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At least 163 records · Page 9Linked to original sources
PubMed1976

Non-T-cell resistance against a mouse Moloney lymphoma.

We have previously shown that spleen cells from normal mice contain lymphocytes that kill certain in vitro-grown Moloney lymphoma lines in a 51Cr release test. The killing activity shows a marked dependence on the genotype of the donor mouse. In vivo rejection studies with a Moloney lymphoma line in various normal semisyngeneic F1 hybrids showed a clear positive correlation between in vitro natural cytotoxicity and in vivo rejection. Thus mice can be grouped as high- or low-reactive according to their in vitro cytolytic behavior as well as their in vivo rejection potential. A lymphoid cell without detectable T- or B-cell markers is responsible for the in vitro killing effect. The present study also shows that the in vivo growth inhibitory function is T-cell-independent. Lymphoid cells depleted of T- and B-cells and transferred together with Moloney lymphoma cells into an irradiated syngeneic recipent were highly efficient in delaying tumor growth. Furthermore, syngeneic or semisyngeneic thymecto-mized, irradiated, fetal-liver-reconstituted mice showed if anything an increased in vivo resistance to a Moloney lymphoma compared to control mice. In contrast, tumor cells histoincompatible with regard to the H-2 locus showed the expected preferential growth in the thymectomized animals. We thus conclude that the major in vivo resistance against transplantation of the syngeneic or semisyngeneic Moloney lymphoma used in this study is T-independent.

Animals↗
PubMed1979

Reproducibility and relation to specific and non-specific anti-tumor resistance of the tumor "sneaking through" phenomenon.

The reproducibility and immunological specificity of the tumor "sneaking through" phenomenon and enhancement of tumor growth were studied in syngeneic and random-bred Syrian hamsters by means of a quantitative modification of the transplantation test. After primary challenge the phenomenon was neither observed in normal animals nor in animals effectively immunized against tumor. However, it was regularly observed in some "immune" animals after secondary challenge. In primary challenge of animals "sneaking through" phenomenon was most often observed in animals pretreated with large doses of heat-inactivated tumor cells. This characteristic could not be transferred with serum of pretreated animals. In contrast to specific tumor immunity, the "sneaking through" pbenomenon appeared to be immunologically non-specific. This was observed in cross-transplantation tests with tumor cells bearing different TSTAs. Thus, TSTA is not an inducer and apparently not a target for a response leading to enhancement of tumor growth in pretreated hamsters. Experiments demonstrating enhanced tumor growth in pretreated animals at the same time demonstrate two other possibly more essential findings: (1) normal animals are naturally resistant to transplantation of 1 to about 1 x 10(3) (or more) tumor cells; and (2) this resistance can be totally abrogated by the pretreatment of normal animals with tumor cell preparations. The preliminary data demonstrate that abrogation of natural anti-tumor resistance in adult hamsters subsequently inoculated with SV40 leads to rapid development of primary tumors in such animals. The development of specific anti-tumor immune response in animals treated with inactivated tumor cell preparations was also studied. Significant non-specific inhibition of sponse in Syrian hamsters treated with inactivated syngeneic tumor cells was observed. The data obtained are considered to demonstrate two anti-tumor defense systems in the animal, i.e., non-specific natural resistance and specific anti-tumor immunity. The first seems to be responsible for elimination of low numbers of tumor cells in the normal organism and also to be esseitial for effective induction and functioning of the specific anti-tumor immunity.

Animals↗
PubMed1982

Metastatic potential of metastases, tumor cell heterogeneity, and therapeutic implications.

The metastasizing capacity of spontaneous metastases of several murine tumors of different histology, origin, and disseminative pattern was investigated to test the hypothesis that metastases originate from various subpopulations within the primary tumor. Overall, tumor cells from individual metastases did not show greater metastasizing capacity than the cells of the original tumor, although a degree of heterogeneity was seen. Differences in the immunologic profile among metastases of the same tumor were also observed. The possible therapeutic implications of these findings are discussed.

Animals↗
PubMed1983

The selective nature of metastasis.

The issue of whether metastases result from the random survival of cells released from a primary tumor or from the selective growth of specialized tumor subpopulations endowed with metastatic properties is important to our understanding of the metastatic process and to the development of therapeutic modalities against metastatic disease. We have found that the tumor cells populating spontaneous metastases are more metastatic than the cells populating the parent neoplasm, clearly indicating that metastasis is selective and not random. The selective nature of metastasis is a consistent observation, however, only when tumor cells are obtained from spontaneous metastases from mice bearing heterogenous, poorly metastatic tumors. Tumor cells from spontaneous metastases from mice bearing tumors that have been selected for metastatic potential or that are homogeneous (cloned) do not differ significantly in metastatic potential from tumor cells populating the parent tumor. Thus, under some conditions the process of metastasis can appear random. Although tumor cells from different individual metastases may be homogeneous with regard to a metastatic phenotype, they may be heterogeneous with regard to their sensitivity to chemotherapeutic agents. Thus, although metastasis selects for metastatic variants, resulting in the population of metastatic foci with tumor cells endowed with metastatic properties, it does not appear to select for phenotypes irrelevant to the process of metastasis such as sensitivity to therapeutic agents.

Animals↗
PubMed1978

Antitumor activity of 1-alkylcarbamoyl derivatives of 5-fluorouracil in a variety of mouse tumors.

The antitumor properties of 1-alkylcarbamoyl derivatives of 5-fluorouracil were examined in various mouse tumor systems to select promising compounds for clinical use. Almost all alkylcarbamoyl derivatives were active against various tumors when given by oral administration. Among them, 1-methyl, 1-ethyl, 1-isopropyl, 1-hexyl and 1-octyl carbamoyl derivatives of 5-fluorouracil were moderately or markedly active in six mouse tumor systems tested. However, 1-methyl, 1-ethyl, and 1-isopropyl carbamoyl derivatives were toxic to mice, though not lethal. As a result, 1-hexyl and 1-octyl carbamoyl derivatives were selected as the best candidates for antitumor agents in further study.

Adenocarcinoma↗
PubMed1980

Experimental gastric carcinoma induced by N-methyl-N'-nitro-N-nitrosoguanidine.

Serial studies by endoscopy and biopsy were made in a Beagle dog during and after oral administration of N-methyl-N'-nitro-N-nitroguanidine (MNNG). Between the 23rd and the 45th week of observation erosions and ulcers appeared at the angulus of the stomach and turned into ulcer scar. A depression with atypical glands was seen in the ulcer scar of the posterior wall of the angulus at the 94th week. It developed elevated margins at the 102nd week, when a well differentiated adenocarcinoma was found histopathologically. Ulceration and reepithelialization were observed in the early carcinoma. The carcinoma progressed into a larger one of Borrmann's type 2 at the 115th week and further into its type 3 at the 181st week. A second carcinoma with signet ring cell carcinoma developed in the anterior wall of the angulus. The two carcinomas fused and formed a single lesion. At autopsy in the 216th week the carcinoma invaded the serosa, and metastasis to regional lymph nodes was observed.

Adenocarcinoma↗
PubMed1977

The spread of cancer in the organism. Facts and problems.

In this review, cancer is conceived as an alteration of the suface-monitored social behavior of cells. Apart from impaired growth controls, loss of residency (tissue affiliation) is the most important consequence of this homeostatic disorder. It results in local spread (penetration) which is initiated by locomotive and/or desctructive activities of the neoplastic cells. Access of cancer elements to the circulation possibly leads to distant spread (metastasis). Penetration and metastasis largely depend upon reactions of the organism, which are of an ill-understood, ambiguous nature favoring both the tumor and the host.

Animals↗