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

The effect of specific priming with alloantigens on the frequency of cytolytic T lymphocyte precursors (CTL-P) has been investigated. Alloimmune lymphoid cells were obtained from the spleen of C57BL/6 (H-2b) mice primed with DBA/2 (H-2d) tumor cells or from 14-day unidirectional mixed leukocyte cultures (C57BL/6 anti-DBA/2). CTL-P frequencies directed against H-2d alloantigens were estimated by limiting dilution analysis in a sensitive micro MLC system. Under these conditions, an apparent increase of 3 to 4-fold in CTL-P frequency was observed in alloimmune (as compared with normal) C57BL/6 spleen cells. Evidence was obtained suggesting that this increase was specific for the priming alloantigens. A much greater increase in CTL-P frequency (25 to 100-fold) was observed after alloimmunization of C57BL/6 spleen cells in unidirectional MLC. Under the latter conditions, 5 to 20% of the surviving splenic MLC cells could be identified operationally as CTL-P. A similar enrichment in CTL-P frequency was obtained when lymph node, peripheral blood, or thymus cells were cultured for 14 days in MLC. These studies provide direct evidence that the pool of specific CTL-P can be expanded after alloimmunization. Furthermore, the very high frequencies observed after in vitro priming indicate that this system should be particularly useful for future studies of the progeny of individual CTL-P.
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PMID:Limiting dilution analysis of alloantigen-reactive T lymphocytes. III. Effect of priming on precursor frequencies. 15 30

Cellular immunity directed against polyoma virus-induced antigen was observed with C3H/HeJ splenic lymphoid cells from mice sensitized by a short-term immunization schedule with syngeneic polyoma 4198 and 4198V tumor cells. Polyoma specificity of the response was shown by demonstration that splenic cells from DBA/2J animals with polyoma virus-induced tumors were cytotoxic for the C3H 4198 and 4198V cells, but not for the L-M cell, another cell line of C3H origin. The polyoma-specific response in the syngeneic system was detectable with the dye exclusion assay but not with the colony inhibition procedure. Colony inhibition with the L-M cell was observed with sensitized lymphoid cells in both allogeneic and syngeneic systems.
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PMID:Evaluation of dye exclusion and colony inhibition techniques for detection of polyoma-specific, cell-mediated immunity. 16 18

Infection of Moloney mouse sarcoma virus (M-MSV) in adult mice of several inbred strains revealed that all strains except AKR are highly susceptible to M-MSV tumor development. F1 hybrids between AKR and CBA, DBA/2 or NIH mice are as resistant (93%) as the parental AKR strain, which indicates that resistance is transmitted as a dominant character. First backcross mice to the susceptible parent show a 3:1 ratio of resistant to susceptible mice. This is the expected ratio for two segregating loci which independently confer resistance. The incidence of resistant F2 mice is somewhat lower than expected. Further support for the two-gene hypothesis was obtained in second backcross mice. None of the major genes affecting MuLV infection (Fv-2 and H-2) seems to play any role in this system and no linkage was found with Thy. 1 and albino, dilute, agouti and brown markers.
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PMID:Genetic control of oncogenesis by murine sarcoma virus Moloney pseudotype. I. Genetics of resistance in AKR mice. 17 Feb 19

Mouse C3H embryo cells were transformed in vitro by avian sarcoma virus Bratislava 77 (B77) released scantily from a mouse cell line transformed earlier by the same virus. B77 virus transformed C3H embryo cells contained B77 viral genome and were transplantable into syngeneic as well as allogeneic DBA/2J young mice in which autochthonous sarcomas were induced. Tumors in both strains of mice were virogenic. The probable reasons for an increased transformation capacity of B77 virus in mammals are discussed.
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PMID:Neoplastic transformation of mouse embryo cells by virus released from tumorigenic mouse cells transformed by avian sarcoma virus B77. 17 2

Mice (female Swiss albino) inoculated when newborn with Visna virus had tumors in 77% of cases when examined 8-12 months later. The tumors were mainly of the mammary carcinoma type. The tumor incidence in non-infected control animals was only 20%. In contrast, no increased incidence of tumors was observed among Visna virus-inoculated inbred mice (BALB/c, CBA and DBA) with low incidence of spontaneous mammary carcinoma.
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PMID:Tumor incidence in Visna virus inoculated mice. 17 28

Spleen cells removed from C57Bl/6J mice bearing a methylcholanthrene-induced fibrosarcoma (MC-16) demonstrate suppressed responsiveness of phytohemagglutinin (PHA) and bacterial lipopolysaccharide (LPS) induced mitogenesis as compared to non-tumorous mice. A similar depression of PHA-induced mitogenesis was observed with spleen cells from C3H/HeJ mice bearing syngeneic mammary adenocarcinomas (C3HBA). The administration of indomethacin, a non-competitive irreversible prostaglandin (Pg) synthesis inhibitor, (75 or 100 mug/mouse, IP) on an alternate day basis to groups of tumor-bearing mice of both strains, significantly enhanced immune cell responsiveness to mitogenic stimulation. The addition of indomethacin (10 mug/ml) to cultures of spleen cells from these tumor-bearing mice, as well as to DBA/1J mice bearing the Cloudman S-91 melanoma, enhanced spleen-cell responsiveness to mitogen-induced DNA synthesis by as much as 156%. Indomethacin administration in vivo or in vitro had no significant effect on mitogen-induced DNA synthesis of spleen cells from non-tumor-bearing animals. It is hypothesized that tumors, or tumor-cell antigens, increase Pg production of a population of spleen cells, and that the increased Pg content of the spleen may be important in controlling immune responsiveness in mice.
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PMID:Indomethacin enhancement of spleen-cell responsiveness to mitogen stimulation in tumorous mice. 18 13

Growth of various fetal tissues and transplantable tumors in syngeneic newborn and adult mice [BALB/c, DBA/2, and (CBA X C57BL/6J)F1] was compared. Fetal skin, a mixture of all fetal tissues, and tumors were transplanted. The tumors arose spontaneously [hepatomas, mammary gland adenocarcinoma (MGAC)] or resulted from malignant conversion of ectopic transplants either of fetal tissues (urinary bladder carcinoma, adenocarcinoma of small intestine, stomach sarcoma) or of adult animal tissues (ovarian carcinoma) in the syngeneic system. The growth of fetal skin transplants and teratomas, which developed after transplantation of minced tissue from 18- to 20-day and 12- to 14-day fetuses, was considerably inferior in newborn syngeneic recipients, as compared with similar transplants in adults. Inhibition of tumor growth observed in newborn animals was manifested in prolongation of latent period before tumor node appearance and in slowing of growth rate of developed tumors. One of six tumors studied (MGAC) grew at the same rate in newborn and adult recipients. It was suggested that a special type of cellular and/or humoral mechanisms controlling tumor growth exists in newborns. The activity of such factors was conceivably based on fetal tumor antigens as targets. We assumed that weakly antigenic and strongly antigenic tumors behaved differently in respect to nonimmune and immune surveillance mechanisms.
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PMID:Nonimmune and immune surveillance. I. Growth of tumors and normal fetal tissues grafted into newborn mice. 18 65

Acetone-fixed smears of DBA/2 mouse leukemia cells that produce clusters of intracytoplasmic A-particles (pronucleocapsids of mouse mammary tumor virus) were employed as an indirect immunofluorescence system to detect the antibody to A-particles in human sera. With positive test sera, specific fluorescence was easily detectable as discrete cytoplasmic granules at the site of A-particle clusters. The antibody was found in 26 (60%) out of 43 breast cancer patient sera and 4 (25%) of 16 mammary fibroadenoma patient sera, while only 4 (11%) out of 37 control woman sera were antibody-positive. In the case of breast cancer patients, occurrence of tha antibody was not specifically related to a particular type of tumor histology. In a considerable number of positive cases, the antibody tended to disappear within various lengths of time after surgical operation of the breast cancer.
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PMID:Occurrence of antibody against intracytoplasmic A-particles of mouse mammary tumor virus in sera from breast cancer patients. 21 37

The strain-specific BALB/c tumor C4092 was conditioned to grow in H-2 incompatible DBA/1 mice by prior maintenance in vitro as an organ culture explant. It then was serially transplantable in DBA/1 mice and regained its specificity with one passage in BALB/c mice. Changes in transplantation behavior were similar in vivo if the recipients were conditioned by neonatal thymectomy, immunologic enhancement, rabbit antimous serum treatment, or immunization with mitomycin C-inactivated C4092 tumor cells. In vivo- and in vitro-modified tumors differed in degree of transplantability and in the stability of immunogenic changes. However, because of conspicuous similarities in the behavior of these lines, it was concluded that ADAPTations of both host and graft ultimately contribute to graft survival.
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PMID:Transplantation behavior of allotransplantable tumor lines derived from immunologically modified hosts. 23 95

To determine if the effector cells responsible for allogeneic marrow stem cell rejections were suppressed in mice with tumors, C57BL/6 (B6) mice were inoculated with 3-methylcholanthrene (MCA)-induced sarcoma cells. When the tumor reached 2.0--2.5 cm in diameter, these mice and control B6 and (BALB/c times A)F1 (CAF1) uninoculated animals were irradiated and given BALB/c marrow cells in the first of a two-step "stem cell rescue" experiment. Four days later, spleen cells of the primary hosts were reinoculated into irradiated CAF1 secondary hosts compatible with BALB/c marrow cells and immunized against B6 antigens. Splenic uptake (percent) of 125I-5-iodo-2'-deoxyuridine 5 days after spleen cell regrafting was used as a measure of cell proliferation and reflected growth of the stem cells in the primary hosts. BALB/c stem cells grew as well in B6 mice with tumors as in CAF1 primary hosts but were rejected by B6 controls. Seeding efficiency of BALB/c stem cells 6 hours after infusion of marrow cells and growth of syngeneic B6 stem cells were enhanced twofold in spleens of tumor-bearing B6 mice. To exclude the possibility that enhanced seeding resulted in greater survival of allogeneic stem cells, more DBA/2 marrow cells were infused into control B6 primary hosts than into tumor-bearing B6 and control DBA/2 mice. Control B6 mice resisted growth of even 7.5 times 10(6) DBA/2 marrow cells, whereas B6 tumor bearers allowed growth of 2.5 times 10(6) cells. No "suppressor cells" capable of inhibiting marrow cell allograft reactions were detected in spleens of tumor-bearing mice. Thus transplanted syngeneic MCA-induced sarcomas abrogated the ability of mice to reject allogeneic marrow stem cells.
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PMID:Loss of marrow allograft resistance in mice with transplanted methylcholanthrene-induced sarcomas. 24 33


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