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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our findings may be summarized as follows: (a) a DNA polymerase is associated with murine type A particles, which is very similar to the reverse transcriptases found in true RNA tumor viruses; (b) the majority of the RNA isolated from A particles is of low molecular weight (probably due to degradation), byt appears to contain an amount of unique sequence information comparable to that found in other oncornavirus particles. These results suggest that A-type particles may be very similar, and perhaps related, to the two other classes (B and C) of oncornaviruses.
Cold Spring Harb Symp Quant Biol 1975
PMID:Reverse transcriptase associated with A-type particles from murine myeloma cells. 5 Sep

This paper points out certain theoretical problems in DNA synthesis associated with antiprimer transcription and with circularization that could oblige RNA tumor viruses to rely on a polyploid genome. It is suggested that each completed act of reverse transcription may be coupled with an act of genetic recombination aimed at recovering the antiprimer information from an adjacent genome subunit in a polyploid train. A partially double-stranded DNA transcript could then be formed with sufficient terminal redundancy to permit circularization. The model provides satisfactory explanations for observed genetic interactions (particularly recombination and heterozygote formation), for inactivation data and for selective subunit transcription.
Cold Spring Harb Symp Quant Biol 1975
PMID:The genome of RNA tumor viruses: a functional requirement for a polyploid structure? 5 Sep 4

Following in vitro stimulation of murine sarcoma virus Moloney isolate (M-MuSV)-immune spleen cells with syngeneic antigenically related Moloney leukemia cells, highly efficient cytotoxic T-lymphocytes (CTL's) were generated. The cytotoxic effect was directed only against H-2-compatible target cells bearing M-MuSV tumor-associated antigens (TAA). However, in a cold target competition assay a weak but detectable capacity to block CTL activity was also obtained when allogeneic Moloney leukemia cells were added. Moreover, when M-MuSV-immune spleen cells from mice inoculated with virus 14 days previously were stimulated by allogeneic Moloney leukemia cells, a strong cytotoxic effect toward syngeneic and allogeneic tumor cells bearing M-MuSV TAA was elicited.
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PMID:Secondary in vitro generation of cytolytic T-lymphocytes (CTL's) in the murine sarcoma virus system. Virus-specific CTL induction across the H-2 barrier. 8 Apr 57

The dissociated cell surface membranes of a rat Moloney sarcoma (MST), derived from a BN rat, were extracted with 2 M KI, with 6 M guanidine thiocyanate, or by papain digestion. Extracts obtained with these three reagents were fractionated on columns of controlled-pore glass, 170 A pore size. A fraction was eluted from each preparation that contained tumor-associated antigens (TAA), viral, fetal, and histocompatibility antigens. With an antibody specific for TAA, the TAA, devoid of detectable viral, fetal, and histocompatibility antigens, were co-precipitated by addition of goat antibody to rat immunoglobulin. After electrophoresis, on slab gels, three bands were detected with estimated m.w. of 185,000, 150,000, and 70,000. No such bands were detected on slab gel electrophoresis with extracts of BC5, a chemically induced tumor, of normal BN lymphoid cells, of M-MuLV, or of fetuses, after incubation with anti-TAA antibody and goat antibody to rat immunoglobulin. TAA extracts prepared with 2 M KI, 6 M guanidine thiocyanate, or papain digestion showed immunologic reactivity. Cold TAA inhibited the co-precipitation of labeled TAA by rat antibody specific for TAA; they elicited antibody in guinea pigs but not in rats; and antibodies specific for TAA were cytotoxic to MST in the presence of C.
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PMID:Tumor-associated antigens of rat moloney sarcoma cells. I. Cell-surface antigens. 8 54

Rat peritoneal cells were made to bind five particle species: immunoglobulin-coated Sheep red cells, glutaraldehyde-treated Sheep red cells, latex beads, leishmania and tumor cells. The dependence of binding on various physico-chemical parameters was studied. The binding of latex beads or Leishmania was not inhibited by cold (4 degrees C), sodium azide, cytochalasin B and ethyleneglycol or dimethylsulphoxide. The binding of immunoglobulin-coated Sheep red cells was unaffected by cold and azide, but it was inhibited by cytochalasin B, ethyleneglycol and dimethylsulphoxide. The binding of glutaraldehyde-treated Sheep red cells was inhibited by cold, azide and ethyleneglycol, but it resisted cytochalasin B and dimethylsulphoxide. The binding of tumor cells was inhibited by azide, cytochalasin B, ethyleneglycol and dimethylsulphoxide. It is concluded that: (a) macrophages are endowed several sets of non-specific binding structures that are differently affected by physico-chemical parameters, which provides a simple way of characterizing them; (b) the expression of a given binding structure on the macrophage membrane is modulated by metabolic inhibitors; (c) some lymphocytes were able to bind tumor cells or Leishmania. Thus, lymphocytes and macrophages might share some non-specific adhesive structures.
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PMID:[Existence of several non-specific recognition systems in macrophages]. 11 24

The induction and effector steps of T cell-mediated cytotoxicity (CMC) have been studied using a mouse tumor cell line and its variant, which is deficient in serologically defined (SD) H-2 antigens. In allogeneic mice the SDxcell line induces CMC, while the SD- cell line does not. However, both cell lines can be lysed by xenogeneic rat lymphocytes. Antiserum specific for rat T cells was used to demonstrate that CMC of both targetss is partially due to T cells. In allogeneic or syngeneic mouse systems the SD- cells coupled with the 2,4,6-trinitrophenyl (TNP) residue can neither induce CMC nor serve as targets for CMC, while TNP-coupled SDxcells can serve both as immunogen and as targets. Thus allogeneic or syngeneic mouse T cells do not interact with the TNP group of targets lacking H-2 SD antigens. However, mouse T killer cells sensitized to TNP-coupled cells may lyse TNP-coupled targets carrying different H-2 haplotypes. These experiments show that the induction and effector steps of CMC executed by mouse T cells, using TNP-coupled cells as immunogen or targets, need not necessarily demonstrate restriction with regard to a certain genetically defined H-2 haplotype. The presence of cell surface H-2 SD antigens is however, absolutely necessary for the induction and effector steps of CMC by mouse T cells. Using cold target inhibition assays, it was not possible to demonstrate recognition of the TNP moiety on TNP-coupled SDxcells.
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PMID:The importance of serologically detectable histocompatibility antigens in the induction and effector step of cell-mediated lysis. 14 72

Regional tumor-draining lymph nodes of 11 of 14 patients with urological tumors and one of four controls studied contained suppressor cell precursors that could be activated by concanavalin A (Con A) to suppress the proliferative response of autologous lymphocytes to Con A. In contrast, no suppression of lymphocyte proliferation by lymph node cells that were not activated with Con A was observed in four patients tested. The suppressive effect was not due to decreased viability or increased release of cold thymidine by Con A-activated cells nor to alteration in the time course of the proliferative response of Con A-activated cells. Mitomycin C treatment of lymph node cells 24 hr after activation did not abrogate their suppressive activity. Peak suppression was observed after 72 hr in culture. The amount of suppression measured could be maximized by treatment of suppressor cells with mitomycin C 24 hr after activation and by washing the cells immediately before pulse labeling with tritiated thymidine. The concentration of Con A required to produce peak suppression varied from patient to patient with optimal doses ranging from 5 to 25 microgram/ml.
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PMID:Concanavalin A-inducible suppressor cells in regional lymph nodes of cancer patients. 15 24

Today, the presence of a hepatic tumor can be diagnosed with considerable accuracy by means of isotope scans, arteriogram and ultrasonic imaging. Its localization to one lobe or other lobes is also generally achievable but with less accuracy because it is not yet possible to visualize the interlobar fissure by a noninvasive technique. Exploratory laparotomy with a view to resection is the preferred approach if the patient is in good general condition. Percutaneous biopsy of a hepatic lesion should be avoided unless laparotomy is not contemplated. Resection is the mainstay of therapy for all forms of hepatic malignant tumors and is the only modality that gives some prospect of cure. The prohibitively high operative mortality rate of former years, mostly due to hemorrhage, has gradually decreased with improved understanding of hepatic anatomy and innovations in surgical technique. By means of adequate vascular control and, if necessary, parenchymal cold perfusion, major resections of difficult and bulky lesions can now be accomplished with safety. Systemic chemotherapy with single agents, intra-arterial infusion chemotherapy and hepatic dearterialization have each been found to be of modest therapeutic value in a variable proportion of patients with diffuse unresectable cancer of the liver. The results of current experience indicate that the response rate is not high and long term control of tumor is rare. Multiple drug combinations with or without infusion therapy or dearterialization are being tried in many centers. Therapeutic strategy and end results for the different forms of benign and malignant neoplasms of the liver are discussed.
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PMID:Current management of hepatic tumors. 16 62

Nonproducer and producer RSV-transformed cells and producer nontransforming virus-infected cells harbor viral DNA specifying the respective avian tumor virus. In nonproducer Rous sarcoma cells, the residing viral DNA is linear, double-stranded and covalently linked to the chromosomal DNA. Both double-stranded and single-stranded forms of RSV DNA transfect chicken cells. The progeny virus is indistinguishable from the DNA parent with respect to the morphological, biological and antigenic properties. Unlike the DNA extracted from nonproducer RSV-transformed mammalian cells, that extracted from producer RSV-transformed chicken cells gives rise, in transfection experiments, to both sarcoma virus and its nontransforming derivative. The DNA from nontransforming virus-infected chicken cells generates only nontransforming viruses. The frequency of nontransforming virus recovery is different from that of sarcoma virus recovery, the latter being a nonlinear function of the amount of transfecting DNA, while the former may suggest a linear relationship. On the other hand, the end-point dilution of transfecting DNA for sarcoma virus recovery is approximately the same as that for nontransforming virus recovery. The following is assumed: Sarcoma viruses and nontransforming derivatives are recovered from two different species of viral DNA which carry or lack, respectively, the transforming genetic material. The size of double-stranded viral DNA is substantially smaller than 20 times 10(6) daltons. In transfection experiments, the sarcoma virus DNA is first integrated into the host cell genome before being expressed, while the nontransforming viral DNA apparently bypasses the integration step. The latter DNA generates the progeny virus when taken up, carried, and transcribed in a permissive cell.
Cold Spring Harb Symp Quant Biol 1975
PMID:Infectious viral DNA in Rous sarcoma virus-transformed nonproducer and producer animal cells. 16 3

The replication of herpes simplex virus types 1 and 2 is defective in XC cells. One lesion is the failure of viral proteins to be transported to the cell nucleus. The resistance of XC cells to the toxic effects of herpes simplex virus is apparently not due directly to the presence of RNA tumor virus in these cells. Other cell lines transformed by RNA tumor viruses exhibited no comparable resistance. The nature of the association between HSV and cell for a number of generations after first selecting "transformants" is not yet established; on prolonged subculture, much of the original HSV information fails to be expressed. Not more than approximately to 0.1 viral genomes per cell remains permanently associated with the host DNA. The "transformants" retain the capacity to synthesize HSV-specific polypeptides, as determined by radioimmunoprecipitation. The "transformants" have a number of characteristics which distinguish them from parental cells, and such characteristics in the light of the immunological data suggest that XC cells exposed to HSV can permanently retain HSV-specific information.
Cold Spring Harb Symp Quant Biol 1975
PMID:Transformation of cells by herpes simplex virus--fact or fantasy? 16 30


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