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

With an L1210 tumor vaccine model, three biological and two chemical agents were tested for their ability to act as adjuvants. Adjuvant was administered with irradiated L1210 cells to immunize mice against this poorly immunogenic tumor. Two chemicals, pyran copolymer and glucan, and one biological, Brucella abortus strain 456 ether extract, were shown to be strong stimulators of antitumor immunity. Vaccination with irradiated tumor cells or adjuvant alone did not produce host resistance. Optimal immunity to challenge was produced by concomitant administration of either pyran copolymer, glucan, or B. abortus strain 456 ether extract with L1210 vaccine. Antitumor immunity was maximally expressed when vaccine and adjuvant were administered i.p. Evidence for systemic immunity was demonstrated when challenge was at a distal s.c. site. Mice immune to challenge were found to be refractory to a later rechallenge.
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PMID:Chemical and biological adjuvants capable of potentiating tumor cell vaccine. 41 6

We have previously shown that irradiated LSTRA cells (LX) were immunogenic and could prolong survival of mice bearing LSTRA tumors. This study demonstrated that addition of Corynebacterium parvum to the LX dramatically improved the strength of tumor immunity. In pretreatment-challenge experiments, C. parvum augmented the immunogenicity of 10(6) LX given intradermally, with an optimum dose of 0.14-1.4 microgram C. parvum per mouse. In therapy experiments (intraperitoneal vaccine treatment after tumor cell challenge), the therapeutic effect of 10(7) LX was improved by admixture of C. parvum, leading to a larger number of cured mice, permitting treatment of a larger challenge inoculum, and allowing later initiation of treatment than was possible with LX alone. Optimal dose of C. parvum for therapy was 1,400 microgram per mouse. Presensitization to C. parvum or use of repeated vaccine injections did not further improve the therapeutic effect. Cure of tumor-bearing mice by the mixed vaccine was tumor-specific. These results suggest that C. parvum is a potent adjuvant for use in active, tumor-specific immunotherapy.
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PMID:Active, specific immunotherapy of murine leukemia. II. Adjuvant effect of Corynebacterium parvum. 52 79

Optimal DNA synthesis in isolated Ehrlich ascites tumor cell nuclei depends upon the presence of ATP. The increased synthesis in the presence of ATP is shown to be due primarily to increased synthesis per active site rather than initiation of synthesis at different sites. The size of the short pieces observed in the presence of ATP is larger than the corresponding pieces observed in the absence of ATP.
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PMID:Nature of DNA synthesized in the presence of ATP in isolated nuclei. 56 77

Certain variables which might influence the outcome of combining cytotoxic drug and immune stimulant therapy were studied to optimize the effectiveness of Corynebacterium parvum combined with cyclophosphamide (CY) as treatment for a murine mammary adenocarcinoma (CaD2). Optimal effects of combined C. parvum-CY treatment in the CaD2 system were obtained when 443 to 1400 microgram of this immune stimulant per mouse were injected 2 to 3 days after CY chemotherapy and when combination treatment was continued on a weekly basis. The most critical factors contributing to the effectiveness of combination treatment in this system were the dose of C. parvum and the treatment frequency. The interval between chemotherapy and immune stimulant therapy was less critical to the outcome of combination treatment. Combination treatment given once or weekly significantly decreased tumor size in comparison to single or weekly CY treatment. A single treatment with CY and C. parvum significantly improved the survival over mice given a single CY treatment, but weekly CY and C. parvum treatment did not increase the survival over mice, given weekly chemotherapy.
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PMID:Effects of dose and schedule of immune stimulant on efficacy of combination Corynebacterium parvum-cyclophosphamide treatment for a murine mammary adenocarcinoma. 76 Nov 79

The antinflammatory ateroids fluocinoine acetonide, fluocinonide, and fluclorolone acetonide were found to be very effectiveinhibitory agents of mouse skin tumor promotion. These steroids also drastically inhibited epidermal DNA synthesis and epidermal cellular proliferation induced by a phorbal ester tumor promoter. In addition, these compounds were potent inhibitors, of plasminogen activator production in tumor cell cultures. The clinically used non-steroidal antiinflammatory agents oxyphenbutazone, indomethacin, and Seclazone also inhibite tumor promotion but were much less effective. Although these agents are useful against inflammatory disorders in general when given p.o., in our studies they had little effect on inflammation and epidermal cellular proliferation induced by a phorbol ester tumor promoter when given topically. The afore mentioned nonsteroidal antiinflammatory agents also had little effect on epidermal DNA synthesis. Oxyphenbutazone and indomethacin were less potent inhibitors of plasminogen activator production in tumor cells than were the antiinflammatory steroids, and Seclazone produced a negligible inhibition. There is, therefore, a general correlation in the potencies of a series of steroidal antiinflammatory agents for inhibition of tumor promotion and their ability to inhibit plasminogen activator production by tumor cell cultures and epidermal DNA synthesis.
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PMID:Effects of antiinflammatory agents on mouse skin tumor promotion, epidermal DNA synthesis, phorbol ester-induced cellular proliferation, and production of plasminogen activator. 85 68

A new microassay which utilizes radioiodinated staphylococcal protein A (SpA) to detect antibodies bound to cell surface antigens (CSA) was developed for monolayers of viable cultured tumor cells. Optimal detection of bound antibodies occurred at 37 degrees C with incubation periods of one hour each for antiserum and 131I-SpA. Labelling target cells with 125I-iododeoxyuridine facilitated expression of results relative to tumor cell number or protein concentration. Quantitation of antibody depended on CSA (tumor cells) and 131I-SpA being in excess of antibody; under these conditions, 0.25 ng of cell surface bound antibody could be detected readily. Initial studies utilized cultured human neurobodies in human serum which bound to CSA were removed by absorption with glutaraldehyde-insolubilized fetal calf serum (FCS) suggesting that FCS or FCS-like determinants can be CSA. Rabbit antisera, after extensive absorption, bound to cultured neuroblastoma and lung adenocarcinoma cells in a cell type specific pattern. These experiments demonstrated the value of this assay in quantitating anti-CSA antibodies and in serological analysis of tumor CSA.
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PMID:Microassay using radioiodinated protein A from Staphylococcus aureus for antibodies bound to cell surface antigens of adherent tumor cells. 90 15

Macrophage-activating factor (MAF) was obtained from cultures of normal F344 rat lymphocytes incubated with insoluble concanavalin A. The MAF rendered macrophages from normal C57BL/6 mice cytotoxic against the syngeneic B16 melanoma and the allogeneic AC 15091. At the same time, normal syngeneic or allogeneic embryo cells were unharmed, even in the presence of susceptible tumor cells. Optimal MAF levels followed incubation of lymphocytes for 48 hr with Sepharose-bound concanavalin A. A 2-hr incubation of macrophages with MAF was sufficient to initiate activation, providing that 46 hr were allowed to elapse before tumor cells were added. The MAF activity was enhanced after heating the supernatant to 199 degrees. Control experiments largely excluded the possibility that residual unbound concanavalin A caused the observed macrophage-mediated tumoricidal effects.
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PMID:Tumoricidal properties of mouse macrophages activated with mediators from rat lymphocytes stimulated with concanavalin A. 95 87

Leiomyosarcoma of vascular origin are rare tumors arising most frequently from the inferior vena cava (IVC). We report on three patients one of whom underwent definitive resection. These tumors most commonly involve the upper segment of the IVC, and appear with manifestations of the Budd-Chiari syndrome. Lesions at this level are not amenable to surgical therapy. Tumors of the middle and lower segments of the IVC usually cause right-sided pain. Diagnosis is difficult, but is best approached preoperatively by angiography and vena cavography. Optimal therapy of lesions at these levels is surgical resection. Resection of the IVC below the hepatic veins is possible with renal function preserved by collateral drainage of the left renal vein.
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PMID:Leiomyosarcoma of the inferior vena cava. Diagnosis and surgical management. 97 Oct 85

Optimal conditions were determined for the distribution of Ehrlich ascites carcinoma (EAC) and L-5178Y mouse tumor cells, proliferating in vivo, by their age within the cell cycle by sedimentation in a buffered linear sacharose density gradient. Measurements of cell size, DNA content and incorporation of tritiated thymidine in successive parts of the gradient confirmed the actual separation of cells of different age: in the upper fractions there were cells in G1 phase, in the middle fractions in S phase and in the lower layers of the gradient there were cells in G2 and/or M phase.
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PMID:Sacharose density gradient separation of Ehrlich ascites carcinoma and L-5178Y tumor cells in different cell cycle phases. 98 Jan 80

The Ca755 solid tumor in the C57B1 mouse has been used as a model to study the interrelationship of surgery and adjuvant chemotherapy on primary tumor growth. Surgery was performed on various days after tumor implantation. Surgical mortality increased with delay in surgery. The mean survival time (MST) was significantly increased by surgery. An increased cure rate in mice with late surgery may be due to immunological factors. Pretreatment cytoxan chemotherapy prior to a number of surgical days on the most effect schedule increased MST in the later surgical days primarily due to shrinkage of tumor and a diminished surgical mortality. Posttreatment chemotherapy significantly increased MST primarily on the basis of reducing tumor cell population after surgery and increasing both the cure rate and the time until death of those mice dying of regrowth of tumor. Optimal chemotherapy alone significantly increased MST compared to untreated controls. Optimal postsurgery chemotherapy increased survival longer than the additive increase of chemotherapy alone and surgery alone. This paper illustrates relationships between day of surgery dose and schedule of chemotherapy and effect on various measurable parameters. The results can best be understood in relationship to each other. It is suggested that adjuvant chemotherapy has specific definable benefits. It is apparent from human studies that carefully devised designs which consider these interrelationships are necessary if optimal therapeutic results are to be achieved.
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PMID:The effect of surgery and pretreatment or posttreatment adjuvant chemotherapy on primary tumor growth in an animal model. 118 67


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