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

The survival time of animals, inhibition of the incorporation of thymidine-[6-3H] (3H-TdR) into DNA, and histopathological observation were made after the injection of Mitomycin-C, Bleomycin, cyclophosphamide, Daunomycin, Actinomycin-D, or 5-fluorouracil into mice transplanted with sarcoma-180 to their liver, kidney, and lung. The most prolonged survival time was obtained by the injection with cyclophosphamide and a moderate prolonged survival by Bleomycin and Actinomycin-D. In the case of 5-fluorouracil and Daunomycin, there were extreme variations in the survival time depending on the site of tumor growth. Cyclophosphamide and 5-fluorouracil showed greater and longer lasting inhibition of the incorporation of 3H-TdR into DNA of the tumor tissue, whereas the remaining agents caused transient inhibition on the tumor tissue. Inhibitory ratio and duration of the incorporation of 3H-TdR into DNA of normal site of the tissue of tumor-bearing organ were found to be more increased or almost the same compared with those of the tumor tissue. The most rapid recovery of the incorporation of 3H-TdR into DNA was observed in the small intestine among various organs and tumor in any treatment groups. From the histopathological observation, the degree of tumor cell damage by the agent was almost in agreement with inhibition of the incorporation of 3H-TdR up to 72 hr after the treatment.
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PMID:Effect of antitumor agents on sarcoma-180 tumor cells transplanted to liver, kidney, and lung. 5 69

(1) Passive hemagglutination and radioimmunoassay are suitable methods for the detection of AFP in the low concentration range. (2) In 3.72% of the cases a clinically unknown carcinoma was found in an unselected group of patients with liver cirrhosis. (3) 21.9% of the patients showed AFP elevations up to 2000 ng/ml. In 10.6% of this group, increasing titers demonstrated a primary liver cell carcinoma. In 89.4% a transitory rise of AFP was not associated with tumor growth. Levels return to normal values within three months in 90% of the cases. (4) Transitory AFP elevations are not correlated to clinical conditions (praecoma, coma, delirium, bleeding, ascites, shunt) or to biochemical parameters (GOT, GPT, bilirubin, prothrombin complex time, gamma-globulin). (5) A temporary rise in AFP is more frequently observed in groups with high hepatoma incidence than in groups with low hepatoma incidence. (6) Therefore, it may be suggested that a transitory rise of AFP could reflect a "primary reaction" of carcinogenesis. (7) Primary liver cell carcinoma is found to be more frequent in posthepatitic than in postalcoholic, cryptogenic, and other cirrhosis and to be more frequent in australia-antigen positive than in australia-antigen negative cases. (8) Routine serological tumor antigen screening of patients with a precancerous disease is useful.
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PMID:Early detection of hepatoma: prospective study in liver cirrhosis using passive hemagglutination and the radioimmunoassay. 5 21

Cell-mediated immune reactions appear to play an important role in resistance against growth of leukemia cells in mice. Possible mechanisms for in vivo protection in two tumor systems are discussed. These tumor models, which are a Friend leukemia virus-induced transplantable tumor, FBL-3, and primary murine sarcoma virus (MSV) -induced tumors, are strongly antigenic; under some conditions, tumors regress completely. In mice with regressing FBL-3 tumors, cell-mediated cytotoxicity was measured by release of [125I]iododeoxyuridine. The response was biphasic, with an initial peak at 10 days and a 2nd peak after 30 days. A boost in reactivity could be elicited by later challenge with tumor cells. All of the reactivity was dependent on T-cells, being eliminated by treatment with anti-theta plus complement. The specificity of the reactions was not completely defined, but it was consistent with Friend type-specific antigen plus broader, common antigens. In mice with regressing MSV tumors, strong cell-mediated cytotoxicity, measured mainly by release of 51Cr, was seen against RBL-5, a Rauscher virus-induced leukemia. A single peak of response occurred at about 14 days after virus inoculation. Upon later challenge with RBL-5 cells, a vigorous and rapid secondary response was elicited, mainly in the region of tumor challenge. This cytotoxic reactivity and in vivo resistance to leukemia.lso was completely dependent on T-cells. In addition, macrophage-mediated inhibition of leukemia cell growth in vitro was seen in this system at the time of peak tumor development. The 51Cr release cytotoxicity was specific and directed primarily against an antigen, MEV-SA1, associated with mouse endogenous C-type viruses. The macrophage-induced growth inhibition appeared to be nonspecific. In both the FBL-3 and MSV tumor systems, protection against tumor growth could be adoptively transferred by immune lymphoid cells. In addition to induction of cell-mediated immunity by tumor cell or virus inoculation, cell-mediated cytotoxic reactivity was found to occur naturally in most young mice. This natural killer activity was quite distinct from the experimentally elicited reactions, being mediated by N-cells, a subpopulation of lymphoid cells with no clearly identifiable cell surface markers. The natural cytotoxicity was also directed against antigenic specificities different from those recognized by the MSV-immune cells. The central issue in all of these studies has been to determine the relationships between the in vitro-detected cell-mediated reactivity and in vivo resistance to leukemia.
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PMID:Cell-mediated immunity to leukemia virus- and tumor-associated antigens in mice. 5 23

W/Fu rats inoculated s.c. with less than or equal to 5 x 10(7) syngeneic (C58NT)D (Gross virus-positive) lymphoma tumor cells normally develop a palpable tumor which reaches its maximum size (12 to 14 mm) at 6 to 8 days and is subsequently rejected by 10 to 12 days. However, rats previously sensitized with soluble tumor antigens from (C58NT)D cells prior to (C58NT)D tumor inoculation demonstrate a significant enhancement of tumor growth (the tumor reaches up to 26 mm and is rejected by 16 to 18 days). This enhancement persisted in antigen-treated rats that continued to receive soluble antigen after tumor inoculation. The in vivo enhancement coincided with a significant in vitro depression of cell-mediated cytotoxicity [assessed with 51Cr-labeled (C58NT)D target cells and peripheral blood leukocytes]. The observed tumor enhancement was specific, inasmuch as presensitization to either soluble tumor antigens from WR6 (Gross virus-negative) tumor, syngeneic to W/Fu rats, or to soluble antigen from W/Fu spleen cells had no enhancing effect on (C58NT)D tumor growth. Interestingly, sensitization to soluble tumor antigen alone did not elicit detectable cell-mediated immunity, cytotoxic antibody, or serum-blocking activity to the (C58NT)D tumor. We conclude that sensitization to soluble tumor antigens specifically impairs the immune apparatus normally acting in tumor rejection. This impairment appears to act primarily at the induction phase of the immune response.
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PMID:Specific enhancement of tumor growth and depression of cell-mediated immunity following sensitization to soluble tumor antigens. 5 98

Spleen cells from W/Fu rats 4 to 6 weeks after immunization with syngeneic Gross virus-induced lymphoma (C58NT)D cells usually lack detectable activity in a short-term 51Cr release assay. The results presented here demonstrate that these spleen cells retain the capacity to generate significant proliferative and cytotoxic activity upon re-exposure to mitomycin C-treated (C58NT)D cells in vitro. Optimal conditions were defined in W/Fu rats for this secondary immune response in vitro to the (C58NT)D cells. The cytotoxic response was observed to be quantitative, reproducible, and specific. Optimal generation occurred 5 days after initiation of cultures with a 30:1 responding cell:stimulating cell ratio. In vitro generated cytotoxic cells inhibit tumor growth in vivo when administered as a mixture with tumor cells.
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PMID:Generation of cytotoxic lymphocytes in vitro: response of immune rat spleen cells to a syngeneic gross virus-induced lymphoma in mixed lymphocyte-tumor culture. 5 29

Primary and secondary cell-mediated cytotoxic responses to FBL-3 cells, a syngeneic Friend virus-induced leukemia in C57BL/6 mice, could be generated by in vitro techniques as tested by the 125IUdR release assay. The specificity of the cytotoxic reactions appeared to be directed against the Friend type-specific antigen and the FMR (Friend, Moloney, Rauscher) antigen which were also the major antigens for transplantation immunity to FBL-3. In comparison to the primary cytotoxic response, the secondary cytotoxic response was accelerated (detected at an earlier time after sensitization), enhanced (gave much higher levels of cytotoxicity), was also longer lasting, and could be induced by a wide dose range of tumor cells. The secondary response could only be induced with lymphocytes obtained from regressors that were resistant to FBL-3 challenge; lymphocytes from mice with progressive tumor growth had no detectable secondary response. It was found that both induction phase and the effector phase of cytotoxic responses were T cell dependent. The characteristics of these reactions were thus very similar to those obtained with in vivo immunization or challenge, providing a good correlation with in vivo tumor immunity.
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PMID:Cell-mediated immunity to friend virus-induced leukemia. IV. In vitro generation of primary and secondary cell-mediated cytotoxic responses. 5 34

Spleen cells at various times after inoculation of W/Fu rats with a syngeneic Gross virus-induced lymphoma, (C58NT)D, were tested for their in vivo activity in adoptive transfer experiments and for their in vitro reactivity in a 4-hr 51Cr release cytotoxicity assay and in a mixed lymphocyte-tumor cell interaction assay. In adoptive transfer, the best protection against tumor growth was observed with immune spleen cells taken at 30 days after tumor cell inoculation (the peak of reactivity in the mixed lymphocyte-tumor cell interaction assay) whereas cells taken at 10 days (the peak reactivity in the 51Cr release cytotoxicity assay) gave only partial protection. The protection detected in the adoptive transfer experiments was specific for (C58NT)D associated antigens, and this correlated well with the specificity observed in the in vitro cell-mediated immunity assays. T cells, but not complement receptor-bearing cells or macrophages, were essential for the protection against tumor growth in vivo, and also for the in vitro reactivity in the 51Cr release cytotoxicity and the mixed lymphocyte-tumor cell interaction assays.
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PMID:In vivo protection against syngeneic Gross virus-induced lymphoma in rats: comparison with in vitro studies of cell-mediated immunity. 5 36

As tables show, hormone treatment may be useful for control of the growth of endometrial and mammary cancers. Although endocrine treatment is to be used only where metastasis has already occurred 70% of all breast cancer patients eventually reach this stage, lending importance to endocrine treatment as well as chemotherapy as life-lengthening (though not curative) methods. Control of tumor growth is possible through altering the hormonal milieu of the host organ and through direct influence on the tumor cells. Measures may be ablative (removal of hormone-producing glands) or additive (e.g., use of steroids, as shown in detail in the tables). Progestagen, in high doses, produces atrophy of the endometrium and is associated with objective remission in at least 30-40% of cases of progressive endometrial carcinomas. In breast cancer cases, endocrine treatment is most suitable for premenopausal women or women at least 5 years past menopause; location of the metastases is among the other factors to be considered.
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PMID:[Endocrine treatment of gynecologic carcinomas]. 5 26

Twenty-six patients are reviewed who had primary carcinomas involving the junction of the hepatic ducts. The majority had had an initial procedure of palliative biliary diversion elsewhere and were referred for further treatment. In three cases, en bloc resection of the tumor with total hepatectomy and orthotopic liver transplantation were performed. All tumor growth was encompassed in each case, but within 4 months all succumbed as a result of allograft rejection. Auxiliary (heterotopic) liver transplantation was performed in another patient because of recurrent disease after previous left hepatic resection in continuity with a hilar duct lesion. Five patients underwent hepatic lobectomy with en bloc resection of the hepatic duct junction. When adequate tumor excision was not feasible, biliary diversion could provide good palliation in some instances for extended periods of time. This is demonstrated by one patient who lived for 4 years and 4 months after the initial operation. In the meantime, the patient underwent 6 subsequent procedures of dilating of constricted bile ducts and tube cannulation of the biliary tree. Biliary diversion was achieved in 4 cases by intrahepatic cholangiojejunostomy. One of these patients, who is on chemotherapy, is asymptomatic one year after surgery.
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PMID:Surgical management of carcinoma of the junction of the main hepatic ducts. 5 80

Effects of continuous administration of bleomycin solution and of intralesional injection of sesame oil-suspended bleomycin on tumor growth were studied. Experimental animal tumors were 3 rd generation isotransplants of a spontaneous C3H mouse mammary carcinoma. Bleomycin treatments were started when transplanted tumors reached 8 mm in diameter and the measurement of tumor volume was followed. Dose administered was fixed as 100 mg/kg in all the groups. Bleomycin solution was given intralesionally in a single or 4 daily doses, or intraperitoneally by continuous infusion. The latter method inhibited tumor growth most effectively, while the single injection was the last effective. Intralesional injection of oil-suspended exhibited similar effectiveness as the continuous infusion, and it was independent of the number of fractions. These results were interpreted by the several features in the response of mammalian cells to the antibiotic.
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PMID:[Effect of continuous bleomycin treatment and of oil-suspended bleomycin on experimental tumor growth (author's transl)]. 6 May


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