concanavalin-a and Fibrosarcoma

Topics: Alginates; Animals; Antibodies, Neoplasm; Antigen-Antibody Complex; Binding Sites, Antibody; Complement System Proteins; Concanavalin A; Cytotoxicity Tests, Immunologic; Epitopes; Fibrosarcoma; Humans; Immunity, Cellular; Immunization; Immunization, Passive; Immunoglobulin Fab Fragments; Immunoglobulin Fc Fragments; Immunoglobulin G; Immunosuppression Therapy; Isoantigens; Lymphocytes; Macrophages; Mice; Neoplasm Transplantation; Sarcoma, Experimental; Splenectomy; Thymectomy; Transplantation Immunology; Transplantation, Homologous

CSA1M tumor-bearing mice exhibited a severe immune dysfunction but the underlying mechanism remained unclear. In this study, we demonstrated that the myeloid suppressor cell (Mac-1(+)Gr-1(+) cells)-(MSC) related T cell immunosuppression in this tumor-bearing model. In mice at the late stage of CSA1M tumor-bearing (Late TB [8-10 weeks after cell inoculation in male BALB/c mice]), the percentages for CD4(+) and CD8(+) T cells decreased but Mac-1(+) cells increased in spleens with severe splenomegaly. There was no deficit for concanavalin A-induced CD4(+) and CD8(+) T cell proliferation, interferon-gamma (IFN-gamma) and interleukin (IL)-4 production, but delayed-type hypersensitivity reaction were attenuated. Analysis of cytokine production in unfractionated spleen cells showed a significant reduction of IFN-gamma and a marked increase of IL-10 and IL-4. In Late-TB mice, splenic MSC number intensively accumulated; the mRNA expressions of the signal transducer and activator of transcription 1, interferon regulatory factor 1 (IRF-1), and inducible nitric-oxide synthase (iNOS) were enhanced in MSC; the nitric oxide production and arginase enzyme activity increased in MSC as well. Furthermore, the concanavalin A-induced T cell proliferation was inhibited in the presence of lipopolysaccharide- or IFN-gamma-activated MSC from Late-TB mice, which could be reversed by the iNOS specific inhibitor L-NMMA. iNOS seemed to be required more than arginase for the suppressive activity of MSC. Taken together, our results suggest that the immune dysfunction in tumor-bearing mice might be causally associated with the accumulation of MSC and its tumor-favoring property.

Topics: Animals; Arginase; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Concanavalin A; Cytokines; Fibrosarcoma; Immune Tolerance; Lymphocyte Activation; Male; Mice; Mice, Inbred BALB C; Myeloid Progenitor Cells; Nitric Oxide; Nitric Oxide Synthase Type II; Spleen; Splenomegaly; T-Lymphocytes, Helper-Inducer; T-Lymphocytes, Regulatory

Binding of tissue inhibitor of metalloproteinase-2 (TIMP-2) to pro-MMP-2 and mature membrane type-1 MMP (MT1-MMP) on the cell surface is required for activation of MMP-2. It has been reported that following binding to cell surface receptors, TIMP-2 undergoes endocytosis and extensive degradation in lysosomes. The purpose of this study was to reexamine the fate of TIMP-2 following binding to transfected HT1080 cell surface MT1-MMP at 4 degrees C. Following 37 degrees C incubation, 125I-TIMP-2 release, endocytosis, and degradation were characterized under varying conditions. More than 85% of the total 125I-TIMP-2 bound to cells was released as intact functional molecules; <15% was degraded. Transfection of HT1080 cells with dominant negative mutant dynamin cDNA resulted in delayed endocytosis and release of 125I-TIMP-2 from cells. Pharmacologic agents that induce clustering of cell surface receptors (concanavalin A) and interfere with endosomal/lysosomal function (bafilomycin A(1)) resulted in enhanced binding of 125I-TIMP-2 to cell surface receptors. Abrogation of activation of proMT1-MMP with a furin inhibitor prevented binding and endocytosis of 125I-TIMP-2. Biotinylation of cell surface MT1-MMP followed by Western blotting confirmed the presence of mature MT1-MMP on the cell surface and degraded MT1-MMP in the intracellular compartment. In conclusion, these studies demonstrate that TIMP-2 is released from cells primarily as an intact functional molecule following binding to MT1-MMP on the cell surface.

Topics: Animals; Cell Line, Tumor; Cell Membrane; Chlorocebus aethiops; Concanavalin A; COS Cells; Endocytosis; Endosomes; Enzyme Activation; Enzyme Inhibitors; Enzyme Precursors; Epithelial Cells; Fibrosarcoma; Humans; Kinetics; Macrolides; Matrix Metalloproteinases, Membrane-Associated; Metalloendopeptidases; Receptors, Cell Surface; Temperature; Tissue Inhibitor of Metalloproteinase-2

Pericellular matrix degradation during cancer invasion and inflammation is dependent on activation of progelatinase A by membrane type 1-matrix metalloproteinase (MT1-MMP); a stoichiometric concentration of tissue inhibitor of metalloproteinase-2 (TIMP-2) is required. Activation of progelatinase A has generally been considered to be a slow process occurring as a result of enhanced expression of MT1-MMP. We herein report that ConA treatment of HT1080 fibrosarcoma cells is followed by MT1-MMP-induced activation of progelatinase A on the cell surface within 1 hour. Cell surface biotinylation, immunohistochemistry, and (125)I-labeled TIMP-2 binding to cell surface MT1-MMP were used to characterize the appearance and function of MT1-MMP on the plasma membrane. Treatment of HT1080 cells with ConA resulted in increased specific binding of (125)I-labeled TIMP-2 to cell surface receptors within 5 minutes. TIMP-2 binds almost exclusively to activated MT1-MMP on the surface of HT1080 cells. MT1-MMP function at the cell surface was also accelerated by treatment of cells with cytochalasin D, an inhibitor of actin filaments, PMA, a stimulator of protein kinase C, and bafilomycin A(1), an inhibitor of lysosome/endosome function. A functional pool of intracellular MT1-MMP available for trafficking to the cell surface was demonstrated by repetitive ConA stimulation. ConA-induced expression of MT1-MMP mRNA (Northern blot analysis) in HT1080 cells was a delayed event (>6 hours). These data suggest that presynthesized MT1-MMP is sorted to a transient storage compartment (trans-Golgi network/endosomes), where it is available for rapid trafficking to the plasma membrane and cell surface proteolytic activity.

Topics: Anti-Bacterial Agents; Cell Membrane; Concanavalin A; Cytochalasin D; Enzyme Activation; Enzyme Precursors; Fibrosarcoma; Fluorescein-5-isothiocyanate; Gelatinases; Humans; Macrolides; Matrix Metalloproteinases, Membrane-Associated; Metalloendopeptidases; Protein Transport; Receptors, Cell Surface; Tetradecanoylphorbol Acetate; Tissue Inhibitor of Metalloproteinase-2; Tumor Cells, Cultured

Matrix metalloproteinase 2 (MMP-2) activation has been described as a "master switch" which triggers tumor spread and metastatic progression. We show here that type IV collagen, a major component of basement membranes, promotes MMP-2 activation by HT1080 cells. When plated on plastic, HT1080 cells constitutively processed the 66-kDa pro-MMP-2 into a 62-kDa intermediate activated form, most probably through a membrane type (MT) 1 MMP-dependent mechanism. In the presence of type IV collagen, part of this intermediate form was further processed to fully activated 59-kDa MMP-2. This activation was prevented by tissue inhibitor of MMP (TIMP)-2 and a broad-spectrum hydroxamic acid-based synthetic MMP inhibitor (GI129471). Type IV collagen-mediated pro-MMP-2 activation did not involve either a transcriptional modulation of MMP-2, MT1-MMP, or TIMP-2 expression nor any alteration of MT1-MMP protein synthesis or processing. An inverse relationship between MMP-2 activation and the concentration of secreted TIMP-2 was observed. This is consistent with our previous report that TIMP-2 degradation is probably linked to the MT1-MMP-dependent MMP-2 activation mechanism. Because invasive tumor cells must breach basement membranes at different steps of the metastatic dissemination, the ability of HT1080 cells to activate pro-MMP-2 in the presence of type IV collagen might represent a key regulatory mechanism for the acquisition of an invasive potential.

Topics: Collagen; Concanavalin A; Culture Media, Conditioned; Extracellular Matrix Proteins; Fibrosarcoma; Humans; Matrix Metalloproteinase 2; Matrix Metalloproteinase Inhibitors; Matrix Metalloproteinases, Membrane-Associated; Metalloendopeptidases; Neoplasm Invasiveness; Protein Biosynthesis; Protein Precursors; RNA, Messenger; Tetradecanoylphorbol Acetate; Tissue Inhibitor of Metalloproteinase-2; Tumor Cells, Cultured

Topics: Animals; Cells, Cultured; Cervix Uteri; Concanavalin A; Enzyme Activation; Enzyme Precursors; Female; Fibroblasts; Fibrosarcoma; Furin; Gelatinases; Gene Expression Regulation, Enzymologic; Humans; Matrix Metalloproteinases, Membrane-Associated; Metalloendopeptidases; Oligonucleotides, Antisense; Oligopeptides; Rabbits; Reverse Transcriptase Polymerase Chain Reaction; Serine Proteinase Inhibitors; Skin; Subtilisins; Tumor Cells, Cultured

It has been reported that the rejection of tumor allografts is mainly mediated by cytotoxic T lymphocytes (CTLs). Here, we characterized the cytotoxic effector cells of C57BL/6 (B6; H-2b) mice infiltrating into the rejection site of the i.p. allografted Meth A fibrosarcoma (or P815 mastocytoma) cells of H-2d origin. Two types of cytotoxic cells (i.e., CD8+ CTLs and macrophages (M phi s)) were identified by flow cytometric fractionation of the infiltrates or by specific in vitro elimination of cells either with antibody (Ab)-coated beads or with an Ab-plus complement. Of particular interest, these effector cells showed distinct and unique target specificities. First, the CTLs were inactive against transplanted tumor (e.g., Meth A) cells, whereas they were cytotoxic against donor-related concanavalin A (Con A) blasts as well as CTLL-2 (H-2b) cells transfected with a class I gene of H-2d origin. A cold target competition assay suggested that the CTLs were composed of multiple sets of T cells, each of which specifically recognized different allo-antigens. Second, the M phi s lysed the allografted tumor cells but were inert toward the Con A blasts and the CTLL-2 transfectants. Unexpectedly, the infiltration of M phi s preceded the infiltration of CTLs by several days during the course of rejection. These results indicate that two distinct populations of unique cytotoxic cells (i.e., CTLs and M phi s) are induced in the allografted tumor rejection site, and that the infiltration of cytotoxic M phi s responsible for rejection precedes that of the CTLs cytotoxic against cells expressing donor-related allo-antigens.

Topics: Animals; Antibodies; CD3 Complex; CD4 Antigens; CD8 Antigens; Cells, Cultured; Complement System Proteins; Concanavalin A; Cytotoxicity Tests, Immunologic; Female; Fibrosarcoma; Flow Cytometry; Graft Rejection; Histocompatibility Antigens Class I; Isoantigens; Killer Cells, Natural; Macrophages; Mice; Mice, Inbred AKR; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred DBA; Mice, Inbred Strains; Neoplasm Transplantation; Peritoneum; Receptors, Antigen, T-Cell, alpha-beta; Receptors, Antigen, T-Cell, gamma-delta; Specific Pathogen-Free Organisms; T-Lymphocyte Subsets; T-Lymphocytes, Cytotoxic; Thy-1 Antigens; Transfection

Overexpression of membrane-type matrix metalloproteinase (MT-MMP-1) results in the activation of both endogenous and exogenous 72-kDa gelatinase. To understand the effects of MT-MMP-1 on 72-kDa gelatinase activation, we analyzed its expression in human fibroblasts and HT-1080 fibrosarcoma cells. Both cell types expressed the MT-MMP-1 mRNA constitutively at a considerable level and treatment of cells with PMA enhanced the expression about 2-3-fold. Concanavalin A treatment increased MT-MMP-1 mRNA levels in fibroblasts about 4-fold. Induction of MT-MMP-1 by phorbol 12-myristate 13-acetate (PMA) required protein synthesis as shown by cycloheximide inhibition. The induction was also inhibited by dexamethasone. Analysis of MT-MMP-1 mRNA stability using actinomycin D indicated that the half-life was rather long and not affected by PMA, suggesting transcriptional regulation. Only HT-1080 cells had significant 72-kDa gelatinase processing activity after treatment with PMA or concanavalin A, while fibroblasts were virtually negative. Immunoblotting analysis of fibroblast lysates indicated that MT-MMP-1 was present mainly in a 60-kDa form. PMA and concanavalin A caused 2-4-fold increases in its protein levels, while in HT-1080 cells PMA, concanavalin A, or overexpression of MT-MMP-1 did not significantly enhance the level of the 60-kDa protein. Instead, an immunoreactive, proteolytically processed 43-kDa form was observed, and its appearance correlated to 72-kDa gelatinase processing activity. Thus 72-kDa gelatinase activation, while enhanced by MT-MMP-1 expression, needs additional co-operating factors.

Topics: Base Sequence; Calcimycin; Cell Line; Collagenases; Concanavalin A; Cycloheximide; Cytokines; Dexamethasone; DNA Primers; Enzyme Activation; Epidermal Growth Factor; Fibroblast Growth Factor 2; Fibroblasts; Fibrosarcoma; Gelatinases; Gene Expression Regulation, Enzymologic; Growth Substances; Humans; Immunoblotting; Interleukin-1; Lung; Matrix Metalloproteinase 1; Molecular Sequence Data; Polymerase Chain Reaction; Recombinant Proteins; RNA, Messenger; Tetradecanoylphorbol Acetate; Transcription, Genetic; Transforming Growth Factor beta; Tumor Cells, Cultured; Tumor Necrosis Factor-alpha

Matrix metalloproteinase-2 (MMP-2) is activated on the cell surface by membrane type 1-MMP (MT1-MMP). Activation of proMMP-2 is induced in vitro by concanavalin A (ConA). The regulation of proMMP-2 activation is, however, not yet fully understood. We investigated the effect of plant lectins, carbohydrates and inhibitors of the cytoskeleton on proMMP-2 activation in normal (HLF1) and malignant fibroblast (HT1080) cells. Native ConA induced proMMP-2 activation in both cell types while dimeric succinyl-ConA had no effect, suggesting that receptor clustering is involved in activation. Wheat germ agglutinin (WGA) also induced proMMP-2 activation. N-acetyl-D-glucosamine (GlcNac) inhibited the effects of ConA and WGA while mannose only inhibited ConA-induced proMMP-2 activation. Mannose also inhibited the expression of MT1-MMP mRNA induced by ConA. Cytochalasin B and colchicine had no effect on the ConA induction of proMMP-2 activation. These studies help to define some of the cellular and molecular mechanisms for the induction of proMMP-2 activation.

Topics: Acetylgalactosamine; Acetylglucosamine; Carbohydrates; Cell Line; Colchicine; Concanavalin A; Cytochalasin B; Cytoskeleton; Enzyme Activation; Enzyme Precursors; Fibroblasts; Fibrosarcoma; Gelatinases; Humans; Lectins; Lung; Mannose; Matrix Metalloproteinase 2; Metalloendopeptidases; Protein Processing, Post-Translational; Tumor Cells, Cultured

Tumor cells interact with the hemostatic system in various ways and may thus influence malignant growth and spread. MC28 fibrosarcoma cells possess a potent procoagulant activity (PCA) and form lung tumors following intravenous injection. The aim of this work was to study the relationship between PCA, intravascular coagulation and lung seeding in the MC28 model. MC28 cells were injected into control, warfarinized and heparinized hooded Lister rats. Coagulation changes were monitored by thromboelastography (TEG) and Sonoclot analysis (SA), lung fibrin formation by light and electron microscopy, tumor seeding by macroscopic counting and tumor cell and platelet deposition in the lungs by radiolabelling. PCA was measured by chromogenic assay. MC28 PCA was characterized as a tissue factor-factor VIIa complex that probably arose during cell culture or disaggregation of solid tumors. Injection of tumor cells caused marked coagulopathy and was rapidly (within 30 min) followed by fibrin deposition in the lungs and accumulation of radiolabelled platelets. Heparin and warfarin significantly reduced lung seeding (p < 0.001) and reduced retention of radiolabelled tumor cells in the pulmonary circulation (p < 0.01). Inhibition of cellular PCA by prior treatment with concanavalin A markedly reduced intravascular coagulation and lung seeding. We conclude that MC28 cells cause intravascular coagulation as a direct result of their procoagulant activity. The data suggest that tumor cells form complexes with platelets and fibrin which are retained in the lungs long enough for extravasation and seeding to occur.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Cell Adhesion; Concanavalin A; Culture Media, Serum-Free; Cysteine Endopeptidases; Disseminated Intravascular Coagulation; Fibrin; Fibrosarcoma; Heparin; Injections, Intravenous; Lung; Lung Neoplasms; Macrophage Activation; Male; Neoplasm Proteins; Neoplasm Transplantation; Neoplastic Cells, Circulating; Pulmonary Circulation; Rats; T-Lymphocytes; Tumor Cells, Cultured; Warfarin

The chemotherapeutic agent bleomycin (BLM) increases cytokine production by mitogen-stimulated healthy rat spleen cells without altering the cellular composition of the spleen. In this study, the chronological production of interleukin (IL)-2, IL-6 and tumor necrosis factor (TNF) by untreated and BLM-treated tumor-bearing rat spleen cells is examined. A significant decrease in the production of both IL-2 and TNF could be observed only 5 days after subcutaneous injection of syngeneic KMT-17 tumor cells. Decrease in cytokine production progressed with time with a slight recovery around day 10 after tumor challenge. Administration of BLM, 5 mg/kg, on day 8, restored IL-2 and IL-6 production and significantly increased TNF production by day 14 of tumor burden as compared with the amounts of cytokine produced by the mitogen-stimulated untreated tumor-bearing rat spleen cells. The response of the tumor-bearing rat spleen cells to concanavalin A (ConA), diminished when compared with that of normal rat spleen cells, could be restored to normal levels by treatment with BLM when examined at low concentrations of mitogen but was unaffected at higher concentrations of ConA. Histological examination of the tumor tissue, following continuous intraperitoneal treatment with BLM, 5 mg/kg, from day 8 to 12, shows disruption of cellular structure with significant infiltration of effector cells as compared with undisrupted organization with no visible infiltration of effector cells in the untreated rat tumors.

Topics: Animals; Bleomycin; Cell Division; Concanavalin A; Cytokines; Female; Fibrosarcoma; Interleukin-2; Interleukin-6; Neoplasm Transplantation; Rats; Rats, Inbred WKY; Rats, Wistar; Splenic Neoplasms; Tumor Cells, Cultured; Tumor Necrosis Factor-alpha

Experimental evidence suggests that many tumours can activate blood coagulation and that such interaction is part of the pathology of metastatic tumour growth. This study aimed to study the procoagulant activity of the methylcholanthrene-induced (MC28) fibrosarcoma to determine whether coagulation activation by these cells could explain the previously reported effects of oral anticoagulants on lung seeding in this model. MC28 cells shortened the recalcification times of normal and factor VII-deficient plasma and directly activated factor X in a chromogenic assay, but did not aggregate platelets in vitro in either whole blood or platelet-rich plasma. Cellular coagulant activity was calcium-dependent, blocked by DFP and concanavalin A but not inhibited by iodoacetamide, E-64 or antibodies to human tissue factor or factor VII. Injection of viable MC28 cells into hooded Lister rats induced a decrease in platelet count (P < 0.001), plasma factor X (P < 0.001) and fibrinogen (P < 0.05) and a marked increase in plasma haemoglobin (P < 0.001). These effects were either not observed or were considerably less marked in heparinized or warfarinized animals. Injection of MC28 cells treated with concanavalin A in vitro completely abolished the clotting changes observed with untreated cells. In conclusion, MC28 cells possessed a potent factor X-activating serine proteinase procoagulant in vitro, which had some of the characteristics of a tissue factor/factor VIIa complex. In vivo, MC28 cells caused clotting activation and intravascular fibrin generation. Since thrombocytopenia was abolished by heparin and the cells lacked platelet aggregating activity in vitro, thrombocytopenia was probably secondary to intravascular coagulation and thrombin generation. The trigger for intravascular clotting activation appeared to be the cellular procoagulant activity since it was abolished by prior in vitro blockade of the latter with concanavalin A.

Topics: Animals; Blood Coagulation; Concanavalin A; Factor X; Fibrinogen; Fibrosarcoma; Hemoglobins; Heparin; Male; Methylcholanthrene; Platelet Aggregation; Platelet Count; Rats; Tumor Cells, Cultured; Warfarin

Mice were injected in the foot pad with either 5 x 10(5) syngeneic plasmacytoma (MOPC104E) or fibrosarcoma cells (Meth A). Lymph nodes containing tumor cells were harvested 14 days later and cultured. In the presence of recombinant interleukin-2 (r-IL-2) predominantly tumor cells proliferated. Culture with T cell growth factor (TCGF) resulted in the growth of lymphoid cells. Concanavalin A (Con A) had only a modest effect on elimination of tumor cells in the culture. Tumor-infiltrating lymphocytes (TIL) prepared from the lymph nodes showed specific tumor-neutralizing activity when grown in the presence of TCGF. In vitro examination revealed that Meth A cells could not be lysed by TIL, while TIL from MOPC tumors showed tumor specific activity. This study may explain negative results in human trials with TIL induced by IL-2 alone.

Topics: Animals; Cell Division; Cells, Cultured; Concanavalin A; Fibrosarcoma; Humans; Interleukin-2; Lymph Nodes; Lymphatic Metastasis; Lymphocytes, Tumor-Infiltrating; Male; Mice; Mice, Inbred BALB C; Neoplasm Transplantation; Plasmacytoma; Rats; Tumor Cells, Cultured

A piece of lymph node containing polyclonally-activated lymphocytes when transplanted in the anterior eye chamber of mouse along with solid piece of fibrosarcoma from syngeneic Swiss mice, dramatically inhibited the tumour-induced-vasodilatation and neo-vascularization. If the tumour explants were incubated in vitro with activated lymphocytes prior to transplantation, such angiogenic reactions was significantly reduced. These explants were incapable of incorporating radioactive thymidine in vitro. Furthermore, the cytotoxic ability of activated lymphocytes towards 51Cr labelled tumour target cells was of significant level indicating the possible mechanism of immunological reactiveness of Con A-stimulated lymphocytes to 3'-methylcholanthrene-induced tumour cells of syngeneic origin.

Topics: Animals; Anterior Chamber; Concanavalin A; Fibrosarcoma; Lymph Nodes; Lymphocyte Activation; Male; Mice; Neoplasm Transplantation; Neovascularization, Pathologic; T-Lymphocytes; Vasodilation

This paper reports on the characteristics of killing by a human and a murine tuberculin (PPD)-specific T helper clone of targets to which PPD was attached via the lectin concanavalin A (Con A). The killing was specific for PPD from M. tuberculosis; and targets coupled to Con A alone or to PPD from M. paratuberculosis were not killed. Target cells carrying Con A-PPD were more effectively lysed than PPD-pulsed cells. This form of lymphocyte killing, though highly significant, was inefficient. Maximum killing of PPD carrying targets was 30-40% at effector to target ratios of 20:1 and at 16 h. Cells carrying 2 x 10(6) molecules of PPD and less than 1.5 x 10(6) molecules Con A per cell were killed most efficiently. A major distinction between this helper T cell killing and that mediated by cytotoxic T cells was that both TH clones displayed bystander lysis and killed PPD uncoupled targets when these were cultured with syngeneic PPD-bound targets. This suggests that the mechanism of cytotoxicity may involve soluble mediators.

Topics: Animals; Cell Line, Transformed; Clone Cells; Concanavalin A; Cytotoxicity, Immunologic; Dose-Response Relationship, Immunologic; Epitopes; Fibrosarcoma; Herpesvirus 4, Human; Humans; Leukemia, Erythroblastic, Acute; Mice; T-Lymphocytes, Helper-Inducer; Time Factors; Tuberculin; Tumor Cells, Cultured

A study was conducted on the activity exerted by prolonged dietary supplementation with progressive amounts of retinoids on cell-mediated immune responses and the growth of transplantable tumors in mice. A few groups of BALB/c mice received 0 (group C), 50 (group A 50), 200 (group A 200), 500 (group A 500), and 1,000 (group A 1000) IU retinol palmitate/mouse/day in drinking water for 150 days. At progressive intervals mice from each group were tested for proliferative responses to concanavalin A (Con A), Escherichia coli lipopolysaccharide, interleukin-2, and interferon-gamma release to Con A. Ten mice from each group were also challenged with the 90-100% tumor-inducing dose of 3 distinct transplantable tumors. At the end of the experiment the principal organs were histologically examined, and the accumulation of vitamin A was evaluated. In groups A 200, A 500, and A 1000, an increase in the proliferative responses and production of lymphokines as compared to those in group C occurred after 60-90 days, but vanished after 150 days. The takes of the 3 tumors were impaired when the challenges were performed on days 75 and 150. This enhancement of distinct functions of cellular reactivity and resistance to transplantable tumors showed a linear relationship with the amount of supplemental retinol palmitate for the first 60-90 days. After 150 days, however, these enhancement effects vanished or tended to decrease.

Topics: Animals; Concanavalin A; Diet; Diterpenes; Dose-Response Relationship, Drug; Female; Fibrosarcoma; Immunity, Cellular; Interferon-gamma; Interleukin-2; Lipopolysaccharides; Lymphocyte Activation; Mammary Neoplasms, Experimental; Mice; Mice, Inbred BALB C; Neoplasm Transplantation; Neoplasms, Experimental; Retinoids; Retinyl Esters; Vitamin A

The local cellular response induced by i.p. injection of mitomycin C (MMC) was studied in C3H/HeN mice and ACI/N rats. MMC-induced peritoneal macrophages showed the maximum in vitro tumoricidal activity against 125I-UdR-labeled syngeneic tumor target cells 4 to 7 days after the i.p. injection of MMC at a single dose of 3 mg/kg and 1 mg/kg in mice and rats, respectively. The tumoricidal activity was dependent on the dose of mitomycin C injected and it was alos detectable against allogeneic and xenogeneic tumor target cells. In addition, these tumoricidal macrophages were found to have augmented functions of 2-deoxy-D-glucose incorporation and phagocytosis. Additional experiments excluded the possibility that the tumor cell cytolysis was the result of direct cytotoxicity of MMC that might have been incorporated into the peritoneal macrophages or of nutrient depletion in the medium during the cytolysis assay. Although the mechanism by which MMC injected i.p. induced the tumoricidal macrophages locally remained undetermined, in vitro production of macrophage-activating factor (MAF) from splenocytes cultured with concanavalin A was enhanced remarkably, following exposure of the spleen to MMC in vivo or in vitro, indicating the involvement of lymphokine in the induction of tumoricidal macrophages by MMC. Among other anticancer drugs, which were used at a dose of three-fifths of LD50, only adriamycin (7.5 mg/kg) was capable of inducing tumoricidal macrophages. A better understanding of the effect of anticancer drugs on macrophage tumoricidal activity may be useful in designing more effective local chemotherapy for cancerous peritoneal effusions.

Topics: Animals; Concanavalin A; Dose-Response Relationship, Drug; Fibrosarcoma; Injections; Lymphokines; Macrophage Activation; Macrophage-Activating Factors; Macrophages; Mice; Mice, Inbred C3H; Mitomycin; Mitomycins; Neoplasms, Experimental; Peritoneal Cavity; Phagocytosis; Rats; Rats, Inbred ACI; Sarcoma, Experimental

The Ly-6.1 alloantigen defined by monoclonal antibody SK70.94 and expressed predominantly on activated lymphocytes has been immunoprecipitated from lysates of cells biosynthetically radiolabeled with 35S-methionine. On SDS-polyacrylamide gel electrophoresis the reduced antigen appeared as a doublet of 17 and 18 kD. The nonreduced polypeptides had higher mobilities indicating intrachain but not interchain disulfide linkages. The nonreduced form was detectable by immunoperoxidase stain on blots after SDS-PAGE. This showed both polypeptide species contained the antigenic epitope. Labeling in the presence of tunicamycin did not change the apparent m.w. suggesting the absence of N-linked carbohydrate. Pulse-chase data are inconsistent with a strict precursor-product relationship between the two polypeptides and give a half-life for the antigen in 2-day Con A blast cells of about 4 1/2 hr. A highly purified preparation of this antigen displayed a similar electrophoretic pattern and, in the presence of deoxycholate, eluted from a Sephacryl S-200 gel filtration column with a partition coefficient equivalent to that of a 31-kD soluble globular protein. Because of the associated detergent and probable deviation from globularity, this is an over-estimate of the size of the native molecule, and is more consistent with the native molecule being a single polypeptide chain rather than a dimer. Isoelectric focusing of this material showed microheterogeneity with at least five bands between pI 4 and 5. Another monoclonal antibody, HD-42, which had been isolated on the basis of its specificity for a fibrosarcoma antigen subsequently found to be Ly-6 related, precipitated the same polypeptides. Furthermore, no obvious difference was evident between precipitates from Con A-activated lymphocytes and Meth A fibrosarcoma cells.

Topics: Animals; Antibodies, Monoclonal; Antigens, Ly; Binding Sites, Antibody; Concanavalin A; Fibrosarcoma; Isoantigens; Isoelectric Focusing; Lymphocyte Activation; Mice; Mice, Inbred A; Mice, Inbred AKR; Mice, Inbred BALB C; Molecular Weight; Peptides; Precipitin Tests; Protein Precursors

Culture fluids of concanavalin A-stimulated rat spleen cells were purified by means of ammonium sulfate precipitation and Sephacryl S-200 column chromatography. Interleukin 2 (IL-2), which can promote the proliferation of mouse lymphocytes was distributed in the fractions of molecular weight of 22,000 to 26,000 daltons. Culture of C57BL/6 mouse spleen cells with the IL-2 fraction resulted in the induction of cells cytotoxic to syngeneic fibrosarcoma cells. Determination of the target specificity of the killer cells revealed that the killer cells could lyse a variety of syngeneic and allogeneic tumor cells in vitro. The results of cold target inhibition tests and cytotoxicity assay after treatment with antisera plus complement indicated that the killer cells mainly consisted of Thy 1.2+, Ly 2.2+, asialoGM1-T cells but included some asialo-GM1+ natural killer (NK) cells. Although the cytotoxicities of both IL-2-activated killer T cells and NK cells were nonspecific in terms of the antigen specificity, their cytotoxic activities against syngeneic fibrosarcomas and NK-sensitive allogeneic lymphomas were complementary. The assay of interferon in culture fluid from IL-2-treated spleen cells suggested that generation of IL-2-activated killer cells was closely associated with the amount of immune interferon released from lymphocytes in the culture.

Topics: Animals; Cell Division; Concanavalin A; Epitopes; Fibrosarcoma; Interferons; Interleukin-2; Killer Cells, Natural; Kinetics; Male; Mice; Mice, Inbred A; Mice, Inbred C57BL; Rats; Spleen; T-Lymphocytes

New Zealand Black ( NBR ) rats that are innately immune to challenge with a syngeneic 3-methylcholanthrene [(MCA) CAS: 56-49-5]-induced fibrosarcoma have spleen cells that produce helper effects for in vitro lymphoproliferative responses in the presence of individual MCA-induced fibrosarcoma cells. Spleen cells from MCA-induced fibrosarcoma progressor rats (which lack innate tumor immunity) do not produce demonstrable helper activity. Supernatants from 48-hour cocultures of spleen cells from tumor-immune (TI) rats and syngeneic MCA-induced fibrosarcoma cells replaced the spleen cell helper activity. Comparable spleen cell supernatants from tumor progressor rats or unchallenged rats (controls) as well as supernatants from MCA-induced fibrosarcoma cells cultured alone did not produce any helper factor activity. Supernatants from TI rat spleen cells following inoculation with MCA-induced fibrosarcoma cells did not affect lymphoproliferative responses of NBR spleen cells induced by concanavalin A or alloantigens. The supernatants also did not contain detectable interleukin 2 activity as determined with the use of the thymocyte costimulator assay. These data indicate that the production of soluble helper factors by TI rat spleen cells may be involved in the augmentation of a protective host antitumor response.

Topics: Animals; Concanavalin A; Fibrosarcoma; Lymphocyte Culture Test, Mixed; Lymphokines; Methylcholanthrene; Neoplasm Transplantation; Rats; Rats, Inbred BUF; Rats, Inbred Strains; Solubility; Spleen; T-Lymphocytes, Helper-Inducer; Transplantation, Isogeneic

A kinetic study assessing the relationship between tumor growth and the ability of BALB/c mouse splenocytes to produce Interleukin 3 (IL 3) indicated a concomitant decrease in IL 3 activity with tumor growth. Tumor-bearing host (TBH) splenocytes produced 600 pmoles/hr/10(8) cells of IL 3 activity at Day 0 but only 62 pmoles/hr/10(8) cells by Day 28 post tumor cell inoculation. Nylon wool fractionation (to remove adherent suppressor cells) did not restore IL 3 activity. Addition of purified IL 3 to mitogen proliferation assays showed that IL 3 alone was mitogenic for normal host but not TBH splenocytes. In concert with concanavalin A (Con A) and phytohemagglutinin, IL 3 augmented in vitro normal host splenocyte responsiveness but significantly further suppressed it in the TBH. An absorption assay indicated that fresh cells had acceptors to remove IL 3 from supernatants. Con A-induced normal or TBH blast cells lost their ability to absorb IL 3. Intravenous inoculation of purified IL 3 into normal and TBH resulted in further suppression of TBH splenocyte mitogen-induced blastogenesis. The exacerbation of TBH spleen cell reactivity by IL 3 may be due to a tumor-induced feedback inhibition mechanism further suppressing cellular differentiation critical to cytotoxic T lymphocyte maturation.

Topics: Animals; Cell Division; Concanavalin A; Fibrosarcoma; Interleukin-3; Kinetics; Lymphokines; Male; Mice; Mice, Inbred BALB C; Neoplasm Transplantation; Phytohemagglutinins; Spleen

Suppressed concanavalin A response of spleen cells which appeared on Day 21 in C3H/He mice bearing methylcholanthrene-induced fibrosarcoma was attributed to macrophages. These macrophages were not only immunoglobulin and Thy 1.2 negative and mitomycin C resistant but were also found in the light-specific-gravity (1.077) fraction and were completely removed by carbonyl iron treatment. These suppressor macrophages, however, disappeared 4 days after surgical resection of the tumor, suggesting that the control mechanism originally resides in tumor tissues. Immunosuppressive acidic protein (IAP) levels in the sera of these tumor-bearing mice increased along with the appearance of these suppressor macrophages. Inasmuch as the suppressor macrophages obtained from the spleens of tumor bearers and cultured in vitro produced 4 times more IAP (88 ng/ml) than did resident macrophages, the elevated levels of IAP in the sera of tumor-bearing mice at the late stage might be explained partly by the appearance of suppressor macrophages. On the other hand, an i.v. administration of IAP (5 mg/mouse) into normal mice not only induced the same unresponsiveness of spleen cells to concanavalin A shown by tumor-bearing mice but also induced suppressor macrophages in the spleens of these mice. This fact may indicate that IAP elevation, even though artificial, triggers the induction of suppressor macrophages in the spleen or at least points to a keen correlation between the appearance of suppressor macrophages and increased IAP level in the serum.

Topics: Animals; Antibody Formation; Concanavalin A; Female; Fibrosarcoma; Macrophages; Male; Mice; Mice, Inbred C3H; Neoplasm Proteins; Spleen; T-Lymphocytes, Regulatory

Tumor pairs, selected on the basis of their different capacities to metastasize in vivo (SP73/AS and ASML from the rat, Eb/ESb from the mouse), have been assayed for their membrane associated actin through the DNase inhibition assay. It is found that, provided inhibitions per cell are corrected for the influence of gross heterogeneities in size distributions, the more metastatic tumor cells have significantly higher DNase I inhibitions than their less invasive counterparts. This observation, which extends our previous study of normal recirculating lymphocytes, is rationalized by postulating a participation of these actin pools to a property critical for both normal recirculation and metastatic spreading, arguments are presented which favor cell surface deformability as a possible candidate.

Topics: Actins; Adenocarcinoma; Animals; Concanavalin A; Deoxyribonuclease I; Endodeoxyribonucleases; Female; Fibrosarcoma; Lymphoma; Male; Neoplasm Metastasis; Neoplasms; Rats

Young New Zealand Black rats (less than 35 wk old) developed progressively growing tumors when given injections of cells from a syngeneic 3-methylcholanthrene (MCA)-induced fibrosarcoma. Spontaneous tumor regression occurred in animals more than 10 months of age. Compared to the responses of spleen cells from age-matched controls, spleen cells from rats in which tumor progression was present progressor rats) showed decreased proliferative responses to concanavalin (Con A), phytohemagglutinin (PHA), and syngeneic MCA tumor cells. Spleen cells from rats in which the tumors had regressed (regressor rats), however, produced significant increases in proliferative responses when compared with the responses of spleen cells from age-matched controls and from progressor rats. Cell-mixing experiments implicated the presence of two spleen suppressor cell populations in progressor rats, one of which was not present in regressor rats. The unique suppressor cell found in progressor rats appeared to be specific for tumor cell-induced proliferative responses. Spleen cells from both progressor and regressor rats produced similar suppressive effects in the PHA and Con A responses of normal cells.

Topics: Animals; Cell Division; Concanavalin A; Fibrosarcoma; Methylcholanthrene; Neoplasm Regression, Spontaneous; Phytohemagglutinins; Rats; Rats, Inbred Strains; Spleen; T-Lymphocytes, Regulatory

Concanavalin A (ConA)-bound-tumor cell vaccine of methylchoranthrene-induced fibrosarcoma (Meth 1) induced tumor-specific immunoprophylactic and immunotherapeutic response against an inoculum of live Meth 1 cells in histocompatible animals. ConA-free Meth 1 vaccine induced much less response under the identical experimental conditions. Immunotherapeutic potency of ConA-bound Meth 1 vaccine was enhanced by levamisole, and 37% of the animals inoculated with 10(4) live Meth 1 cells at day 0 were cured when they were administered 10(6) cells of ConA-bound Meth 1 vaccine at days 1 and 8 and 0.63 mg/kg levamisole at days 1,2 and 3. Delayed administration of levamisole at day 8,9 and 10 was less effective than the earlier administration, but still produced a 17% cure of Meth 1-bearing animals when combined with ConA-bound Meth 1 vaccine. Immunotherapeutic response under these regimens was further enhanced by mitomycin C, and approximately 60% of the animals inoculated with 10(5) Meth 1 cells were cured when three agents were administered at the defined intervals. These results suggest the feasibility of the regimen in which the therapeutic response induced by immunotherapeutic agents is further enhanced by the selected chemotherapeutic agents.

Topics: Animals; Concanavalin A; Drug Therapy, Combination; Fibrosarcoma; Immunotherapy; Levamisole; Male; Methylcholanthrene; Mice; Mice, Inbred Strains; Mitomycin; Mitomycins; Sarcoma, Experimental

Topics: Animals; Cell Division; Cell Line; Concanavalin A; DNA; Female; Fibrosarcoma; Kupffer Cells; Male; Mitogens; Rats; Rats, Inbred Strains; Receptors, Mitogen

Experiments were carried out to determine whether the growth of tumors could be influenced by local inflammatory reactions induced by mitogens; Gram-negative bacterial lipopolysaccharide (LPS), concanavalin A (Con A) and phytohemagglutinin (PHA). Mice received injections, beneath the footpad or subcutaneously in the flank, of cells of syngeneic chemically induced fibrosarcomas with or without varying doses of mitogen. In the footpad (a) LPS caused a dose-dependent increase in the size; (b) Con A caused a decrease in the size of one of the three tumors, the decrease being inversely related to the dose of Con A; (c) PHA caused a dose-dependent decrease in the size of all three tumors: (d) PHA caused much smaller macroscopic inflammatory reactions than LPS or Con A. Subcutaneously injected tumor growth was inhibited by all three agents. Subcutaneous tumors contained a higher proportion of host inflammatory cells when mitogens had been mixed with the tumor inoculum. It is concluded that mitogens that can induce inflammatory reactions in mice can also bring about some suppression of tumor growth but that the depression is site-dependent and not clearly related to the apparent intensity of inflammation.

Topics: Animals; Concanavalin A; Dose-Response Relationship, Drug; Female; Fibrosarcoma; Gram-Negative Aerobic Bacteria; Inflammation; Injections, Subcutaneous; Lipopolysaccharides; Male; Mice; Mitogens; Neoplasms, Experimental; Phytohemagglutinins; Time Factors

An increase in natural (innate) immunity with age (through 65 weeks) of NBR rats to a syngeneic methylcholanthrene-induced fibrosarcoma (MCA) is described. This increase is characterized by the appearance of spontaneous tumor regressor animals and an increase in the incidence of tumor non-takes by rats 45 weeks of age and older when compared to younger animals. Age-related changes were observed in the in vitro proliferative responses of normal unfractionated and nylon wool fractionated spleen cells to Con A, PHA and irradiated MCA tumor cells. Certain of these different proliferative responses either increased and/or decreases independently at different ages. Relative to normal spleen cell proliferative responses, tumor progressors have decreased proliferative responses and tumor regressors display increased proliferative responses. The significance of this in light of current aging research is discussed.

Topics: Aging; Animals; Cell Division; Concanavalin A; Fibrosarcoma; Immunity, Innate; Methylcholanthrene; Mitosis; Neoplasm Transplantation; Phytohemagglutinins; Rats; Rats, Inbred Strains; Spleen

Concanavalin A (Con A) potentiated the BCG-contact-mediated antitumor action when both Con A (10 microgram) and BCG (50 micrograms) were injected with fibrosarcoma cells (5 x 10(4)) into inbred Swiss mice. BCG (50 micrograms) alone had no antitumor effect. The Con A-potentiated BCG-contact-mediated phenomenon was shown to be immunologically mediated, inasmuch as tumors developed in immunosuppressed mice inoculated with tumor cells mixed with Con A and BCG. The same dose of 50 micrograms BCG was effective in controlling the growth of 10(6) fibrosarcoma cells in the presence of Con A. The specific inhibitor of Con A, alpha-methyl D-mannoside, abrogated the potentiation of the BCG effect seen with Con A. Con A also increased the antitumor effect of BCG in sarcoma 180 ascites tumor. Another lectin, peanut agglutinin, also induced an antitumor effect in the presence of BCG only when the tumor cells were treated with Vibrio cholerae neuraminidase.

Topics: Animals; BCG Vaccine; Concanavalin A; Fibrosarcoma; Graft Rejection; Immunosuppression Therapy; Lectins; Male; Mice; Mice, Inbred Strains; Neoplasm Transplantation; Neoplasms, Experimental; Sarcoma, Experimental; Transplantation Immunology

The effect of in vivo treatment with THF (thymus humoral factor) on the response of mouse lymphocytes to mitogens was investigated. Different preparations of THF were tested by daily i.m. injections into normal mice. Spleen, peripheral lymph node and thymus cells were tested for reactivity to several mitogens at various intervals after initiation of treatment. Our results indicate that the administration of THF to normal mice causes an inhibitory trend in the response of spleen cells to T-cell mitogens. It was found that the response of spleen cells to phytohemagglutinin (PHA) and concanavalin A (Con A) was strongly depressed after 7 days of treatment with 50 micrograms of THF. This was followed by a recovery of the response to normal levels after 14 days of treatment. The response of spleen cells to lipopolysaccharide (LPS) a B-cell mitogen, did not change throughout 14 days of treatmnent with THF. Lymph node cells of THF-treated mice behaved qualitatively in a similar manner to spleen cells, while thymus cells from THF-treated mice showed a significantly increased response to Con A. In contrast to normal mice, the injection of THF into mice with an impaired reactivity to PHA, such as thymectomized mice and tumor-bearing mice, caused an augmentation of the mitogenic response of spleen cells. These results suggest that in vivo administration of THF causes regulatory changes in the lymphocyte reactivity to T-cell mitogens.

Topics: Animals; Chromatography, Gel; Concanavalin A; Fibrosarcoma; Kinetics; Lymph Nodes; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; Mitogens; Phytohemagglutinins; Spleen; T-Lymphocytes; Thymectomy; Thymus Hormones

Neoplastic transformation of primary fibroblast culture derived from esophagus tissue of a 52-year old male esophageal cancer patient was induced by chemical carcinogen (N-methyl-N'-nitro-N-nitrosoguanidine, MNNG) treatment. The transformed cells showed the biological and morphological properties characteristic of malignant cells, such as loss of contact inhibition, unlimited growth in vitro, aneuploidy, agglutinability by concanavalin A, formation of microvilli on the cell surface, growth on solid agar medium and tumor (fibrosarcoma) formation after heterotransplantation into immunosuppressed newborn mice.

Topics: Aneuploidy; Animals; Cell Division; Cell Transformation, Neoplastic; Cells, Cultured; Concanavalin A; Disease Susceptibility; Esophageal Neoplasms; Esophagus; Fibroblasts; Fibrosarcoma; Humans; Male; Methylnitronitrosoguanidine; Mice; Middle Aged; Neoplasm Transplantation

Topics: Animals; Cell Count; Cell Transformation, Neoplastic; Concanavalin A; Cricetinae; Female; Fibrosarcoma; Lymphocyte Activation; Lymphocyte Culture Test, Mixed; Lymphocytes; Male; Mitogens; Simian virus 40; Spleen; Thymus Gland

Topics: Animals; Concanavalin A; Cytotoxicity, Immunologic; Dextrans; Erythrocytes; Fibrosarcoma; Lipopolysaccharides; Macrophages; Mannose; Peptones; Phytohemagglutinins; Rats; Sheep; Solubility

Two ascites tumors in syngeneic CBA mice are described, viz., MCB 21-AA and MCB 31-AA, with their solid progenitors: A sarcoma (MCB 21-SS) and a squamous cell carcinoma (MCB 31-SC), induced by gastric feeding of 20-methylcholanthrene. The ascites tumor cells have certain characteristics in common, which they do not share with either cells from the solid tumors or even with cells from solid ascites tumors (-21-AS and -31-AS=ascites tumor transplanted s.c.). Presumably some of these differences, for instance, in PAS stainability, electrophoretic mobility and lectin agglutinability, are due to enzyme treatment required to bring solid tumors into suspension. Between the two ascites tumors there are certain differences in cell size, aggregability, and growth rate. They are similar, however, in requiring large cell doses for transplantation in syngeneic animals, which is also true for the solid (SS and SC) tumors. MCB 21 and -AA even required fewer cells for transplantation in allogeneic A mice than in syngeneic CBA mice. MCB 31-AA is also allotransplantable. The pattern of spread, after i.v. cell injection, is almost exclusively to the lungs for all tumor lines.

Topics: Animals; Ascites; Carcinoma, Squamous Cell; Cell Nucleus; Chromosomes; Concanavalin A; Electrophoresis; Fibrosarcoma; Lectins; Methylcholanthrene; Mice; Mice, Inbred CBA; Neoplasm Transplantation; Neoplasms, Experimental; Surface Properties; Transplantation, Homologous; Transplantation, Isogeneic

Topics: Animals; Bone Marrow; Concanavalin A; Cytotoxicity, Immunologic; Female; Fibrosarcoma; Lymphocyte Activation; Lymphocytes; Macrophages; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; Neoplasms, Experimental

The effects of in vivo-administered concanavalin A (Con A) on the kinetics of the primary and secondary cellular immune responses to simian virus 40-transformed tumor cells were investigated in BALB/c mice. Either a single initial dose of 400 mug Con A or daily doses of 50 mug depressed the cell-mediated immune response to tumor cells during the progressive growth of tumors, as determined by a radioisotopic foot-pad assay. The immune depression correlated with an increase in ultimate tumor weight. Similarly, Con A suppressed the antitumor cellular immune response in tumor-immune animals. Immune reactivity returned within 6 days after a single injection of 400 mug Con. Continuous administration 50 mug Con A resulted in a gradual decline in antitumor cellular immune responsiveness, which reached a plateau by the 5th day. Splenic lymphocytes from Con A-treated, immune mice failed to elicit a local adoptive transfer reaction; their immune responsiveness tended to return after incubation with alpha-methyl-D-pyranosyl sugars.

Topics: Animals; Concanavalin A; Fibrosarcoma; Immunity, Cellular; Immunization, Passive; Kinetics; Lymphocytes; Mice; Mice, Inbred BALB C; Sarcoma, Experimental; Simian virus 40; Spleen; Time Factors

Topics: Adenoviridae; Animals; Antibody Formation; Bromodeoxyuridine; Cells, Cultured; Concanavalin A; Culture Media; Female; Fibrosarcoma; Guinea Pigs; Immunodiffusion; Inclusion Bodies, Viral; Injections, Subcutaneous; Liposarcoma; Methylcholanthrene; Osteosarcoma; Sarcoma, Experimental; Thymidine; Tritium

Topics: Adenocarcinoma; Animals; Concanavalin A; Female; Fibrosarcoma; Immunotherapy; Mammary Neoplasms, Experimental; Methylcholanthrene; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; Mitomycins; Neoplasm Transplantation; Neoplasms, Experimental; Neuraminidase; Sarcoma, Experimental; Transplantation, Homologous; Vibrio cholerae

Topics: Adenocarcinoma; Animals; Antigens, Neoplasm; Cell Membrane; Concanavalin A; Epitopes; Female; Fibrosarcoma; Immunotherapy; Mammary Neoplasms, Experimental; Melanoma; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; Neoplasm Transplantation; Neoplasms, Experimental; Neuraminidase; Sarcoma, Experimental; Transplantation, Homologous; Vibrio cholerae

Tumors induced by SV40 virus in newborn and adult Syrian hamsters were analyzed for their growth properties in vitro, transplantation, agglutination with concanavalin A and chromosome constitution. Following transfer to culture flasks tumor cells grew for 2-3 weeks, then went through a "degenerative phase". Eventually lines were established which became adapted to in vitro culture conditions. Agglutination properties of these tumor cells were similar to those of cells transformed in vitro with SV40 virus. Of five subcutaneous and six intratesticular tumors that were analyzed for their chromosome constitution, all had a hypotetraploid chromosome number distribution. The results of the chromosome studies suggest a similiar pattern in the evolution of malignant properties of cells transformed in vitro and in vivo following infection with SV40 virus.

Topics: Agglutination; Animals; Antigens, Neoplasm; Antigens, Viral; Cell Line; Cell Transformation, Neoplastic; Cells, Cultured; Chromosome Aberrations; Chromosomes; Concanavalin A; Cricetinae; Diploidy; Fibrosarcoma; Karyotyping; Male; Neoplasm Transplantation; Neoplasms, Experimental; Polyploidy; Simian virus 40; Testicular Neoplasms; Transplantation, Homologous

Topics: Adenocarcinoma; Animals; Antigens, Neoplasm; Concanavalin A; Female; Fibrosarcoma; Immunotherapy; Mammary Neoplasms, Experimental; Melanoma; Methylcholanthrene; Mice; Mice, Inbred Strains; Mitomycins; Neoplasm Transplantation; Neuraminidase; Sarcoma, Experimental; Vibrio cholerae

Topics: Animals; Antibodies, Neoplasm; Antibody Formation; Antigen-Antibody Reactions; Antigens, Neoplasm; Antilymphocyte Serum; Autoantibodies; Concanavalin A; Cytotoxicity Tests, Immunologic; Fibrosarcoma; Histocompatibility Antigens; Humans; Immunotherapy; Lymphocytes; Mammary Neoplasms, Experimental; Melanoma; Methylcholanthrene; Mice; Neoplasm Transplantation; Neoplasms; Neuraminidase; Rats; Sarcoma, Experimental; Vibrio cholerae

Topics: Animals; Antigens; Antigens, Bacterial; Antilymphocyte Serum; Ascitic Fluid; Autoradiography; Cell Migration Inhibition; Cells, Cultured; Concanavalin A; DNA; Endotoxins; Fibrosarcoma; Graft vs Host Reaction; Immunity, Cellular; Immunization, Passive; Lectins; Lymphocytes; Macrophages; Mice; Mice, Inbred A; Mice, Inbred CBA; Salmonella typhimurium; Serum Albumin; Spleen; Thymidine; Tritium

Topics: Agglutination Tests; Animals; Carcinogens; Cell Division; Cell Line; Cell Transformation, Neoplastic; Concanavalin A; Contact Inhibition; Cricetinae; Dextrans; Embryo, Mammalian; Female; Fibroblasts; Fibrosarcoma; Mice; Mitosis; Molecular Weight; Pregnancy; Sulfuric Acids; Time Factors

Topics: Agglutination; Animals; Cell Division; Cells, Cultured; Concanavalin A; Fibrosarcoma; Lectins; Mice; Neoplasms, Experimental