Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transplantation immunity of Donryu rats against ascites hepatoma AH-64A induced by azo dye was demonstrated by intraperitoneal injection of tumor cells pretreated with heteroantibodies in vitro. Hyper-immunity was induced by successive challenges with fresh tumor cells. The cytotoxic effect of the serum of resistant rats (RRS) against AH-64A tumor cells was not reduced after absorption with normal rat liver cells, but was slightly reduced after absorption with normal rat spleen cells. The cytotoxicity was absorbed completely with 5 times 10(6) AH-64A tumor cells. AH-64A, -B, -C, and -D are ascites hepatoma cell lines originating from a single Donryu rat. AH-64A and AH-64B cross-reacted with RRS while AH-64C and AH-64D, chemically induced DBLA-6 leukemia cells and normal lymph node cells of rats, did not react with RRS in indirect immunofluorescence and cytotoxicity tests. A neutralization test was carried out by treating 2 times 10(5) tumor cell with either RRS or immune spleen cell in vitro and then injecting them subcutaneously into irradiated rats (400 R). It was found that 1:20 dilution of RRS protected the rats against AH-64A tumor cell growth while 1:40 and 1:80 dilutions of RRS caused some protection. A subcutaneous tumor mass developed after transplantation of tumor cells treated with RRS, but after about 2 weeks this began to decrease in size and disappeared completely within 6 weeks after transplantation. Treatment of AH-64A tumor cells with immune spleen cells at cell-to-cell ratios of 1:200 and 1:100 caused complete neutralization while normal spleen cells at a ratio of 1:200 had slight effect. Treat;ent with immune spleen cells prevented tumor growth from t;e start. Most of the surviving animals were resistant to c,allenge with 1 times 10(5) fresh AH-64A cells. RRS was fractionated by cellulose acetate membrane electrophoresis and the amounts of beta1- and gamma-globulin fractions were found to be 48 and 42% more than in normal rat serum. The immunoelectrophoretic pattern of resistant rat serum showed a stronger IgM precipitin line than that of normal rat serum.
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PMID:A tumor-specific cytotoxic and neutralizing factor in rats immunized with ascites hepatoma induced by azo dyes. 16 13

Syngeneic tumor cell lines free of endogenous type C virus or viral antigen antigen expression were derived from spontaneously occurring tumors of the BALB/cCr mouse. Two cell lines free of endogenous type C virus were examined and found to be highly tumorigenic in tumor growth kinetic studies. In vitro inoculation of these cell lines with Rauscher-murine leukemia virus (R-MuLV) resulted in their chronic infection in which 95 to 100% of the cells were scored as virus positive. These infected lines showed a highly significant increase in their immunogenicity as compared to their uninfected controls. Animals in which these virus-positive tumors regressed were then shown to be highly resistant to challenge with the uninfected tumor cell lines as well as to live R-MuLV. This observed resistance to uninfected tumor cell lines could not be induced by immunization of the mouse with uninfected tumor cells and R-MuLV simultaneously at the same injection site, nor could it be induced with lethally irradiated virus-infected tumor cells, subtumorigenic doses of uninfected cells, or inactivated R-MuLV or Gross leukemia virus (G-MuLV). Cell-mediated cytotoxicity studies revealed that spleen cells obtained from animals whose virus-infected tumors regressed were cytotoxic to homologous infected and uninfected tumor cells as well as to other uninfected tumor cell lines syngeneic to the BALB/c mouse. Correlation of in vitro cytotoxicity with in vivo immunity was provided by the Winn assay, by inoculation into susceptible mice of immune and nonimmune spleen cells premixed with uninfected tumor cells. The immune cells were highly effective in preventing this tumor cell transplantation. It was concluded that type-C virus infection of these syngeneic tumor cells resulted in their acquiring strong transplantation antigens that were in part due to the virion, but were at least in part due to alterations of antigens or haptens that are present in a less immunogenic form on the uninfected tumor cell.
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PMID:Immunity to virus-free syngeneic tumor cell transplantation in the BALB/c mouse after immunization with homologous tumor cells infected with type C virus. 18 39

The immune response to progressor murine sarcoma virus (P-MuSV)2 and regressor murine sarcoma virus (R-MuSV) was analyzed by the radioisotopic footpad assay (FPA) for delayed hypersensitivity (DH) and by the membrane immunofluorescence assay for anti-tumor antibodies. In mice injected with P-MuSV, the footpad response remained at a low level for 7 weeks, while membrane immunofluorescence antibody titers reached their maximum levels after 5 weeks. By contrast, in mice injected with R-MuSV, the footpad response rose to a maximum by 4 weeks and membrane immunofluorescence antibody titers reached a maximum after 4 weeks. The adoptive footpad response reached its highest level in 2 weeks. A most striking difference between the P-MuSV and the R-MuSV systems was the lower immunogenicity of tumor cells induced by the P-MuSV as measured by the FPA. Considerable differences between the two stocks were also observed in oncogenic activity and tumor growth patterns. The P-MuSV contained one-tenth the amount of helper Moloney leukemia virus found in R-MuSV. Addition of more helper Moloney leukemia virus to the P-MuSV did not produce regressor tumors.
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PMID:Immunological study of two stocks of Moloney sarcoma virus producing regressor and progressor tumors in C57BL/6 mice. 20 43

Complement-dependent cytotoxic antibodies against the cells of mammary tumor MMTI appeared in the blood of C3H/He and C3Hf mice at the terminal stage of tumor growth; at the same time the mice of the above-mentioned substrains showed no difference in the degree of reaction. The level of natural cytotoxic antibodies against MMTI tumor cells detected in old C3H/He and C3Hf mice significantly exceeded their level in young mice affected with tumor; however, MMTI tumor cells grew equally fast in both old and young animals. The sera of mice affected with tumor had a weak cytolytic activity against the cells of hepatoma 22a and did not affect L cells and embryonal fibroblasts. The sera were partially exhasted by spleen and renal tissues, as well as the cells of spontaneous mammary tumor obtained from syngeneic animals and were not exhausted by allogenic cells infected with Rauscher murine leukemia virus.
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PMID:[Cytotoxic antibodies in the serum of C3H mice after inoculating them with spontaneous mammary gland tumor cells]. 22 96

Red blood cell deformability is a major determinant of capillary blood flow. In mice with L1210 leukemia and with Lewis lung carcinoma, red blood cell deformability was significantly decreased during tumor growth. In mice with L1210 leukemia, deformability was significantly decreased by day 5 after transplantation and progressively decreased through day 9. Terminally, red blood cell deformability returned to normal or above normal values. In mice with Lewis lung carcinoma, significant decreases in deformability were noted 21--28 days after transplantation and persisted throughout the remainder of the tumor course. Impaired capillary blood flow, secondary to abnormal red blood cell deformability, is therefore associated with advanced cancer.
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PMID:Impairment of red blood cell deformability by tumor growth. 28 42

We have found that poly(L-lysine) can be a very effective agent in preventing the growth of Ehrlich ascites tumors in mice. When given optimal doses of poly(L-lysine) (Mr 60 x 10(3)) intraperitoneally for 5 consecutive days, beginning on day 1 after inoculation with Ehrlich ascites cells. White Swiss mice show nearly a 100% remission from subsequent tumor growth. Rechallenge of "cured" animals with tumor cells, however shows no long-term immunological protection. In tissue culture, poly(L-lysine) shows a related potent cytotoxicity with HeLa cells; interestingly, the D isomer. In addition, there is a strong molecular weight dependence in that the small polylysine (Mr 3 x 10(3)) possesses less than 1/20th the cytotoxicity of large polymers (Mr 70 x 10(3)) on a weight basis in both cell culture and animal studies. At the same time, none of these lysine polymers gives any significant increase in life span to BDF1 mice infected with L1210 murine leukemia cells. We have also further explored the mechanism by which the polylysines express their cytotoxicity. These data indicate that lysine polymers show cell specificity in their action and in some cases they may be beneficial as potent antineoplastic agents, particularly when molecular weight is taken into consideration.
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PMID:Antineoplastic activity of poly(L-lysine) with some ascites tumor cells. 29 Oct

Sera from 134 selected patients with various types of cancer were tested for soluble antigen-antibody complexes by the C1q binding method. Sera from 85 healthy blood bank donors served as normal controls. C1q binding activity (C1q BA) values above the 95th percentile for healthy subjects were found in 83% of sera from patients with neoplastic diseases. The incidence of abnormal C1q BA values among patients with malignant melanoma was 83%, with breast cancer 74%, with colon cancer 75%, with lung cancer 88%, with leukemia and lymphoma 85%, and with miscellaneous tumors 94%. High C1q BA values were found most frequently in sera of patients who had been diagnosed relatively recently (within 5 mo) and who had evident residual disease after surgical treatment. Recurrence or progression of tumor growth occurred significantly more frequently in lung cancer patients with high C1q BA. DNA was not detected in cancer patients' sera and treatment with DNase did not decrease in C1q BA. C1q BA in sera could not be explained by the presence of antiglobulin antibodies. Sucrose density gradient ultracentrifugation studies of the serum C1q BA in 4 cancer patients showed that the major binding activity was found between 19S and 7S.
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PMID:The C1q binding test for soluble immune complexes: clinical correlations obtained in patients with cancer. 32 5

The life history of a transplantable B cell leukemia (BCL1) that arose spontaneously in a BALB/c mouse is described. Animals bearing this tumor live from 2 to 4 months in apparently good health despite massive splenomegaly and leukemia. Antibody to the idiotype or gamma light chain of the tumor IgM was used in conjunction with the fluorescence-activated cell sorter to identify tumor cells in the BCL1-bearing mice. The results suggest that these cells multiply and differentiate in the spleen and subsequently emigrate to the blood. Tumor cells do not recirculate as evidenced by their failure to enter the thoracic duct or to infiltrate lymph nodes to a significant extent. During tumor growth, a population of T cell blasts appears that may be involved with an immune response against the tumor.
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PMID:Murine B cell leukemia (BCL1): organ distribution and kinetics of growth as determined by fluorescence analysis with an anti-idiotypic antibody. 38 72

A stable phenol, gamma-L-glutaminyl-4-hydroxybenzene (GHB), is oxidized by tyrosinase in the gill tissues of the mushroom Agaricus bisporus to a quinone and a second oxidation product which together suppress mitochondrial energy production and the synthesis of proteins and nucleic acids in the zygote, thus establishing dormancy in the spores. Brief incubation of cultured murine L1210 leukemia and B-16 melanoma cells with muM concentrations of the purified quinone notably prolonged survival times or blocked tumor growth in histocompatible mice inoculated i.p. with high concentrations of the exposed cells. The instability of the quinone precluded in vivo administration. The short incubation of cultured B-16 melanoma cells with mM concentrations of GHB markedly prolonged survival times or abolished tumor growth in histocompatible C57BL/6J mice inoculated i.p. with 5 X 10(6) exposed cells. This response did not occur with L1210 leukemia cells, which lack the enzyme tyrosinase. The survival times of mice bearing B-16 melanoma, but not of those with L1210 leukemia, were slightly prolonged by a single injection and were significantly extended by daily i.p. injections of GHB. Normal C57BL/6J mice, given GHB i.p. as single or multiple 400-mg/kg doses, manifested no systemic toxicity but showed depigmentation of the hair after 2 to 3 weeks. These studies provide evidence that GHB exerts cytotoxicity specifically for cells that by their content of tyrosinase convert the phenol to the quinone. This targeted response minimizes systemic toxocity and underscores the potential therapeutic application of this agent to melanocarcinoma.
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PMID:gamma-L-Glutaminyl-4-hydroxybenzene, an inducer of cryptobiosis in Agaricus bisporus and a source of specific metabolic inhibitors for melanogenic cells. 40

The effect of heat-killed Pseudomonas aeruginosa (10 serotypes) on antibody formation, macrophage activation and leukemia growth was investigated in relation to the dose injected and to the time and the route of administration. It appeared that intravenous administration of the preparation (10(9) bacteria per ml) was the most efficient at the dose of 0.1 ml since: 1) it increased the number of PFC against SRBC when injected 10 days before the antigen (higher doses and shorter time intervals resulted either in no modification or an significant inhibition of the PFC response; 2) it induced a slight activation of peritoneal macrophages as measured by their cytostatic activity for tumor cells in vitro, when injected 3 or 7 days before testing whereas higher doses were ineffective; 3) it increased the survival time of leukemic mice when administered 2.5 days before the injection of L1210 tumor cells, and higher doses were also effective in this immunoprophylaxis assay. When the subcutaneous route was used, large doses appeared to be the most effective: 1) potentiation of the PFC response was obtained only when 0.5 or 0.2 ml were given 10 days before the antigen; 2) macrophage activation was demonstrated 7 and 10 days after 0.5 ml; 3) leukemia growth was retared when 0.5 or 0.2 ml was injected 2.5 days prior to L1210 tumor cell inoculation and also when 0.2 and 0.1 ml were injected 7 days before tumor cells. No correlation between macrophage activation and the inhibition of tumor growth could be found.
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PMID:Heat-killed Pseudomonas aeruginosa as a systemic adjuvant in cancer immunotherapy. 41


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