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 ribonuclease activity of cerebrospinal fluid of 219 patients was studied. The normal level was 269 +/- 95 units/ml. Consistent elevations above 550 units/ml were found in: 1. Chronic cerebrovascular disease; 2. Spinal cord compression; 3. Tumors. The molecular weights of the ribonucleases in the cerebrospinal fluid are approximately 33,000; 21,000 and 15,000; the major species is the one with m.w. 33,000. Although the increase in the CSF ribonuclease activity is not disease specific, the measurement has provided corroborative help in cases when the CSF protein is normal. The increase in CSF RNAase is not due to red or white blood cells and the immunologic data suggest that the CSF enzyme activity is derived from the blood stream. Further studies are necessary to rule out a nerve cell origin of the CSF ribonuclease activity.
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PMID:Ribonuclease activity of human cerebrospinal fluid. 85 26

The cross-linked dimer of bovine pancreatic RNase (M.W. 28,000) is significantly more effective than the monomer in inhibiting tumor development in mice when administered i.p. 1 day after inoculation with sarcoma 180J ascites cells. Animals bearing solid tumors were not affected. In AKR/J mice with advanced leukemia, a single i.p. injection of 100 mug of the dimer led to about 50% reduction in the enlarged lymph nodes and the spleen at 24 hr. The half-life of the dimer in the bloodstream has been determined to be 10 min in rats and 6 min in mice, compared to values of 5 and 3.5 min, respectively, for the monomer. Analyses of the tissues of untreated leukemic mice for RNase and RNase inhibitors show that the tumor tissues are not deficient in RNase activity. Considerations of possible mechanisms of action of the dimer indicate that other basic proteins in this size range may merit examination as cytostatic agents toward transformed cells.
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PMID:Comparison of antitumor activities of pancreatic ribonuclease and its cross-linked dimer. 97 50

Fifty-one previously untreated cases of lung carcinoma and 7 normal healthy controls were evaluated with respect to serum ribonuclease (S-RNase) levels. Cellular immunity was tested in 22 of these 51 cases by leukocyte migration inhibition test (MIT) using extract of culture cell line of lung carcinoma. S-RNase levels in lung carcinomas were significantly elevated. There appeared to be no difference in S-RNase levels by histological classification. More striking was high S-RNase level in disseminated versus localized cases. MIT results indicated impairment of cellular immunity in those cases of more elevated S-RNase. S-RNase may be implicated in blocking phenomenon associated with neoplastic disease.
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PMID:Serum ribonuclease in patients with lung carcinoma. 99 11

Ehrlich ascites tumor cells were labeled with [5,6-3H]uridine in vivo during the exponential growth phase of the tumor in the mouse. Hydroxyapatite column chromatography of the total cell nucleic acid revealed a level of activity in the DNA approaching 50% of the incorporated activity of the RNA after 24 hours. After perchloric acid hydrolysis, the constituent bases of the DNA, separated by paper chromatography, contained more than 90% of the tritium radioactivity in the cytosine and thymine, at a ratio of approximately 2:1. Prior to digestion of the polymer, the level of label in the DNA was not sensitive to RNase, alkaline, or heat denaturation. Equilibrium density gradient centrifugation produced a single peak, coincidental for radioactivity and optical density at 260 nm. Our results indicate that tumor cells under replicative stress incorporated more than one-third of the tritium radioactivity of uridine into the DNA, whereas those at a growth plateau had less than 10% of the label in the DNA. This exogenous uridine radioactivity observed in the DNA represented neither a DNA-RNA hybrid, RNA primer pieces in DNA synthesis, nor any other RNase-sensitive species, but was apparently the consequence of amination and methylation of the tritium-labeled uracil moiety to satisfy the metabolic needs of the replicating cells for cytosine and thymine bases.
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PMID:Incorporation of tritiated uridine into DNA of Ehrlich ascites tumor cells. 100 13

Six transplantable murine tumor models were evaluated for changes in RNase activity. This study was conducted with spleen and thymus homogenates, as well as with plasma collected from tumor-bearing mice. Nuclease activity directed against the synthetic substrates, polyadenylic acid, polyuridylic acid, and polycytidylic acid, was measured and the data obtained for tumor-bearing animals were compared to their normal counterparts. Elevated activity against polyuridylic acid was observed in the plasma of all tumor-bearing mice. Although not as all inclusive, RNase levels in both the spleen and thymus were generally altered as well. The observance of unilateral changes in nuclease activity directed against the synthetic substrates demonstrated that, in most cases, two or more enzymes were being detected. The assay may have some eventual value in the monitoring of cancer
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PMID:Alterations in ribonuclease activities in the plasma, spleen, and thymus of tumor-bearing mice. 105 98

Mice were actively immunized against Friend leukemia virus tumorigenesis by vaccination with cell-free homogenates derived from infected splenocytes emulsified in Freund's adjuvant. Adoptive immunity was also achieved by transferring splenocytes from actively immunized donor animals intravenously into syngeneic recipient animals challenged with the virus. Furthermore, RNA-rich extracts derived from spleens of actively immunized donor animals were capable of transferring immunity to FLV leukemia when injected into recipient animals challenged with the virus. The "immune RNA," when incubated with normal splenocytes in vitro, followed by washing, resulted in a cell population that also induced adoptive immunity after transfer to normal animals challenged with virus either before, simultaneously with, or after injection of the treated splenocytes. RNase, but not DNase or other enzymes, inactivated the biologie activity of the protective RNA from immune donors. In addition, isogeneic mouse serum that contained neutralizing antibody to FLV also inhibited the protective effect of the specific RNA; sera from control mice immunized with unrelated antigens failed to neutralize the specific RNA. These results indicate that an RNA extract that contains a virus-associated or -induced antigen is formed in the spleens of actively immunized animals and possesses the ability to either directly induce protective immunity in recipient animals challenged with virus or, indirectly, to convert normal splenocytes in vitro to adoptively confer immunity to similar recipients. Further investigations concerning the mechanism by which such immunogenic RNA functions in vivo and in vitro, as well as the physicochemical nature of the RNA complex, especially that portion associated with the tumor virus-associated antigen, are needed.
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PMID:Discussion paper: protective immunity in leukemic mice treated with specific "immunogenic" RNA. 106 68

It was shown that normal nonimmune C3H mouse spleen cells became specifically cytotoxic to chemically-induced syngeneic C3H tumor cells by incubation with xenogeneic I-RNA extracted from the lymphoid organs of specifically immunized guinea pigs. This response was specific for the tumor used to immunize the I-RNA donor. In a totally syngeneic system, we showed that syngeneic I-RNA extracted from the spleens of tumor-bearing rats mediated cytotoxic immune reactions which were directed specifically against the tumor-associated antigens of syngeneic rat tumor target cells. Active antitumor I-RNA synthesis in the lymphoid organs of I-RNA donor animals reached a maximum between days 14 and 21, depending on the route of administration and the nature of the immunizing tumor. Active I-RNA preparations were insensitive to treatment with deoxyribonuclease or pronase, but were inactivated by ribonuclease treatment; thereby indicating that the active moiety was one or more species of RNA. The active fractions of the I-RNA preparations had sedimentation values in sucrose density gradients of 12-16S, and comprised only a small fraction of the total RNA present in the lymphoid cells. Active antitumor I-RNA appeared to be localized in the cytoplasm of sensitized lymphoid cells, rather than in the nucleus. Lymphocytes from normal human donors as well as from cancer patients, when incubated with xenogeneic or allogeneic I-RNA, became specifically cytotoxic for human tumor cells in vitro. Crossreactivity among tumors of the same histologic type was observed, but not crossreactivity with tumors of other histologic types. Xenogeneic I-RNA extracted from the lymphoid organs of donor animals immunized either iwth tumor cells or normal tissues, following incubation with normal allogeneic lymphocytes, mediated cytotoxic immune reactions which were directed both against tumor-associated antigens and normal transplantation antigens. However, when autologous lymphocytes were used as effector cells, only immune reactions directed against tumor-associated antigens were observed. Allogeneic I-RNA extracted from peripheral blood lymphocytes of human cancer patients mediated specific cytotoxic immune reactions that were directed against common tumor-associated antigens shared by human tumors of similar histologic type. I-RNA's directed against "self" normal cell surface antigens appear to be recognized as self by lymphocytes, and immune responses against these self antigens are not elicited. On the other hand, I-RNA's directed against "nonself" tumor-associated antigens induce lymphocytes to effect specific antitumor immune responses. Our data are consistent with the hypothesis that I-RNA is an information-containing ribonucleic acid molecule capable of mediating immune reactions in vitro which are specific for the tumor-associated antigens of the tumor used to immunize the I-RNA donor.
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PMID:Mediation of immune responses to tumor antigens in vitro by immune RNA. 107 64

Infusion of cycloheximide i.v., an antibiotic known to inhibit synthesis of protein, at a rate of 0.2 mg/kg/hr, reliably caused lysis of fever in 15 chronically febrile patients with Hodgkin's disease who did not have detectable bacterial, fungal, or viral infection. Antipyretic effects were also seen in some patients with reticulum cell sarcoma, lymphosarcoma, acute leukemia, histiocytic medullary reticulosis, plasma cell myeloma, carcinoma of the lung, and carcinoma of the cervix. The drug failed to produce defervescence in four patients with normal granulocyte reserves, who were febrile due to bacterial infection. When infused at a rate of 0.2 mg/kg/hr, the drug apparently caused an acute alteration of protein metabolism in man in that plasma amino acid nitrogen rose acutely while plasma levels of muramidase and ribonuclease fell during the period of the infusion. The data suggest that continuing synthesis of protein may be involved in nonbacterial fever of neoplastic disease. Mammalian granulocytes and monocytes are known to elaborate a pyrogenic protein following appropriate stimulation; it is suggested that in some types of neoplastic disease, particularly Hodgkin's disease, tumor cells may produce and release a pyrogenic protein and that drug-induced inhibition of its synthesis is responsible for the observed lysis of fever.
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PMID:Antipyretic effect of cycloheximide, and inhibitor of protein synthesis, in patients with Hodgkin's disease or other malignant neoplasms. 109 49

Ribonuclease activity in cell-free thymus homogenates was elevated for five strains of mice genetically predisposed toward leukemia or reticulum cell neoplasms (AKR, C58, PL, RF, and SJL). Such increased activity was directed against polyuridylic acid and was observed in 8-wk old mice, well before the onset of neoplastic transformation. Similarly, white blood cell ribonuclease activity was elevated in mice of the strains AKR, C2H/He, PL and RF. Statistical analysis indicated that such elevated activity in these strains related to their high incidence of spontaneous neoplastic disease. Elevated ribonuclease activity thus represents a new biochemical marker relating to the genetic propensity of some strains of mice to die prematurely of spontaneous neoplasia.
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PMID:Elevated ribonuclease activity in the thymus and white blood cells of genetically cancer prone mice. 109 92

The RNase activity observed in the sera of leukemic guinea pigs was compared to that observed in white blood cell (WBC) lysates of the same animals. The WBC-associated RNase activity directed against polyuridylic acid decreased with the progression of neoplastic disease, though serum RNase activity remained unchanged. With certain forms of cancer, therefore, variations in cell RNase may be more sensitive markers than changes in serum RNase for the evaluation of the progression or regression of disease.
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PMID:A white blood cell RNase assay for the possible monitoring of malignancy. 113 54


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