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

The expression of receptors for the Fc portion of IgG immunoglobin molecules was studied on tumor cell lines with high and low metastatic capacity. Two tumor cell lines from DBA/2 mice that had high metastatic activity, ESb and MDAY-D2, contained a high percentage of Fc receptor positive cells, as detected in a rosette assay with IgG antibody-coated erythrocytes (EA). In contrast, the low metastatic parental line Eb, from which ESb was derived, contained only a low percentage of EA-rosette-forming cells. ESb ascites tumor cells adapted to tissue culture in the presence of 2-mercaptoethanol (2ME) had a high expression of Fc receptors, whereas a cell line adapted to tissue culture in the absence of 2ME had a low expression of Fc receptors. "Soluble" Fc receptors were detectable by their ability to bind to EA and to cause blocking of rosette formation. They were found to be present in fluids from tumor-bearing animals, such as serum and cell-free ascites. Even animals with an ascites tumor of the low-metastatic line Eb contained "soluble" Fc receptors. The results are discussed with regard to their possible significance for tumor metastasis.
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PMID:Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. VIII. Expression and shedding of Fc gamma receptors on metastatic tumor cell variants. 52 81

A dual-antigen, dual-isotope assay has been used to monitor the migratory behavior of selectively labeled antiallogeneic lymphocytes in mice challenged subcutaneously in all four foot pads with semiallogeneic spleen cells. 3H-labeled anti-C3H and 14C-labeled anti-C57BL lymphocytes of DBA/2J origin were pooled and adoptively transferred to multiple groups of previously challenged DBA/2J recipients. In some of the studies, separate groups of recipients were challenged with either CDF or BDF spleen cells in all four paws, whereas in others CDF spleen cells were used to challenge the right paws of each mouse in the group and BDF spleen cells to challenge the left paws of each mouse in the group. At intervals varying from 24 to 96 h after challenge, a subgroup of four mice from each appropriate group was sacrificed and the relative numbers of anti-C3H and anti-C57BL lymphocytes present in the challenged paws, draining lymph nodes, and other tissues of each mouse were inferred from the mean 3H/14C ratios of the respective tissues of that subgroup. The results of these studies firmly establish that specific antiallogeneic lymphocytes are selectively recruited to the paws and draining lymph nodes of mice challenged subcutaneously in the foot pads with semiallogeneic spleen cells and are deleted from their circulating blood and nondraining lymph nodes. A mechanism for antigen-induced selective recruitment and its possible functional significance in tumor immunology are discussed.
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PMID:Migratory behavior of lymphocytes with specific reactivity to alloantigens. II. Selective recruitment to lymphoid cell allografts and their draining lymph nodes. 62 33

The respective role of anti-H-2 K/D and anti-H-2 Ia antibodies in allotransplanted tumor enhancement was tested in vivo on two experimental tumors. Sa I A/4 (H-2a, i.e., H-2k/d) was enhanced in CBA (H-2k) and C57BL/Ks (H-2d) strains with anti-A/J immune sera prepared in CBA and C57BL/Ks, respectively. EL 4, C57BL/6 (H-2b) lymphoma, was enhanced in DBA/2 (H-2d) and BALB/c (H-2d) with immune sera prepared in DBA/2 and BALB/c. Anti-K/D antibodies were obtrained by elution from glutaraldehyde-treated RBC previously incubated with corresponding alloimmune sera prepared in mice immunized with spleen cells, thymocytes, or two consecutive skin grafts syngeneic to the RBC. The residual complement-dependent serocytotoxicity for target lymphocytes observed after complete hemagglutinin absorption on corresponding RBC was attributed to anti-Ia antibodies. RBC eluates (anti-K/D) were found to be enhancing for both experimental tumors and for all studied sera. After RBC absorption, the sera lost all enhancing activity when they were prepared by immunization with spleen or thymus cells, but remained enhancing in some sera prepared by immunization with skin grafts. Both types of antibodies (anti-K/D and anti-Ia) therefore appear able to enhance allografts. These results are compatible with the in vitro correlates of the two phases of the transplantation reaction: initiation phase (mixed lymphocyte reaction) inhibitable by anti-Ia and effector phase (cell-mediated cytotoxicity) inhibitable by anti-K/D.
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PMID:Ia versus K/D antigens in immunological enhancement of tumor allografts. 63 85

Incorporation of 3H-TdR into EL4 leukemic cells in vitro was inhibited by peritoneal exudate cells (PEC) harvested from syngeneic C57BL/6J mice given an intraperitoneal (i.p.) injection of 1x10(7) viable Mycobacterium smegmatis ATCC 607 (Smeg) 4 days before. This phenomenon was also observed in the following five systems of PEC from animals and syngeneic tumor cells: C57BL/6J mice and B16 melanoma; DBA/2 mice and P815 mastocytoma; SWM/Ms mice and K5 fibrosarcoma; BALB/c, nu/nu mice and KKN-1 fibrosarcoma; and strain 2 guinea pigs and line-10 hepatoma. The in vitro cytotoxicity of the PEC activated by viable Smeg was much higher than those activated by dead-Smeg, viable BCG or proteose peptone. The activity of the adherent fraction of the PEC was stronger than that of the nonadherent one, and not influenced by either anti-theta or anti-mouse lymphocyte rabbit sera. The PEC induced with Smeg 4 days before contained a large population of mononuclear cells (88.9%) and a significant level of polymorphonuclear cells (PMN) (3.2%), and showed a much higher cytotoxicity than the PEC induced with Smeg 3 hr before, which contained a much larger population of PMN (71.9%), suggesting that PMN were not the effector cells in this system. In vitro and in vivo treatment with macrophage-inhibitors such as carrageenan, trypan blue and cytochalacin B, reduced the activity of the PEC. All of these facts suggested macrophages as the effector. Viable macrophages were required for the growth inhibition of EL4 in vitro: gamma-ray irradiated or freeze-thawed macrophages were ineffective. Kinetic studies revealed that inhibition of 3H-TdR incorporation into EL4 cells started within 3 hr of incubation together with the activated macrophages at an effector to target (E/T) ratio of 5, and the incorporation decreased gradually with the lapse of incubation time. On the other hand, 51Cr release from labelled EL4 was undetected when the E/T ratio was 5 but detected at on E/T of 10 or more. Even at the higher E/T ratio, at least 10 hr were needed until the release of 51Cr, suggesting that the activated macrophages produced growth inhibition of tumor cells followed by cell destruction.
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PMID:In vitro cytotoxicity of peritoneal macrophages activated with Mycobacterium smegmatis. 66 26

The in vivo growth of EL-4 ascites tumor cells in peritoneal cavities of syngeneic (C57BL/6) and allogeneic (DBA/2) mice was monitored by electronic volume analysis. In the growth of EL-4 cells in the C57BL/6 mice, daily decrease in electronic modal cell volume and labeling indices was observed. After day 7, the rejection of EL-4 cells in DBA/2 mice was indicated by increase in the percentage of small cytotoxic lymphocytes and decrease in the labeling indices of tumor cells.
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PMID:Electronic cell volume analysis of growth and rejection of EL-4 ascites tumor cells. 71 86

An H-2 heterozygous sarcoma, MDAY, originally induced with methylcholanthrene in an (A X DBA/2)F1 ((H-2a X H-2d) hybrid host was selected for growth in the H-2d homoxygous parental DBA/2 strain by serial intraperitoneal transplantation of ascites tumor cells. An apparent variant, designated MDAY-D2, was obtained which showed the expected loss of the private and public H-2Kk haplotype antigens normally associated with the A strain parent and the original MDAY tumor. Comparison of the original and variant lines revealed a wide variety of a cell surface antigen and receptor differences. Both tumors were found to be highly anaplastic and histologically unclasssifiable. Examination of the two tumor lines growing in vivo revealed a remarkable difference in their metastatic growth potential. The original MDAY line showed little propensity to spread to any organ site, with the occasional exception of liver, after subcutaneous inoculation of (A X DBA/2)F1 mice. In striking contrast, there was a rapid and massive spread of MDAY-D2 to liver, spleen, lungs and kidneys within 12-16 days: liver and spleen could be totally replaced by tumor within 2-3 weeks. These characteristics were observed in both (A X DBA/2)F1 and DBA/2 mice. The tendency to metastasize, as well as loss of the H-2Kk haplotype, appeared stable and irreversible. Although the precise origin of MDAY-D2 is not clear, its metastasizing properties are unique, making it a useful and desirable model to study the biology of metastasis.
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PMID:Induction of a tumor with greatly increased metastatic growth potential by injection of cells from a low-metastatic H-2 heterozygous tumor cell line into an H-2 incompatible parental strain. 72 18

Low numbers (10(4)) of peritoneal exudate L1210 mouse lymphoma cells were injected into DBA/2 mice subcutaneously and the development of tumours was followed. Tumour takes occurred in 100% of the animals within 9 days after tumour transplantation. The latent period of tumour development was prolonged by 6-10 days when tumour cells of the peritoneal exudate, depleted of adherent/phagocytic cells, were used in the inoculum or when tumour cells derived from continuous cell cultures were used. Addition of adherent cells in high numbers to in-vitro-derived L1210 cells accelerated tumour growth. This effect was found to be not specific for adherent/phagocytic cells, as liver cells had the same influence on tumour growth. It is concluded that, under certain experimental conditions, a cell population with the functional properties of macrophages is able to promote tumour development, most likely due to their non-specific effect on the micro-environment of the growing tumour.
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PMID:Promotion of L1210 tumour growth by macrophages. 72 47

The efficacy of glucan in combination with local radiation therapy was measured using three solid murine tumors of differing abilities to induce a host defense. Using the KHT fibrosarcoma which induces no measurable host defense, glucan did not improve tumor-free survival over radiation alone; the combination produced a marginal improvement in tumor-free survival in animals bearing the highly immunogenic EMT-6 tumor. The most marked improvement in tumor-free survival was found with the mildly immunogenic 6C3HED lymphosarcoma. The efficacy of glucan in combination with BCNU chemotherapy was measured using the disseminated AKR transplantable leukemia; the combination yielded a high level of cures compared to no survival for either agent alone. Using the AKR transplantable leukemia in an F1 model, the effect of amphotericin B (AmB) alone or in combination with BCNU was tested. AmB or BCNU alone had little or no curative effect when tested in (AKR X DBA)F1 mice, but 56% of mice were cured when combined therapy was employed. When tested in (AKR X C57BL)F1 or (AKR X A)F1 mice, a small fraction was cured with AmB alone while about 90% were cured with either BCNU alone or the combination.
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PMID:Preliminary observations on the effect of glucan in combination with radiation and chemotherapy in four murine tumors. 72 4

The role of host hematopoietic stem cells in the formation of tumor colonies in the spleen of (C57BL/6 X DBA/2) F1 mice after grafts of spleen cells from Friend virus (FVP)-infected donors has been investigated. Hematopoietic stem cell compartments of recipient mice were destroyed by Myleran treatment or gamma-ray irradiation. A single injection of Myleran reduced the pluripotent hematopoietic stem cells (CFU) and the erythropoietin responsive cells (ERC) in polycythemic mice to around 1% of that of controls. Repeated injections of erythropoietin (EPO) restored the erythropoietic precursor cell (ERC) population. Pretreatment of polycythemic hosts with Myleran totally suppressed the tumor colony forming ability of grafted Friend virus-infected spleen cells, whereas it had no effect on tumor colonies produced by inoculation of true tumoral Friend cells. After EPO injections in such Myleran-treated recipients, with a consequent appreciable ERC repopulation, splenic colonies again occurred. Similar results were obtained in hosts whose ERC populations were damaged by irradiation. These data strongly suggest that splenic colonies result from the proliferation of the host cells transformed by virus released by Friend virus-infected cells and not from the proliferation of donor tumor cells.
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PMID:Incapacity of hematopoietic stem cell-deprived mice to produce tumor colonies induced by Friend virus-infected cells. 74 2

Serum samples from about 10 males and 10 females from each of 15 genetically defined strains of rabbits and from one hybrid were tested as sources of complement for the microtiter lymphocytotoxicity test using as target cells lymph node cells from C3H/HeJ, B10/Sn, BALB/cJ, and DBA/2J strain mice. The lynph node cells were tested with appropriate H-2 alloantisera. Results indicated marked strain differences. Correlation analysis of these data with data using primarily aliquots from the same serum samples tested against lymph node cells from B10.A/Sn mice showed clearly that a genetically defined population of rabbits that provided serum of high quality for one of these test systems would in general work reasonably well in any one of the other four. The correlation coefficients in all possible combinations ranged from +0.49 to +0.92. Of the five strains tested, the results obtained from BALB/cJ appear to be the best predictors of the results in the other four strains (r values were +0.74, +0.57, "0.76, and +0.92). Studies are in progress to test rabbit serum complement samples against the more demanding tumor cells.
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PMID:Effect of rabbit strain on activity level and cytotoxicity of serum complement. II. Comparison of five murine target cells. 74 74


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