Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The RNA-directed DNA polymerase of murine mammary tumor virus, a type B RNA tumor virus, was purified sequentially through DEAE-cellulose, phosphocellulose (step gradient), and phosphocellulose (linear salt gradient) chromatography followed by glycerol sedimentation centrifugation. During all stages of purification, coincident peaks of RNA-directed DNA polymerase activity, templated by polyribocytidylate-oligodeoxyguanidylate, and RNase H digestion of [3H]polyriboadenylate-polydeoxythymidylate were observed, and both enzymatic activities displayed a cation preference for magnesium. Under conditions that removed adventitiously associated nucleases, RNase H activity was found to co-purify with polymerase. The specificity of this nuclease was assayed with various prepared substrates, which indicated that the polymerase-associated RNase H activity was directed only against the RNA strand of an RNA-DNA hybrid. It is highly probable that RNase H (RNA-DNA hybrid: ribonucleotide-hydrolase, EC 3.1.4..34) and RNA-directed DNA polymerase of type B viruses are associated enzymatic activities analogous to those observed for avian and mammalian type C RNA tumor viruses.
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PMID:RNase H and RNA-directed DNA polymerase: associated enzymatic activities of murine mammary tumor virus. 6 21

Firmly established transplantable C3H/HeJ mammary carcinomas can be inhibited by host challenge with Vibrio cholerae neuraminidase (VCN)-treated tumor cells. The effect is totally immunospecific, even VCN-treated tumors bearing shared mammary tumor virus (MTV) antigen cannot induce the regression. Thus, VCN is capable of increasing the immunogenicity of the private, unique-unshared tumor antigens on mammary carcinomas; VCN is incapable of increasing the immunogenicity of the shared MTV-associated tumor antigen even in syngeneic C3HeB/FeJ MTV-free mice. The immunoregressive effect of VCN-treated tumor cells can be augmented by subtotal or total surgical excision of large transplantable tumors. Spontaneous mammary tumors in retired breeder C3H/HeJ female mice can be made to regress by two immunological maneuvers: (1) repeated intratumor injections of VCN and/or BCG; and (2) total excision and immunotherapy with VCN-treated autochthonous mammary tumor cells. The use of VCN-treated transplantable mammary tumor cells sharing the MTV-associated antigen was not better than excision alone. The evidence supports the idea that active specific immunotherapy of spontaneous tumors with VCN-altered tumor cells may require the use of autochthonous cells.
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PMID:Experimental cancer immunotherapy: modification of tumor cells to increase immunogenicity. 6 99

Similarities have been observed for some time between oncornavirus-induced malignancies in laboratory animals and leukemias and solid tumors in man. Particles similar to type C oncornaviruses have been detected by electron microscopy both in cells or plasma from leukemia patients and in solid-tumor human malignancies such as Hodgkin's lymphoma, lymphosarcomas, and sarcomas. Likewise, particles resembling type B oncornaviruses in shape and appearance have been found in human breast cancer. In neither case has the infectious nature of the particles been confirmed. However, DNA synthesized in vitro by the enzyme of murine mammary tumor virus was found to hybridize with polysomal RNA obtained from human mammary adenocarcinomas. The presence of RNA complementary to RNA from the Rauscher strain of murine leukemia virus has been observed in other human malignancies unrelated to breast cancer. It has also been found that cells of patients with myelogenous leukemia possess an oncornaviral-type reverse transcriptase that is distinguishable from other cell DNA polymerases and serologically related to the reverse transcriptase of primate oncornaviruses.
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PMID:Human studies following animal models of tumorigenesis by oncornaviruses. 7 Nov 81

BALB/cfC3H female mice which develop mammary tumor virus (MTV)-induced mammary tumors possess not only serun antibodies directed against virus-associated antigens which are expressed on mammary tumor cells but also antibodies directed against antigenic specificities which are unique to each tumor. The possible range of unique specificities is considerable; a survey of serum samples from 18 tumor-bearing females revealed only two which reacted with a tumor-unique specificity of another isologous MTV-induced mammary tumor. A retrospective study revealed that in multiparous females, the serum activity against tumor-unique antigenicity could be detected 1 to 4 months before the tumor was grossly visible. On the other hand, in virgin females, the serum activity was detectable only when the tumor was visible. On the basis of this difference in time of origin of reactivity, we speculate that the mechanism of tumor formation in parous females may involve a longer preneoplastic or latent neoplastic period than in virgin females; in the latter the change from normal to overtly neoplastic appears to be more abrupt.
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PMID:Early detection of tumor-specific antibodies to mammary carcinoma. 7 10

Fucosyltransferase levels in 6 established strains of spontaneously metastasizing rat mammary tumors (STMT-058, MT-449, DMBA-4, SMT-077, TMT-081, and SMT-2A) were compared with 4 nonmetastasizing strains (MT-W9B, MT-W9A, MT-100, and MT-66) as controls. Two acceptors were prepared from fetuin for the assay, one by acid hydrolysis of N-acetylneuraminic acid and the other by the stepwise removal of N-acetylneuraminic acid and penultimate galactose by Smith degradation. The enzyme that transfers fucose to the first acceptor was designated fucosyltransferase A, whereas the one that uses the second acceptor was designated fucosyltransferase B. Both types of fucosyltransferases were found in this rat mammary tumor system. Whereas the levels of fucosyltransferase A in the 2 tumor groups were comparable, those of fucosyltransferase B were sixfold to sevenfold higher in the metastasizing tumors. This difference in the level of fucosyltransferase B was not caused either by differential hydrolysis of GDP-fucose by pyrophosphatase in the 2 groups or by hydrolysis of the product by fucosidases. Presence of any other inhibitor(s) or activator(s) of fucosyltransferase was excluded by mixing experiments. Optimal conditions for the assay of this enzyme were determined in a representative strain from each group. Under all circumstances, the activity of fucosyltransferase B was higher in the metastasizing tumors. The enzyme was inhibited by nucleoside diphosphates and triphosphates, and guanosine nucleotides were the most efficient inhibitors. Subcellular distributions of the two fucosyltransferases were similar, 35-50% of the enzyme activity being present in the crude microsomes. When plasma membrane factions were prepared from the microsomes, the major part (50-70%) of the enzyme was associated with the light and heavy plasma membrane fractions. Increased activity of fucosyltransferase B in the group of metastasizing tumors may have reflected faster synthesis and shedding of fucose-containing glycoprotein antigens. Similar molecules possibly were also synthesized in the nonmetastasizing cells but at a much slower rate, because the antigen is not easily lost from the cell surface. Any alteration of the specificity of this focosyltransferase in the metastasizing tumors, in addition, may have caused antigen modulation.
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PMID:Fucosyltransferase activity in metastasizing and nonmetastasizing rat mammary carcinomas. 7 84

The tumorigenicity of dexamethasone-treated tissue-cultured mammary tumor cells was compared to that of untreated mammary tumor cells. The dexamethasone-induced cells progressed faster in normal syngeneic animals than did untreated mammary tumor cells. The fact that the growth rate differential was also observed in athymic mice suggests that T-lymphocyte-mediated immunity was not a factor in the accelerated progression in vivo of the tumor cells that had been cultured in the presence of dexamethasone.
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PMID:Accelerated growth of mammary tumor cells in normal and athymic mice after treatment in vitro with dexamethasone. 8 Feb 60

Two DNA probes representative of either the entire mouse mammary tumor virus (MMTV) genome or the poly(A)-adjacent sequences at the 3' end of MMTV RNA were synthesized with calf thymus DNA or oligo(dT) primers, respectively. These probes were used to study the expression of endogenous MMTV sequences in several BALB/c mammary tumor cell lines, in normal lactating BALB/c tissue, and in a cloned C3H tumor cell line. Both probes were characterized with respect to their rates of hybridization with template RNA, their size as determined by alkaline sucrose gradient centrifugation, and the thermal stability of the cDNA.MMTV RNA hybrids. In addition, the ability of the calf thymus oligodeoxy-nucleotide- or oligo(dT)-primed probes to protect (125)I-labeled MMTV RNA or (125)I-labeled poly(A)-adjacent MMTV RNA sequences from S1 nuclease digestion was determined. Hybridization analysis with these two probes indicated that (i) there were approximately 20-fold more oligo(dT)-primed sequences in BALB/c lactating tissue than there were sequences representing the entire genome; (ii) in BALB/c tumor cells, the oligo(dT):random oligonucleotide-primed cDNA sequence ratio was reduced to 4:1; and (iii) in virus-producer C3H tumor cells, there was only a 2-fold excess of oligo(dT)-primed sequences over that observed with a representative cDNA. These results are consistent with the presence of subgenomic viral mRNA species, integration of partial proviral copies, or altered mRNA processing.
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PMID:Differential expression of poly(A)-adjacent sequences of mammary tumor virus RNA in murine mammary cells. 8 48

Specific inhibition of cell-mediated cytotoxicity can be used as a quantitative measure of soluble tumor antigen if highly cytolytic cells are obtained. In vitro secondary stimulation of spleen cells sensitized in vivo to the syngeneic 13762A mammary adenocarcinoma results in a lymphocyte population consistently more cytolytic than lymphocytes after primary stimulation. Maximal cytolysis requires removal of dead lymphocytes from the effector population. Soluble tumor antigen (STA) is detected only in supernatants of 13762A mammary tumor cultures grown in the presence of the proteolytic enzyme inhibitor, epsilon-amino caproic acid. Soluble MTM antigen preparations block lymphocytes immune to the mammary tumor but not lymphocytes immune to a second mammary adenocarcinoma (R3230) or to allogeneic spleen cells. Soluble antigen preparations from other tumors do not inhibit lymphocytes specifically cytolytic to the 13762A tumor. Additional evidence that the STA preparation contains tumor antigen is its ability to induce specific cytolytic lymphocytes and partial protection from challenge with live MTA tumor cells.
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PMID:A quantitative assay for tumor antigen based on inhibition of cytotoxicity of sensitized lymphocytes. 8 68

We have shown [Mesa-Tejada, R., Keydar, I., Ramanarayanan, M., Ohno, T., Fenoglio, C. & Spiegelman, S. (1978) Proc. Natl. Acad. Sci. USA 75, 1529--1533] that an antigen immunologically related to gp52, a 52,000-dalton glycoprotein of the mouse mammary tumor virus, can be identified in sections of human breast cancer by means of an indirect immunoperoxidase technique. The specificity of the reaction was established by absorption experiments which revealed that only purified gp52, or material containing it, served to eliminate the IgG molecules responsible for the immunohistochemical reaction in the human breast tumors. We show here that the cross-reactivity between the human and murine tumor antigens is due to the polypeptide rather than the polysaccharide components of gp.52. Sugar-free gp52 prepared by deglycosylation with a mixture of glycosidases was as fully effective as the intact gp52 in removing from anti-MMTV the IgG responsible for the reaction with the human tumor antigen. In contrast, the isolated polysaccharide of gp52 was unable to exert blocking activity.
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PMID:Human breast carcinoma antigen is immunologically related to the polypeptide of the group-specific glycoprotein of mouse mammary tumor virus. 8 56

Mouse mammary tumor virus (MMTV) p10 and gp52 were purified and used as radiolabeled antigens in sensitive radioimmunoassays. These radioimmunoassays were specific for MMTV proteins since detergent-disrupted MMTV from C3H/HeN, RIII, and GR/N mice gave complete competition, whereas C3H/HeNf liver extracts and other lysed retroviruses did not. Both gp52 and p10 are coded by the viral genome, since MMTV grown in a heterologous cell line (feline kidney cells) competed in these assays. Sera from mammary tumor-bearing mice and mammary tumors from C3H/HeN and C3H/HeNf mice competed in both the gp52 and the p10 assays. Although these radioimmunoassays detected predominantly group-specific antigenic determinants in C3H/HeN and C3H/HeNf tumor extracts, type specificity was also found with gp52. Absorption of the anti-MMTV serum with C3H/HeNf tumor extracts removed all antibodies directed against p10 and decreased the anti-gp52 titer approximately 30-fold. When this absorbed antiserum was used at limiting dilution in the gp52 radioimmunoassay, C3H/HeN tumor extracts gave complete competition, whereas no competition was found with C3H/HeNf tumor extracts.
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PMID:Immunological characterization of mouse mammary tumor virus p10 and its presence in mammary tumors and sera of tumor-bearing mice. 9 Jan 56


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