cells. 5 Aug 78
A C-type virus continuously released from a cell line (WR-9) derived from a spontaneous epidermoid carcinoma was purified by means of large-scale tissue culture techniques and high-volume zonal centrifuges. With the use of relatively pure virus concentrates, partial characterization of the virus has been accomplished. Up to 60 liters of spent culture medium from relatively low virus-yielding cultures were processed at a time through the Model K ultracentrifuge in order to obtain quantities of virus sufficient for convenient Tween-ether extraction of the major polypeptide (30,000 daltons). This structural protein having group-specific reactivity was purified and isolated by isoelectric-focusing techniques. A UV absorption peak (A280) was found to be coincident with a major peak of radioacticity at pH 8.6, the isoelectric point (pI) for rat virus gs antigen previously reported by other investigators. Because species-specific (gs-1) and cross-reactive (gs-3) determinants coexist on this protein, fractions containing the group-specific antigen were identified on the basis of the mammalian interspecies determinant (gs-3), using antiserum prepared against Tween-ether-disrupted feline
leukemia
virus. At the same time, reactivity to the gs-1 determinants in identical fractions was observed in complement fixation and gel diffusion assays, using guinea pig antiserum known to contain principally antibodies to rat gs-1 determinants. Presently, the principal source of rat type C viral gs antigen is rat cell line MSB, which continuously releases a rat
leukemia
virus pseudotype of murine sarcoma virus. The WR-9 rat virus line may be of use in providing an additional source of C-type particles that are capable of yielding good gs reagents.
Cancer
Res 1975 Oct
PMID:Partial characterization of C-type particles in a cell line (WR-9) derived from a rat epidermoid carcinoma of spontaneous origin. 5 Aug 83
RADA-1 cells [H-2a thy-1b; thymus-
leukemia
(TL) 1, 2, 3], a radiation-induced murine
leukemia
cell line maintained by serial transfer in histocompatible recipients, resisted lysis by guinea pig complement (GPC) and TL 1, 3; TL 2; or TL 1, 2, 3 antiserum. The cells expressed TL antigenic specificities as determined by indirect fluorescent antibody methods, the direct isolation of TL antigens from the cells, and the capacity of the cells to reduce known titers of TL antisera. GPC was consumed to the same extent during the reaction of resistant cells and TL antisera as occurred in the reaction of sensitive cells (killed under similar conditions) and TL antisera. RADA-1 cells were not nonspecifically resistant to complement (C)-mediated lysis; they were killed in the presence of H-2a antiserum and GPC. The TL antisera contained antibodies for TL determinants. They stimulated the C-mediated lysis of ASL-1 cells (TL 1, 2, 3) and thymocytes from strain A mice (TL 1, 2, 3). The TL antigens of resistant RADA-1 cells underwent antigenic modulation, the reversible disappearance of TL antigens from the cells stimulated by specific antiserum. After the cells were treated with neuraminidase, they became susceptible to the cytotoxic effects of aliquots of the same TL antisera and GPC used previously.
J Natl
Cancer
Inst 1975 Aug
PMID:Detection of a TL(+) murine leukemia cell line that resists the cytotoxic effects of guinea pig complement and specific antiserum. 5 Oct 85
RADA-1 cells (H-2a), a murine
leukemia
cell line maintained by serial transfer in histocompatible recipients expressing thymus-
leukemia
(TL) 1, 2, 3 antigenic determinants, resisted the cytotoxic effects of guinea pig complement (GPC) and TL antiserum. The cells expressed a lower density of TL antigens than did ASL-1 cells, another TL(+)
leukemia
cell line expressing the same determinants and susceptible to complement (C)-mediated lysis. Stable somatic cell hybrids of RADA-1 cells and LM(TK)- cells (H2k), a TL(minus) thymidine kinase-deficient mutant of mouse L cells, were selected in hypoxanthine-aminopterin-thymidine medium. The hybrid cells expressed the H-2 antigens of both parents and shared a hybrid karyotype. They formed TL 1, 2, 3 antigens as determined by immunofluorescence, mixed hemagglutination methods, the direct isolation of TL antigens from Nonidet P40 extracts of the cells, and the capacity of the cells to reduce by absorption the known titers of TL antiserum. These hybrid cells lost the capacity to resist lysis by TL antiserum and GPC. They were susceptible to the cytotoxic effects of TL 1, 2, 3; TL 2; OR TL 1, 3 antiserum and GPC, even though the density of TL antigens associated with the cells was approximately 25% of their resistant RADA-1 parental cells. These results indicated that the mechanism of resistance to C-mediated lysis was genetically separable from the expression of TL antigens by the cells and that the susceptibility of the cells to the cytotoxic effects of antiserum was related only in part to the density of TL antigens expressed by the cells.
J Natl
Cancer
Inst 1975 Aug
PMID:Complement sensitivity of somatic hybrids of a complement-resistant murine leukemia cell line. 5 Oct 86
Tumor-specific immunoprophylaxis was achieved in C57BL/6J mice against EL 4 leukosis cell challenge by sensitization of the syngeneic host with multiple ip injections of irradiated EL 4 cells. A minimal radiation dose was used to replication-block EL 4 cells before inoculation, as defined by dose-response analysis of irradiated EL 4 cells. Multiple ip injections of irradiated EL 4 cells stimulated development of significant, yet relatively low, levels of cytotoxic lymphoid activity (CLA) in lymphoid cells of the peritoneal exudate as measured by in vitro 51Cr-release cytotoxicity assays. The specific temporal and frequency dependencies of the inoculation regimen for achieving immunoprophylaxis indicated that, in addition to CLA, other, short-lived, immune processes were important in the tumor rejection. These observations showed the capacity of the C57BL/6J host for tumor-specific immune recognition and rejection of the syngeneic EL 4
leukemia
. The tumor rejection could be elicited solely by inoculations of irradiated EL 4 cells and did not require exogenous amplifiers, such as immunoadjuvants, chemical modifiers, and/or allogeneic immune information transfer.
J Natl
Cancer
Inst 1975 Sep
PMID:Immunoprophylaxis and cytotoxic effector cells against EL 4 leukemia induced in syngeneic C57BL/6J mice by use of irradiated EL 4 cells. 5 Oct 89
DNA-RNA hybridization was used to explore whether human neoplasias contain RNA molecules having sequence homologies to those of the RNA tumor viruses known to cause similar diseases in animals. The pattern of specific RNAs found in the human tumors showed a remarkable concordance with the predictions deducible from the animal systems. Thus human breast cancer contains RNA homologous only to that of the murine mammary tumor virus (MMTV). Human leukemias, sarcomas, and lymphomas (including Hodgkin's and Burkitt's) all contain RNA with sequence homology to the murine
leukemia
virus (RLV) and not to MMTV RNA. Finally, as in the case of the mouse, none of the human tumors examined contain RNA related in sequence to that of the avian myeloblastosis virus (AMV). The RNA detected in all of the human neoplasias was demonstrated to be of high molecular weight (1 times 10(7) daltons) and encapsulated with a reverse transcriptase in particles having densities between 1.16-1.19 g/ml. Further, the RNA of these human tumor particles was related in sequence to the murine viruses that cause the corresponding neoplasias in mice. Thus, 4 features diagnostic for the murine oncogenic viruses are satisfied by the particles found in the human cancers. Finally, it was shown by "recycling" experiments that the DNA from human leukemic cells and from lymphomatous tissue contained particle-related sequences that could not be detected in normal DNA. This finding was further substantiated by studies with identical twins in which it was shown that the leukemic twin contained particle-related sequences that could not be detected in the leukocytes of his identical healthy sibling. These findings are inconsistent with hypotheses that require chromosomal transmission in the germ line of complete copies of the information required to produce
malignancy
and the associated virus particles.
...
PMID:Sequences related to the RNA tumor viruses in the RNA and DNA of human leukemias and lymphomas. 5 26
Gibbon
malignancy
frequently involves the hematopoietic system and can occur in clusters. Virus isolated from gibbon neoplasms possessed typical type C virus morphology, and the virion measured 100 nm in diameter with an electron-dense nucleoid measuring approximately 75 nm. The virus incorporated 3H-uridine into the nucleic acid and rested at a buoyant density of 1.14-1.16 g/cm3. Intra-and interspecific antigenic determinants were present, and the intraspecific antigenic determinant was shared with the woolly monkey sarcoma virus but not with feline or murine type C viruses. The virus and antibody reactive to the virus are more prevalent in gibbon groups that experience
leukemia
than those free of hematopoietic neoplasms.
...
PMID:Studies on the prevalence of type C virus associated with gibbon hematopoietic neoplasms. 5 28
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>