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

The tumor dormant state established in L5178Y immunized and challenged mice is characterized by a prolonged period of clinical normalcy followed by rapid tumor outgrowth. The tumor cells which emerged after termination of the tumor dormant state had abnormal marker chromosomes identical to those in the L5178Y cells used in the original challenge inoculum, indicating that the emergent tumor cells were progeny of the challenge inoculum. Original and emergent L5178Y cells had equivalent in vivo growth rates, when inoculated into normal DBA/2 mice. The emergent L5178Y cells were less susceptible than original cells to in vitro lysis by tumor dormant PC. Original and emergent L5178Y cells expressed common tumor-associated target antigens for cytolytic effector cells. Both modulation and masking of these target antigens were ruled out as mechanisms for decreased susceptibility to cell-mediated cytolysis. Immunofluorescence revealed heterogeneity in tumor-associated antigen expression within both original and emergent cell populations, with a decreased intensity of staining in the emergent population. Both populations were equally susceptible to lysis by alloimmune cells, alloantiserum, and anti-Thy 1.2 serum, but emergent cells were less susceptible to lysis by serum directed against L5178Y TAA. Quantitative absorption revealed that the emergent L5178Y cells expressed eightfold less serologically detectable TAA than the original cells. These findings indicate that the host immune response developing during establishment of the tumor dormant state selects a stable tumor cell subpopulation which expresses decreased amounts of surface tumor-associated target antigens.
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PMID:The tumor dormant state. Comparison of L5178Y cells used to establish dormancy with those that emerge after its termination. 42 62

The content and activity of the components of liver microsomal aryl hydrocarbon monooxygenase system change biphasically during long-term 3,4-benzo(a)pyrene administration of C57BL/6 mice as well as to (C57BL/6 X DBA/2)F1 hybrids. The first activity peak (4--14 days) is associated with the induction of aryl hydrocarbon monooxygenase by 3,4-benzo(a)pyrene; the second peak (70--84 days) is related to noninductive mechanism. In DBA/2 mice, the second peak is absent while the slight increase in aryl hydrocarbon monooxygenase activity observed on days 14--28 indicates the aberrant inductive capacity of 3,4-benzo(a)pyrene under its prolonged administration. It is suggested that the weak sensitivity to the blastogenesis caused by 3,4-benzo(a)pyrene observed in C57BL/6 mice and in (C57BL/6 X DBA/2)F1 hybrids is due to the high level of liver aryl hydrocarbon monooxygenase activity at the time of tumor appearance.
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PMID:A comparison of the activities of aryl hydrocarbon monooxygenase in liver microsomes from mice of different strains during prolonged 3,4-benzo(a)pyrene administration. 44 73

Ehrlich ascites tumor grows in almost any mouse host. We have found a strain of dystrophic mice to be strongly resistant to Ehrlich ascites tumor. Mice of the dystrophic strain survived injection of Ehrlich Ascites tumor cells that had just been passaged through either dystrophic mice or C57BL X DBA/2 F1, (hereafter known as BD2F1) mice. However, most of the dystrophic mice died when they were given injections of Ehrlich ascites tumor cells that had just been passaged through Swiss white mice. All Swiss white and BD2F1 mice died when they were inoculated with Ehrlich ascites tumor cells, regardless of the type of mouse through which the Ehrlich ascites tumor cells had just been passaged. In some dystrophic mice, the tumor grew to a palpabale size and then disappeared. This provided the opportunity to passage the tumor from one dystrophic mouse to another and thereby to demonstrate resistance in the dystrophic mice to tumor that had grown previously in dystrophic mice. There was no detectable difference in the rate of tumor growth in either Swiss white or BD2F1 mice.
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PMID:Resistance to Ehrlich ascites tumor in a strain of dystrophic mice. 44 11

A/J, C3H/HeJ, DBA/2J, and C57BL/6J mice have different susceptibilities to polycyclic aromatic hydrocarbon-induced pulmonary neoplasia, whereas the livers from these animals are uniformly resistant to the carcinogenic actions of these substances. After i.v. injection of [3H]-3-methylcholanthrene, radiolabel was detected in the DNA of both lung and liver of all these strains. The DNA was digested to deoxyribonucleosides and chromatographed on Sephadex LH-20. The amounts of nucleoside-bound adducts detected varied markedly with the different tissues and strains. These adducts were undetectable in liver DNA by 28 days. Although all lung preparations showed some reduction in adducts by 28 days, the amounts in A/J lung were always highest; this correlated with its high susceptibility to neoplastic transformation. In all preparations, radioactivity eluted from Sephadex LH-20 with the column void volume or with underivatized nucleosides. Tissue, but not strain differences were observed in these chromatographic profiles. The predominance of these early-eluting peaks in liver, rather than lung, suggests that they may represent noncarcinogenic lesions. This radiolabeled material remains uncharacterized, but some possibilities are discussed.
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PMID:Persistent binding of 3-methylcholanthrene to mouse lung DNA and its correlation with susceptibility to pulmonary neoplasia. 44 39

Effect of 1,1,1-trichloropropene 2,3-oxide and 7,8-benzoflavone on benzo[a]-pyrene and 3-methylcholanthrene carcinogenesis in the subcutaneous tissues of C3H/He and DBA/2 mice was examined. By a single application of the carcinogen, the incidence of fibrosarcoma was higher and the latency of tumorigenesis was shorter in C3H/He mice than in DBA/2 mice. Treatment with 1,1,1-trichloropropene 2,3-oxide increased the incidence of fibrosarcoma in DBA/2 mice, but decreased the rate in C3H/He mice, when benzo[a]pyrene was used as a carcinogen. On the other hand, in 3-methylcholanthrene carcinogenesis, no effect of the oxide on the tumor incidence was observed. By the simultaneous application of 7,8-benzoflavone with benzo[a]pyrene, the tumor incidence increased, but not so significantly in DBA/2 mice, compared to that treated with benzo[a]pyrene alone, and no appreciable effect was observed in C3H/He mice treated with benzo[a]pyrene, and in both strains of mice with 3-methylcholanthrene. The relationship between the activity of arylhydrocarbon hydroxylase and the change in polycyclic hydrocarbon carcinogenesis is briefly discussed.
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PMID:Effect of trichloropropene oxide and benzoflavone on polycyclic hydrocarbon carcinogenesis in C3H/He and DBA/2 mice. 44 77

Genetic control of hybrid resistance to the BALB/c plasmacytoma MPC-11 was investigated. The results indicate that a single dominant autosomal gene or gene complex, which segregates independently of H-2 and the coat color c and b-loci, controls resistance to this tumor. This gene has the same strain distribution pattern in the CXB Bailey recombinant inbred strains as three unlinked genes, H-2, Ly-4, and Ea-4. It is possible, therefore, that it could be linked to either of the latter two loci. Strains that carry a positive allele for resistance are C57BL/10 and all of its congenic resistant partners tested, C57BL/6, C57L, C57BL/Ks, AKR, and DBA/1. BALB/c and its congenic resistant partners are presumed to carry a negative allele of the gene for resistance to MPC-11. Strains such as SJL, DBA/2, and A and its congenic resistant partners, which form susceptible hybrids with BALB/c, could carry either the negative allele of the gene for resistance, like BALB/c, or could carry both a positive allele of the gene and some other gene conferring susceptibility on the hybrids. Heterozygosity within the H-2 complex increases resistance only in the presence of this non-H-2 linked gene for resistance, and the effect maps to the left of the H-2D region.
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PMID:Hybrid resistance to BALB/c plasmacytomas. I. Resistance to MPC-11 controlled by a locus not linked to H-2. 44 97

The biochemical and biological effects of the combination of 5-aza-2'-deoxycytidine (5-aza-dCyd) and 3-deazauridine (3-DU) on L1210 leukemic cells and EMT6 tumor cells were investigated. The cytotoxic action of 5-aza-dCyd and 3-DU on both L1210 and EMT6 cells in vitro was synergistic when these agents were used in combination. The combination of 5-aza-dCyd and 3-DU produced a greater inhibition of in vitro growth of L1210 and EMT6 cells than did either agent alone. The in vivo antineoplastic activity of this combination was synergistic with respect to the increased survival time of BALB/c x DBA/2 F1 mice with L1210 leukemia. 3-DU, an agent that reduces the intracellular pool size of cytosine nucleotides, stimulated the incorporation of [3H]-5-aza-dCyd into DNA of both L1210 and EMT6 cells, suggesting that the synergistic action of this combination is related to the increased incorporation of 5-aza-dCyd in the presence of 3-DU.
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PMID:Synergistic action of 5-aza-2'-deoxycytidine and 3-deazauridine on L1210 leukemic cells and EMT6 tumor cells. 47 19

The metastasizing MDAY-D2 tumor of DBA/2 mice disseminates in BALB/c allogeneic athymic nude (nu/nu) mice in a manner identical to that observed in the syngeneic host. Both the kinetics and organ distribution pattern of metastases from s.c. implants of MDAY-D2 are routinely predictable at any given tumor dose. BALB/c heterozygote (nu/+) litter-mates reject MDAY-D2 grafts on the basis of the multiple minor histocompatibility differences that exist between DBA/2 and BALB/c mice. The in vitro cell-mediated cytotoxic response detected in tumor-bearing BALB/c nu/+ mice is "low grade" (isotope release is approximately 40 to 50% by 24-hr 111-indium-8-hydroxyquinoline assay and approximately 6 to 8% by 6-hr 51Cr assay) and yet correlates directly with tumor rejection. BALB/c nu/nu mice can be protected against MDAY-D2 by previous reconstitution with lymphoid cells from normal or MDAY-D2-sensitized BALB/c nu/+ mice. In addition, surgically documented, established visceral metastases in BALB/c nu/nu mice can be arrested and regressed by the adoptive transfer of MDAY-D2-sensitized BALB/c nu/+ spleen cells. This represents one of the few models where established metastases have been immunotherapeutically regressed. As such, the MDAY-D2 BALB/c nu/nu mouse model offers unique advantages for studying the role of the immune system in regulating the metastatic process.
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PMID:Immune-mediated arrest and reversal of established visceral metastases in athymic mice. 47 40

The distribution of purified 125I-labeled alloantibodies, prepared from the serum of DBA/2J mice obtained after immunization with C3H/HeJ spleen cells, was studied in immunosuppressed DBA/2J mice bearing either allogeneic C3H/HeJ 3-methylcholanthrene sarcomas growing s.c. or syngeneic SaD2 3-methylcholanthrene sarcomas. Once purified radiolabeled antibody was isolated from 125I-labeled immune gamma-globulin by a single adsorption onto C3H/HeJ RBC and elution from stroma prepared from these cells, by using 0.1 M glycine buffer (pH 3.0). Twice-purified alloantibody was then produced by Bio-Gel P-200 or Sephadex G-200 gel filtration chromatography or DEAE A-50 ion-exchange chromatography. In vitro, such purified antibodies bound specifically to C3H/HeJ RBC. In vivo, they localized to a significant extent following i.p. injection, preferentially in C3H/HeJ 3-methylcholanthrene sarcomas (4.4 to 8.9% of the injected dose per g of tumor equal to 1% of mouse weight), with mean tumor/blood ratios of 4.0 to 7.8, at 24 or 48 hr after injection. The percentage of injected dose localized in tumor and the tumor/blood ratio did not show significant differences with respect to time or method of antibody purification. Normal tissue/blood ratios in C3H/HeJ or SaD2 sarcoma-bearing mice were less than 0.9. The tumor/blood ratios in SaD2 sarcomas were approximately 0.6. Injection of 131I-labeled normal DBA/2J gamma-globulin resulted in normal tissue/blood and tumor/blood ratios of less than 0.9 in C3H/HeJ tumor-bearing mice.
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PMID:Distribution of radiolabeled alloantibodies in mice bearing 3-methylcholanthrene-induced sarcoma. 47 67

MDAY-D2 is a highly tumorigenic and anaplastic DBA/2 strain murine transplantable tumor capable of rapid and widespread spontaneous metastatic growth. It was therefore chosen as an ideal murine tumor model for the study of factors affecting metastatic growth. Two approaches were taken in an effort to obtain stable qualitative and quantitative low-metastatic variants of MDAY-D2, namely, cloning of multiple sublines and derivation of lectin-resistant (LecR) mutants. In the first method, 20 clones were isolated, and of these, three initially showed a marked reducstion in ability to metastasize from a subcutaneous site. However, these clones proved to be unstable both in vivo and in vitro. In the LecR selection experiments, 18 independent variants were obtained using chemical mutagenesis followed by treatment with wheat germ agglutinin (WGA), phytohemagglutinin (PHA), or concanavalin A (Con A). All of the variants proved to be highly metastatic except two WGAR variants, designated MDWI and MDW3. They proved to be nontumorigenic in normal DBA/2 hosts even when as many as 5 X 10(6) cells were injected, and this was found to be a stable change. Despite this fact, the nontumorigens an unchanged expression of H-2d and Ly-6.2 alloantigens and Fc receptors. The variants were, however, tumorigenic and metastatic in severely immunosuppressed (nude) mice, but not in moderately immunosuppressed 250-R-irradiated DBA/2 hosts. The results demonstrate that 1) stable membrane mutant sublines possessing radically altered growth properties in vivo can occasionally be obtained by selection of LecR variants, and 2) their growth and metastatic properties can be greatly affected by the immunologic status of the host. The possibility that the chemical mutagen treatment itself induced, or was responsible for, MDW1 and MDW3 variant formation is also discussed.
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PMID:Immunologic studies of membrane mutants of a highly metastatic murine tumor. 50 93


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