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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spleen cells from C57BL mice carrying the metastatic Lewis lung carcinoma (3LL) developed a transient cytotoxic response towards the tumor shortly after tumor transplantation. Later on, the cytotoxic activity was lost and enhancing lymphocytes could be demonstrated in the spleens of the tumor-bearing mice (TBM). Spleen cells that were transferred together with tumor cells into syngeneic recipients enhanced tumor growth. The enhancing activity could be eliminated by the removal of a cell population that bound to histamine/rabbit serum albumin/Sepharose (HRS). The adherent population was enriched for enhancing lymphocytes, since it enhanced tumor growth more than the unfractionated population. The non-adherent cells, on the other hand, lost their enhancing activity in vivo and were sometimes protective against tumor growth. In addition, these cells manifested in vitro cytotoxicity against tumor cells. Hence the suppression of the cytotoxic expression in TBM is, at least in part, due to suppressor lymphocytes that bind to unsolubilized histamine. These cells seem to enhance tumor growth by suppressing host reactivity. Thus the enhancing lymphocyte populations can be separated into two subpopulations, of which one is enriched while the other is depleted of suppressor cells.
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PMID:Enhancing lymphocytes in spleens of tumor-bearing mice: affinity chromatography on insolubilized histamine. 89 34

The production of tumor-specific cell-mediated cytotoxicity following in vitro sensitization of C57BL spleen cells against a syngeneic 3LL Lewis lung carcinoma was studied. Lymphocytes were sensitized on monolayers of the tumor cells for 4-5 days. The cytotoxicity was assayed by measuring the reduction in 3H-leucine and 3H-thymidine incorporation by target cells after interaction with the sensitized lymphocytes. Spleen lymphocytes sensitized on monolayers of 3LL tumor cells caused a high extent of lysis; such cells tested on C57BL or C3H fibroblast targets evoked only a low level of cytotoxicity. C57BL spleen cells sensitized on C57BL fibroblasts caused a low level of cytotoxicity when tested on a 3LL target. Thus cytotoxicity appeared to be tumor specific. The reduced incorporation into protein and DNA of target tumor cells caused by the sensitized lymphocytes was a measure of cell injury, which was more sensitive than direct cell count or uptake of 51CR. Lymphocytes from syngeneic tumor-bearing mice, tested 13-25 days after tumor inoculation, did not manifest in vitro cytotoxicity. On the contrary, such lymphocytes sometimes appeared to have a promoting effect on the tumor cells.
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PMID:Specific cytotoxicity in vitro of lymphocytes sensitized in culture against tumor cells. 99 7

Spleen cells from inbred Biozzi mice, immunized against the human breast cancer cell line T47D, were fused with murine myeloma SP2O cells to generate monoclonal antibodies. One of these, 1BE12, of IgM isotype, reacted with five of six human breast tumor cell lines, while no binding was detectable with normal lymphocytes, RBC, or fibroblasts. The antigen recognized by monoclonal antibody 1BE12 was localized on the surface of T47D and MCF7 cells and was detected in cell-free supernatants of cultures. The antigen was found also on the surface of milk secretory cells. Immunohistochemical staining of frozen and paraffin-embedded sections of human tissues showed apical polarized reactivity in normal breast glands, while in all breast cancers staining was either cytoplasmic or membranous and heterogeneously distributed. Immunostaining was also observed in some other normal epithelia, including salivary gland, gastroduodenal mucosa, exocrine pancreas, and cervix. The antigen was not detectable in secretory endometrium, whereas proliferative endometrium was strongly stained. Colon carcinoma, and cancers of the bladder and endometrium were strongly reactive. No staining was detected in melanoma, lymphoma, mesothelioma, non-small cell lung carcinoma, and thyroid, renal, and ovarian carcinomas. Lectin absorption of MCF7 membrane extracts reduced 1BE12 binding. A large reduction in 1BE12 reactivity was observed after digestion of T47D and MCF7 membrane extracts with proteases. Treatment with sodium periodate resulted in complete loss of antigenicity, while neuraminidase treatment did not affect 1BE12 binding. These findings suggest that the 1BE12 epitope is expressed on the carbohydrate moiety of a glycoprotein and does not contain sialic acid. Immunoblotting of the perchloric acid-soluble fraction of MCF7 membrane extracts after electrophoresis in 1% agarose detected the antigen as a high molecular weight species (Mr greater than 900,000). The antigen was purified by perchloric acid extraction of MCF7 membrane preparations followed by affinity chromatography on 1BE12 antibody coupled to Sepharose-4B and gel exclusion fast protein liquid chromatography. No reactivity of the purified material was found with monoclonal antibodies directed against human milk fat globule membrane-associated mucins HMFG1 and DF3.
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PMID:Characterization and distribution in human tissues of a glycoproteic antigen defined by monoclonal antibody 1BE12 raised against the human breast cancer cell line T47D. 222 61

A rat monoclonal antibody 133-13A to a mouse lung carcinoma cell line was found to react with macrophages in mouse lung [1]. This monoclonal antibody is different from previously described antibodies to macrophages. Immunogold electron-microscopy and immunoperoxidase light microscopy have been used to show that MoAb 133-13A binds specifically to macrophages in normal and in BHT treated mouse lungs. This MoAb recognizes a protein of approximately 100 kDa (P100) on cultured lung carcinoma cells and a 87 kDa protein on macrophages from lung or the peritoneal cavity which is different from other macrophage antigens. The surface glycoprotein has been purified from cultured cells using immunoaffinity chromatography. The purified protein was radioiodinated and MoAb 133-13A was used to develop a competition radioimmunoassay to quantitate P100. Spleen, intestines, lung, skin and uterus all have high levels of P100. P100 on peritoneal macrophages has been determined to be about 94,000 molecules/cell. Analyses of lung lavage and whole lung homogenates from mice treated with BHT, BHT plus 70% O2, and 70% O2 alone show that treated animals have elevated P100 content compared to corn oil treated mice.
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PMID:A new monoclonal antibody to study mouse macrophage antigen during BHT-induced lung injury and repair. 246 38

Killer helper factor (KHF) was previously found to be produced by a human T cell hybridoma, 24A . CA2. We studied the therapeutic effects of interleukin-2 (IL-2) and KHF on the inhibition of pulmonary metastases of syngeneic Lewis lung carcinoma (3LL) in C57BL/6N mice. Multiple subcutaneous (sc) injections of IL-2 plus KHF had significantly more effect than injections of IL-2 alone in inhibiting spontaneous pulmonary metastases and prolonging survival of the mice. The effect of KHF with IL-2 on induction of lymphokine (IL-2)-activated killer (LAK) activity against P-29 cells was examined in the murine system. Spleen cells generated LAK activity after incubation for 4 days with more than 500 U/ml of IL-2. In contrast, KHF alone did not render spleen cells cytotoxic. The combination of these lymphokines at subthreshold concentrations, however, resulted in significant in vitro induction of LAK activity. The LAK activity of splenocytes incubated with IL-2 plus KHF was maximal after 4 days, and persisted for longer than that of cells treated with IL-2 alone. The LAK cells induced by KHF plus IL-2 were also cytotoxic to FBL and YAC-1 cells. Moreover, spleen cells of mice bearing lung metastases could be induced to the cytotoxic state by sc injections of IL-2 plus KHF. These results indicate that combination treatment with IL-2 and the new lymphokine KHF should be useful clinically in inducing LAK activity for inhibition of pulmonary metastases.
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PMID:Enhancement of therapeutic effect of interleukin-2 on spontaneous pulmonary metastases of Lewis lung carcinoma by killer helper factor associated with increased induction of killer activity. 250 76

This study was undertaken to determine whether in vitro treatment of Lewis lung carcinoma (3LL) cells with ultraviolet (UV) radiation could increase their immunogenicity. Tumor cells were irradiated with UV light from a germicidal lamp (254 nm; UV-C) at a dose of 720 J/sq m. After 2 weeks of culture, the surviving cell population was cloned by limiting dilution. Cell suspensions of each clone were injected intrafootpad in C57BL/6 mice at a dose of 2.5 X 10(5) cells per mouse. Eighty independent clones were tested. Fifty-one clones showed decreased tumorigenicity and failed to grow in 20 to 95% of immunocompetent mice, whereas they produced tumors in 100% of irradiated (550 R) and athymic nude mice. These clones were designated "tum-" (nontumorigenic) clones. In contrast, all 25 clones selected from the untreated parental 3LL induced progressively growing tumors in 100% of the mice. After two courses of UV treatment, the uncloned 3LL population was rejected in 45% of inoculated mice. Mice rejecting an inoculum of a tum- clone were completely resistant to subsequent challenge with higher doses of the same or unrelated tum- clones. This resistance was fully expressed even after irradiation of immune mice with 550 R. Mice immune to a tum- clone also were able to prevent the growth of various tum+ clones or untreated 3LL tumor cells. When tum- and tum+ clone cells were simultaneously inoculated intrafootpad in opposite legs, rejection of tum- clone resulted also in the prevention of the growth of tum+ clone. Spleen cells of immune mice caused rapid elimination of radiolabeled 3LL tumor cells from the place of their inoculation (intrafootpad) and prevented tumor growth. In an in vitro cytotoxic assay, spleen cells after in vivo and in vitro immunization with tum- clones demonstrated high cytotoxic activity against various tum+ clones and parental 3LL cells, as well as against tum- clones. In addition, parental 3LL tumor cells and tum- cells were similarly able to inhibit cytotoxic activity in the cold target inhibition assay. However, in contrast to tum- cells, 3LL cells were less efficient in in vitro restimulation of cytotoxic activity of immune spleen cells. Therefore, these data suggest that tum-, tum+, and parental 3LL cells share a common antigenic specificity, which is not immunogenic in 3LL cells. UV treatment presumably converted the antigenic determinants present in the 3LL cells into an immunogenic form.
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PMID:Induction of highly immunogenic variants of Lewis lung carcinoma tumor by ultraviolet irradiation. 258 Jun 24

We studied the properties of activated peritoneal cells (PC) inhibiting the take of SP4 spontaneous adenocarcinoma and Lewis lung carcinoma in syngeneic mice. Treatment of the poly I:C activated PC from Balb/c mice suppressing the take of SP4 tumour with anti-asialo GM1 antibody and complement before transfer did not affect their tumour-inhibitory potential. PC from Balb/c nude mice treated with poly I:C also inhibited the take of SP4 tumour. Spleen cells from untreated or poly I:C treated Balb/c and Balb/c nude mice, however, did not inhibit the take of SP4 adenocarcinoma. Treatment of peritoneal cells activated by a combination of poly I:C, indomethacin and Syncumar (referred to as "combined treatment") with anti-asialo GM1 antibody and complement could not, or could only partly abolish their tumour-inhibitory potential. The cells mediating the suppression of the take of Lewis lung tumour proved to be Thy-1,2+/-, Lyt-1-, Lyt 2.2- cells. We conclude that the activated peritoneal cells inhibiting the take of SP4 adenocarcinoma and Lewis lung tumour are different from NK cells, NC cells and LAK cells and represent a distinct antitumoural effector cell population.
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PMID:Characterization of activated peritoneal cells inhibiting the take of transplantable murine tumours. 260 45

Spleen cells from BALB/c mice hyperimmunized with the human epidermoid lung carcinoma cell line T222 were fused with NS-1 mouse myeloma cells to produce monoclonal antibodies to human lung cancer antigens. Hybridoma culture supernatants were tested by an enzyme-linked immunosorbent assay for reactivity against a panel of human lung tumor cell lines. Supernatant from hybridoma EA1 (immunoglobulin G1) displayed strong reactivity with four of four non-small cell lung carcinomas but did not react with three of three small cell lung carcinoma (SCLC) cell lines. This hybridoma was cloned by limiting dilution and utilized to generate ascites antibody for subsequent immunohistochemical and antigen characterization studies. Evaluation of fresh frozen tumor tissue sections by immunoperoxidase staining methods revealed EA1 reactivity with the vast majority of non-SCLCs tested (21 of 21 epidermoid, 17 of 18 adenocarcinomas, four of four large cell, two of two bronchioloalveolar) and no reactivity with nine of nine small cell lung carcinomas. EA1 also stained bronchial epithelium and other benign and malignant epithelial tissues. The EA1 antigen was determined to have a molecular weight of 75,000 by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis of human non-SCLC tumor extracts. These data imply that EA1 recognizes a novel antigen expressed by non-SCLCs and other epithelial tissues. The absence of EA1 reactivity with SCLCs suggests that this monoclonal antibody may find future application in distinguishing non-SCLC from SCLC and prove useful in furthering our understanding of the histogenesis of lung carcinomas.
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PMID:A novel monoclonal antibody-defined antigen which distinguishes human non-small cell from small cell lung carcinomas. 301 95

In the present study, some basic effects of Eubacterium lentum (TYH-11), isolated from normal intestinal flora, upon the immune system and various experimental tumor cell lines were investigated. E. lentum showed no direct cytotoxicity against Ehrlich ascites tumor, while Serratia marcescens (TY-142) did show direct cytotoxicity. E. lentum presented striking antitumor activity which differed according to the injection route and time. This strain showed antitumor activity against 11 experimental tumor cell lines including Ehrlich ascites tumor, Meth-A, etc., but not against EL4 or Lewis lung carcinoma. The antitumor activity in this strain was recognized to lie in the cell wall and granular fractions. The effect of this strain on the immune system was studied by using plaque formation and the footpad reaction. When mice received 5 injections of E. lentum, the plaque number increased to treble the control level. Spleen weight was also increased following administration of E. lentum. In normal and tumor-bearing mice immunized with SRBC alone, the footpad reaction was increased significantly to the control level by administration of E. lentum.
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PMID:Antitumor activity and its properties of Eubacterium lentum. 312 99

Human embryonal carcinoma cells sometimes display the developmental potential of early embryonic stem cells. While available data do not clearly identify a counterpart of these tumor cells in normal development, previous comparisons of human embryonal carcinoma and yolk sac carcinomas indicated that these cell types are closely related, and suggested that embryonal carcinoma cells might resemble the progenitors of extraembryonic endoderm. To analyse further cell-differentiation lineage in these tumors, we produced monoclonal antibodies to cytostructurally associated antigens of human embryonal carcinoma cells. Spleen cells from mice immunized with a detergent-insoluble extract of cultured human embryonal carcinoma cells were fused to NS-1 myeloma cells, and hybridoma supernatants were screened by indirect immunofluorescence on the immunizing cell line, then on a panel of cell lines derived from human embryonal carcinomas, yolk sac carcinomas, and a range of neoplastic and normal tissues. Monoclonal antibody GCTM-1 stained the nuclei of all human cells tested and served as a positive control; this antibody immunoprecipitated proteins of 85 and 66 k Da from human embryonal carcinoma cells. GCTM-2 recognized an epitope on a 200-k Da extracellular protein present on the surface of embryonal carcinoma cells, and stained the surface of visceral yolk sac-type carcinoma and colorectal carcinoma cells as well. Enzymatic analysis of carbohydrate residues on the GCTM-2 antigen revealed that it was a keratan sulphate proteoglycan, and suggested that the epitope recognized by the antibody lies on the core protein. In immunoblots, antibody GCTM-3 bound to a 57-k Da cytoskeletal protein expressed in human embryonal carcinoma. This antibody decorated filamentous arrays in cell lines from human embryonal carcinoma, visceral yolk sac carcinoma, parietal yolk sac carcinoma (endodermal sinus tumour), and adenocarcinoma and large cell carcinoma of the lung. Antibody GCTM-4 recognized a determinant present on a 69-k Da polypeptide, associated with a component of the lysosomal compartment, which was expressed in embryonal carcinoma cells, but no other cell type tested. The results with this antibody panel thus allow distinction between human embryonal carcinoma and yolk sac carcinoma, but provide further evidence of a close relationship between these cell types.
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PMID:Analysis of cell-differentiation lineage in human teratomas using new monoclonal antibodies to cytostructural antigens of embryonal carcinoma cells. 324 84


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