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PubMed1984

[Induction of tumor necrosis factor (TNF) in tumor-bearing mice].

Tumor necrosis factor (TNF) can be induced in BALB/c mice bearing syngeneic tumor RL male 1 lymphoma or Meth A fibrosarcoma, by initial injection of either Corynebacterium parvum or BCG, in combination with a second injection of endotoxin (LPS) almost 10 days later. Either treatment resulted in hemorrhagic necrosis and complete regression of tumors in mice. The term, "endogenous induction of TNF therapy" was proposed for this trial. Although the TNF of tumor-bearing mice was identical to that of normal mice in molecular weight (about 40,000 daltons) and isoelectric point (4.4), and differed from IFN, the in vivo effect of endogenous TNF was much more remarkable than in mice receiving passive TNF administration. The mice bearing RL male 1 lymphoma cured after endogenous induction of TNF, rejected rechallenge of the same tumor cells but not Meth-A tumor cells. Splenocytes obtained from these cured mice were also found to be inhibitory in Winn's neutralization assay. The data indicate that tumor-specific immunity can be induced in mice receiving endogenous induction of TNF.

Animals↗
PubMed1984

Immunotherapy of cancer by systemic administration of lymphoid cells plus interleukin-2.

The adoptive transfer of specifically immune lymphocytes is capable of mediating the regression of a variety of established experimental tumors. We have studied the factors responsible for successful adoptive immunotherapy. Following injection of FBL-3 lymphoma into the footpad of syngeneic mice, this tumor forms a local nodule and is disseminated throughout the mouse within 5 days. Systemic administration of fresh immune lymphocytes on day 5, or of in vitro boosted immune splenocytes, or immune lymphoid cells expanded in interleukin-2 (IL-2), is capable of mediating total regression of both local and disseminated tumor. The efficacy of this immunotherapy can be enhanced by the simultaneous administration of IL-2. Because specifically immune cells can be difficult to obtain in many murine and human tumor systems, we have investigated the use of nonspecifically sensitized cells for use in adoptive immunotherapy. Lymphokine-activated killer cells (LAK) can easily be generated by incubating fresh murine or human lymphocytes in IL-2. Systemic injection of LAK cells can reduce the growth of established pulmonary metastases in murine tumor models when the LAK cells are administered in conjunction with IL-2. A variety of methods for activating human lymphoid cells to become lytic for fresh human tumors have been developed, including activation by IL-2, activation by lectins such as phytohemagglutinin and concanavalin A, and by allosensitization with pooled stimulator cells. The characteristics of these different activated killer cells have been defined. In a series of Phase I studies, we have demonstrated that activated killer cells can be safely administered to humans with advanced cancer. Studies are actively proceeding to develop an effective and practical method for the adoptive immunotherapy of cancer in humans, using both specifically activated and nonspecifically activated lymphoid cells.

Animals↗
PubMed1984

[Growth of human tumor transplanted into nude mice with various genetic backgrounds].

Nude mice with different genetic backgrounds were used for the experiment to evaluate the growth of human and murine tumors in the different hosts. Twelve human tumors including 5 gastric carcinomas (St-4, St-10, St-15, St-40, KS-1), 2 colon carcinomas (Co-3, Exp-42), 1 breast carcinoma (MX-1), 1 bile duct carcinoma (Ch-1), 1 hepatocellular hepatoma (Li-4) and 2 hemangiosarcomas (LC-27-R, LC-27-UR), and one murine tumor spontaneously arisen from C3H/HeN nu/+ mouse were transplanted into the subcutaneous tissue of nude mice with genetic backgrounds of BALB/cA, DDD and ICR (CD-1). BALB/cA-nu was originated from the Central Institute for Experimental Animals, DDD-nu was supplied from the Institute of Medical Science, University of Tokyo and ICR (CD-1)-nu was supplied from Charles River Co., Ltd. Tumors were measured by the width (W) and length (L) three times a week by the same person. The tumor volume (V) was estimated by the formula V = W2 X L/2. Tumor doubling time (Td) during the exponential growth phase was compared between the nude mice with different genetic backgrounds. It was found that Td of MX-1 in DDD-nu mice and Td of St-40 and Exp-42 in BALB/cA-nu mice were shortened in comparison with those of tumors transplanted into nude mice with the other strains. However, no statistically significant differences were observed when t-test of matched pairs and coefficients of correlation were applied to compare Td in the other kinds of nude mice. Nude mice with genetic backgrounds of DDD and ICR (CD-1) were thought to be also useful for various kinds of therapeutic experiments in human tumor xenografts/nude mice system.

Adenocarcinoma↗
PubMed1983

[Coombs-positive reactions in mice during transplantation of syngeneic tumors].

The effect of the growth of syngeneic transplantable tumors on Coombs' positive test in mice was studied. The modification of the hemagglutination test permitting one to minimize the amount of reagents used is described. Tumor transplantation induced Coombs' positive reactions in most recipients. The phenomenon could be observed in 4 murine strains and 6 tumor systems. Sometimes autoimmune reactions occurred before the emergence of palpable tumors. It is concluded that despite the influence of nonspecific factors, the principal cause of autoimmune reactivity is tumor growth. It seems that the appearance of alien "normal" histocompatibility antigens is a characteristic feature of all the tumors; besides, the host response pattern to these antigen is cross-reactive, including autoimmune component. Coombs' positive test may be one of numerous manifestations of such an autoimmune process.

Animals↗
PubMed1978

An in vitro quantitative assay for tumor cell invasion.

An in vitro quantitative assay of tumor cell invasion is described. The assay measures the rate at which [125I]iododeoxyuridine-labeled tumor cells migrate through the chorioallantoic membrane of developing chicken embryos. Invasion chambers were prepared from amber latex cylinders, chorioallantoic membrane, and thread ligatures. The chambers were placed in glass vials to rest on discs of photographic sponge immersed in tissue culture medium. Labeled tumor cells were added to the chamber, and the vial was incubated at 37 degrees. At various time points individual chambers were monitored to determine the number of viable, labeled cells that had passed through the membrane and were present in the medium, on the glass vial, or in the sponge. The application of the assay may be of use in delineating the mechanisms of tumor cell invasion.

Allantois↗
PubMed1977

Regulation of the immune response to tumor antigens. III. Characterization of thymic suppressor factor(s) produced by tumor-bearing hosts.

Immunosuppressor T cells (IST),6 capable of inhibiting the rejection of a methylcholanthrene-induced fibrosarcoma (S1509a) in A/Jax mice immune to this tumor, produced soluble factors with similar suppressive activity. The immunosuppressive factor(s) (ISF) has been shown to be immunologically specific, as demonstrated by the complete loss of suppressive activity after absorption with S1509a cells, but not with cells of an unrelated syngeneic tumor. From its behavior on gel filtration, the size of ISF was deduced to be less than 70,000 daltons. The ISF was not removed by passage through a rabbit anti-mouse F(ab')2 reverse immunosorbent and, hence, it was concluded that ISF was not likely to be an immunoglobulin. The (immunosuppressive) activity of ISF was destroyed by treatment with Pronase, but not with RNase. The ISF was found to share the antigenic determinant(s) of the product(s) of the K end of the major histocompatibility complex of the mouse. Moreover, antibodies to ISF were induced by immunization with ISF-tumor cell complexes. Thus, IST and their factor(s) appear to play an important role in the regulation of the immune response to tumor antigens.

Animals↗
PubMed1982

Suppression of cell-mediated antitumor immunity by complete Freund's adjuvant.

The effect of complete Freund's adjuvant (CFA), which is one of the strong immunoadjuvants, on the induction of either cytotoxic or suppressor T-cells against syngeneic tumors was investigated by an in vitro assay system. CFA did not show the apparent augmenting activity in the induction of cytotoxic T-cells against syngeneic tumors when it was administered i.p. to mice receiving s.c. inoculations of mitomycin C-treated tumor cells. The treated animals failed to develop stronger resistance against the second inoculum of the same viable tumor cells. Furthermore, CFA had an effect on the induction of suppressor T-cells in tumor-bearing hosts in which suppressor T-cells had been readily activated. Suppressor T-cells developed in syngeneic tumor-bearing mice treated with CFA was tumor specific. Tumor growth was enhanced when CFA was administered to mice given s.c. inoculations of the homologous tumor.

Animals↗
PubMed1982

Antitumor effect of polysaccharide TC-13 on allogeneic and syngeneic tumors in mice.

The antitumor activity of TC-13, a protein-bound polysaccharide extracted from a rare actinomycetes was tested on allogeneic and syngeneic tumors in mice. In the allogeneic Ehrlich carcinoma system, TC-13 showed antitumor activity over a broad optimal dose range, when administered by various routes such as ip, iv, sc, it (intratumorally) or po, even when given before tumor inoculation. TC-13 showed synergistic antitumor effects in combination with other immunomodulators, e.g., lipopolysaccharide, lentinan and picibanil. It showed antitumor activity against syngeneic tumors, MM46 mammary carcinoma and MCS-8 and Meth A fibrosarcoma.

Animals↗
PubMed1982

[Activation of the membrane toxicity and cytotoxicity of the tumor cell by leukocyte and fibroblast interferon].

The effect of exogenous interferon on membrane toxicity and cytotoxicity of mouse tumor cells (MX-II, SA-I, thymomas, IAC) was studied with respect to target IAC-I cells. The treatment with leukocyte interferon made tumor cell membrane toxicity rise by 27-40%, while that with fibroblast one by 30-47%. As a result of the treatment with leukocyte interferon, tumor cell cytotoxicity increased by 26-47%. Antiserum against fibroblast interferon reversed its activation effect on tumor cells. It is assumed that the effect described is linked with the increased resistance of tumor cells as regards normal killers under interferon action.

Animals↗
PubMed1978

Preliminary observations on the effect of glucan in combination with radiation and chemotherapy in four murine tumors.

The efficacy of glucan in combination with local radiation therapy was measured using three solid murine tumors of differing abilities to induce a host defense. Using the KHT fibrosarcoma which induces no measurable host defense, glucan did not improve tumor-free survival over radiation alone; the combination produced a marginal improvement in tumor-free survival in animals bearing the highly immunogenic EMT-6 tumor. The most marked improvement in tumor-free survival was found with the mildly immunogenic 6C3HED lymphosarcoma. The efficacy of glucan in combination with BCNU chemotherapy was measured using the disseminated AKR transplantable leukemia; the combination yielded a high level of cures compared to no survival for either agent alone. Using the AKR transplantable leukemia in an F1 model, the effect of amphotericin B (AmB) alone or in combination with BCNU was tested. AmB or BCNU alone had little or no curative effect when tested in (AKR X DBA)F1 mice, but 56% of mice were cured when combined therapy was employed. When tested in (AKR X C57BL)F1 or (AKR X A)F1 mice, a small fraction was cured with AmB alone while about 90% were cured with either BCNU alone or the combination.

Amphotericin B↗