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

The differential immunogenicity of DBA/2 lymphoma L1210 and three L1210 sublines, each resistant to a different anti-leukemic agent (guanazole, methylglyoxal-bis-guanylhydrazone, and 4,4-diacetyldiphenylurea-bis-guanylhydrazone), was evaluated in vitro. Syngeneic spleen cells from nonimmunized DBA/2 mice were cultured in the presence of graded numbers of irradiated cells of L1210 or its sublines. The stimulation elicited a T-independent primary antibody response in vitro which was measured by determining the number of plaque-forming cells by using the immunizing lymphoma cells as target. Cells of all three sublines exhibited an increased immunogenicity, as compared to that of the parental L1210 cells, in eliciting the response directed to tumor-associated antigens which were common to all sublines. Dose-response experiments showed that high doses of the parental cells did stimulate responses which were detectable with subline cells as target. The results indicated that the differential immunogenicity of L1210 and its sublines, as demonstrated in the present assay system, is primarily quantitative, and was apparently due to increased amount or density of common tumor-associated antigens on the subline cells. The implications of these observations are discussed in relation to the possible mechanisms underlying the emergence of highly immunogenic drug-resistant sublines.
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PMID:Differential tumor immunogenicity of L1210 and its sublines. I. Effect of an increased antigen density on tumor cell surfaces on primary B cell responses in vitro. 33 Jul 61

Subcutaneous injection of normal allogeneic kidney and liver tissues extended survival of DBA/2Cr mice challenged with a lethal dose of syngeneic L5178Y lymphoma cells. Immunization with a combination of tissues from five strains provided far more protection than immunization with tissue from any single strain. It is suggested that the basis of this protective effect is a cross-reactivity or identity between tumor-associated transplantation antigens (TATA) on the L5178Y tumor and non-H-2 alloantigens normally expressed by some allogeneic tissues.
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PMID:Protection against syngeneic tumor grafts induced by inoculation with normal allogeneic tissues. 34 93

The thymus dependency of humoral immunity to syngeneic tumor antigens was investigated in T cell-deficient DBA/2 mice. ATXBM animals bearing the T1699 mammary tumor in the subcutaneous abdominal area displayed normal immediate but not delayed hypersensitivity reactions (DHR) to 3 M KCl-extracted T1699 antigens injected into the footpad. Sera from ATXBM tumor-bearers passively transferred immediate hypersensitivity but failed to support tumor-specific macrophage-mediated ADCC reactions. The synthesis of macrophage-mediated ADCC antibody was greatly reduced in the CXBM animals when compared to nonirradiated tumor-bearers. The CXBM mice, however, showed normal T cell function as measured by allograft rejection, antibody response to sheep erythrocytes, and DHR to T1699 antigens. Of all antibody classes and subclasses tested by indirect membrane fluorescence, only IgG2b was found to be produced at normal levels by either ATXBM or CXBM tumor-bearers. The results show that IgG2b antibody production in response to T1699 syngeneic tumor antigens is thymus independent and suggest that this antibody is the mediator of immediate hypersensitivity. The synthesis of macrophage-mediated ADCC antibody (IgG2a) was found to be not only thymus dependent but also sensitive to the long-term effects of irradiation and bone marrow repopulation.
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PMID:Immunity to the T1699 murine mammary tumor. I. Thymic influence and long-term effect of irradiation on the humoral response. 38 22

ARyl hydrocarbon hydroxylase (AHH) in mouse epidermis was inducible by topical application of several tumor-initiating polycylic aromatic hydrocarbons. The weak tumor initiator 1,2,3,4-dibenazanthracene (1,2,3,4-DBA), at dose level of 200 nmoles, increased AHH activity more than 10-fold over that of the acetone controls at 12 hr after treatment. Administration of the same quantity of the potent initiator 7,12-dimethylbenz(a)anthracene (DMBA) increased AHH activity approximately 4-fold over that of the control at 12 hr after treatment. Simultaneous treatment with 200 or 100 nmoles of DMBA and 1,2,3,4-DBA resulted in AHH activity that was 546 and 732% that of the controls, respectively, 12 hr after treatment: this was less AHH activity than was observed when 1,2,3,4-DBA was administered alone. Doses of 20 nmoles or more of 1,2,3,4-DBA, when given at about the same time as DMBA, effectively inhibited DMBA initiation of skin tumors in a two stage system of tumorigenesis. The results suggest that the weak initiator 1,2,3,4-DBA may program the epidermal AHH system to metabolize the strong carcinogen DMBA to noncarcinogenic intermediate(s).
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PMID:Inhibition of the tumor-initiating ability of the potent carcinogen 7,12-dimethylbenz(a)anthracene by the weak tumor initiator 1,2,3,4-dibenzanthracene. 40 69

The immune reactivity to tumor cells within a progressively growing tumor mass in the syngeneic host has been analyzed by studying the cell-mediated cytolytic response of DBA/2 mice to the ascitic mastocytoma P815Y. Peritoneal cells from P815Y tumor-bearing hosts were fractionated by velocity sedimentation at unit gravity. Cell-mediated cytotoxicity of fractionated and unfractionated cells was measured by 51Cr-release from tumor target cells. The cell separation procedure revealed significant levels of specific cell-mediated cytotoxicity to P815Y within peritoneal cell populations at 8-16 days after tumor cell inoculation. Tumor cells purified from the peritoneal cell populations of mice injected with 10(3) tumor cells 10 days previously were as susceptible to syngeneic and allogeneic cell-mediated cytotoxicity as P815Y grown in vitro. However, tumor cells obtained from mice 16 days after tumor inoculation were resistant to cytolysis by syngeneic, but not allogeneic, effector cells. In addition, day 16 tumor cells did not inhibit syngeneic cell-mediated cytotoxicity against P815Y grown in vitro. Immunoglobulin was not detected on day 16 tumor cells and no circulating antibody to P815Y was found in the ascitic fluid of day 16 tumor-bearing mice. These results indicate that tumor cells may escape immune attack by loss of expression of cell surface tumor-associated antigens in the absence of circulating antibody against tumor.
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PMID:Development of tumor cell resistance to syngeneic cell-mediated cytotoxicity during growth of ascitic mastocytoma P815Y. 40 6

The tumor-inhibitory effect of an intralesional injection of Propionibacterium acnes was of limited duration ("finite"). Our model was the DBA/2 syngeneic mouse injected with P815 mastocytoma cells (5 X 10(5)) into each rear footpad; only the left was treated, leaving the right as a "pseudometastasis." The finite effect occurred at approximately 21 days after the first treatment. Subsequent i.p. treatments with P. acnes did not alter this effect, although they increased mean survival time. With one footpad tumor, we achieved 22% cures with complete regression and no sign of metastatic growth. A RNA fraction from P. acnes produced inhibition of tumor growth, but crude cell walls and cell walls treated with Pronase had no effect. A P. acnes cytoplasmic fraction with tumor-inhibitory activity was pelleted by high-speed centrifugation; this fraction inhibited P815 mastocytoma as fully as whole cells injected in one-fifth the dose on a nitrogen basis and did not cause a local inflammatory reaction. The activity of the pellet also differed from whole cells in that it was equally inhibitory to the pseudometastasis in the contralateral right rear footpad. The cytoplasmic fraction apparently contained at least two active components since activity was obtained at two dilution levels. Such activity was relatively stable at 5 degrees, but it was unstable at -30 degrees.
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PMID:Antitumor activity of Propionibacterium acnes (Corynebacterium parvum) and isolated cytoplasmic fractions. 40 91

The growth of L 1210 leukemia in DBA/2 strain mouse, provokes in the grafted animals intraleucocytic enzymatic modifications. As increase of acid phosphatase and a decrease of beta-glucuronidase were observed in the lymphocytes, the level of polymorphonuclear non-specific esterase being decreased. The implications of these modifications in the host response toward the tumor is discussed.
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PMID:[Cytochemical study of leucocytes of DBA/2 Mice after leukemia L1210 tumor graft]. 41 May 51

DBA/2 mice were treated with four successive subcutaneous injections of rabbit anti-theta-gamma-globulin followed by the subcutaneous implantation of chemically induced mastocytoma (P-815-X2). Another series of animals received rabbit anti-thymus-gammaglobulin according to the same schedule and still another series of animals served as non-treated controls. A definite augmentation of the tumor growth, as evidenced by the dissemination of the tumor into the spleen, liver and kidney, was evident in the globulin-treated series. Such dissemination was not observed in the control animals, where the metastases were limited to the reginal lymph nodes. The studied gammaglobulins were different in two important respects; the death rate of animals and the frequency of thymic metastases were higher in the anti-theta-globulin series. These findings advocate the conclusion that anti-theta-globulin, prepared against the brain tissue, is the more specific and more potent T-lymphocyte suppressor of these two globulins studied. T-lymphocyte population seems to play an important role in host resistance against experimental neoplasia.
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PMID:The influence of anti-theta-globulin treatment on the growth of mastocytoma in mice. 41

In DBA/2 mice bearing transplanted, syngeneic P815 mastocytoma, macrophage accumulation was impaired in the tumor when the cancer grew intraperitoneally. By varying the number of transplanted mastocytoma cells and quantitating the macrophage response to a standardized stimulus of proteose peptone, we determined that 4-16x10(6) mastocytoma cells were required to inhibit monocyte inflammation. That interference with monocyte inflammation required a threshold number of tumor cells was consistent with an increase in tumor-associated macrophages proportional to tumor growth during early cancer. It was also consonant with a greater number of macrophages in tumors initiated with small rather than large tumor inocula. Impairment of monocyte inflammation could be passively transferred with ascitic fluid.
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PMID:Tumor cell threshold required for suppression of macrophage inflammation. 41 87

The effects of 5-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC), 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (MeCCNU), and L-phenylalanine mustard (L-PAM) have been compared by using three i.p. transplanted mouse melanomas: the B16 melanoma in C57BL/6 mice; the Harding-Passey (HP) malanoma in BALB/c X DBA/2F1 (hereafter called CD2F1) mice; and the Cloudman S91 melanoma in DBA/2 mice. HP melanoma responds well to all three drugs. S91 responds only to L-PAM and MeCCNU. DTIC may accelerate death in mice bearing this tumor. B16 responds well to L-PAM and moderately well to MeCCNU and to multiple injections of DTIC. The best response to DTIC and MeCCNU is given by HP, while the best response to L-PAM is given by S91. Tumor cell-doubling times were found to be 1.5 days for B16, 2 DAYS FOR HP, and 3 days for S91. HP would seem to be the most responsive malanmoma with respect to the 3 agents studied. This may be due to an interaction between the chemotherapeutic agents and the host immune response, since the HP tumor arose in a noninbred mouse and is thus nonsyngeneic with the CD2F1 host. All three tumors appear to be interesting biological models for studying drug combinations and combined therapeutic modalities against melanoma.
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PMID:Effects of 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide, 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea, and L-phenylalanine mustard on B16, Cloudman S91, and Harding-Passey mouse melanomas. 42 82


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