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At least 865 records · Page 48Linked to original sources
PubMed1975

Stimulation of syngeneic and allogeneic lymphoid cells by tumour cells in vitro.

August and Wistar rat lymph node cells were found to respond well to PHA stimulation and in mixed lymphocyte culture, as determined by an increased incorporation of 3H-thymidine. August rat lymph node cells were also stimulated by incubation with irradiated syngeneic tumour cells. Allogeneic Wistar rat lymph node cells produced a larger response to the August tumour cells. The response of syngeneic and allogeneic lymph node cells was reduced by pretreating the tumour cells with a Wistar anti-tumour serum. Pretreating the tumour cells with sera from normal or tumour bearing rats also reduced the response of syngeneic lymph node cells but did not reduce the response of allogeneic lymph node cells.

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PubMed1977

Evaluation of 51Cr release for detecting cell-mediated cytotoxic responses to solid chemically induced rat tumours.

A 51Cr-release test was developed for the detection of cell-mediated cytotoxicity against transplanted solid chemically induced rat tumours, and the findings were compared with those obtained in parallel tests using a microcytotoxicity assay. It was necessary to incorporate several modifications of the original Brunner assay (Brunner et al., 1968) in order to increase the sensitivity of the test as applied to long-term tumour lines maintained as glass-adherent cultures. These included: 1. preincubation of labelled tumour cells at 37 degrees C for 3-4 h before addition of effector cells; 2. preincubation of effector cells at 37 degrees C for 12 h before addition to target cells; 3. upon admixture of target and effector cells, intimate cell contact was established by gentle centrifugation; 4. after incubation of target and effector cells at 37 degrees C, a further incubation for 1 h at 45 degrees C was included to complete the release of 51Cr from non-viable cells. Maximal cytotoxicity of tumour-bearer effector cells was detected after 12 h incubation of lymphoid and target cells at a ratio of 200:1. Spleen cells from tumour-bearing rats during the first 2 weeks of tumour growth exhibited the same pattern of reactivity in the 51Cr-release test and the microcytotoxicity assay, although significant reduction in target-cell numbers was more frequently recorded using the microcytotoxicity assay. Tumour-bearer spleen cells showed reactivity against the homologous tumour as well as against unrelated tumours. Using either assay, pre-exposure of effector cells to 3M KC1 extracts of tumour was found to inhibit their effect on tumour cells most frequently in tests in which the effector-cell donor, soluble extract and target cell were of the same tumour line.

Animals↗
PubMed1983

Do metastases arise from pre-existing subpopulations of cancer cells?

The hypothesis that metastases arise from pre-existing metastatic sub-populations of cancer cells with heritable metastasis-related characteristics, was tested by comparing the metastatic behaviour of cancer cells derived from pulmonary metastases with those from corresponding primary tumours, after implanting them subcutaneously in mice. In the case of KHT osteosarcomas and B16 melanomas, injected minces of metastases gave rise to more pulmonary metastases than cells derived from minces of the primary cancers generating them. However, in the case of 3LL and T241 cancers, the primary tumour minces gave rise to more pulmonary metastases than those derived from minced metastases. It is therefore concluded that the subpopulation hypothesis cannot be accepted as a general rule. When fragments of solid tumours were implanted into animals, no differences were detected between the metastatic behaviour of implants taken randomly from pulmonary metastases and the volume/age matched primary tumours generating them. These experiments thus provide no support for the hypothesis that metastases arise exclusively or predominantly from pre-existing metastatic subpopulations of cancer cells. Finally, implants of matched fragments from 3LL tumours of different volume and age, essentially produced no statistically significant differences in numbers of metastases. These observations do not therefore support the concept of a progressive evolution of subpopulations of cancer cells with heritable metastatic phenotypes during tumour growth.

Animals↗
PubMed1991

Flow cytometric evaluation of hypoxic cells in solid experimental tumours using fluorescence immunodetection.

Numerous methods have been proposed for the detection of hypoxic cells using nitroimidazoles labelled with both radioactive and stable isotopes where the isotopic label becomes bound as a result of reductive metabolism of the nitro group. A new probe for hypoxia, 7-(4'-(2-nitroimidazol-l-yl)-butyl)-theophylline, is described where an immunologically recognisable hapten (theophylline) is covalently linked to a 2-nitroimidazole. Bioreduction of the nitroimidazole leads to binding of bioreductive metabolites, and hence the theophylline side-chain, to intracellular molecules. Immunochemical procedures are then used to stain cells containing the bound theophylline using an FITC-conjugated anti-serum. Flow cytometric analysis of stained cells is facilitated by co-staining cellular DNA, which allows discrimination of single cells in the sample and rejection of cell clumps and debris. The alternative use of an immunoperoxidase-conjugated anti-serum has been used to demonstrate the localisation of hypoxic cells in frozen tumour sections.

Animals↗
PubMed1981

Increasing metastatic potential is associated with increasing genetic instability of clones isolated from murine neoplasms.

The metastatic stability of clones, which were derived from the murine UV-2237 fibrosarcoma and which exhibit low or high metastatic potential, was examined after 60-72 days of continuous growth in vitro and in vivo. Subclones of the high metastatic clone exhibited a 140-fold variation in the production of experimental pulmonary metastases after intravenous injection into syngeneic C3H- mice. In contrast, subclones from the low metastatic clone varied only slightly (8-fold). Using cloned cells from three mouse tumors with differing metastatic potential, we determined the spontaneous mutation rates of cells with low or high metastatic capacities with respect to the selective genetic markers, 6-thiopurine resistance or ouabain resistance, or both. In all cases, cells with high metastatic potential had a 3- to 7-fold increase in the rate of mutation (per cell generation) at both genetic loci, as compared with their low metastatic but tumorigenic cell controls. These results support the hypothesis that the evolution of tumors from the benign to the malignant state could be the consequence of acquired genetic instability in the neoplastic cells.

Animals↗
PubMed1976

Immunity to tumor antigens: potential implications in human neuroblastoma.

Immune reactions to tumor-specific and tumor-associated antigens have been demonstrated in animals with neoplasms with in vitro and in vovo techniques. Some of the antigens detected in vitro induce transplantation resistance in vivo, while others do not. Human neuroblastoma cells cultivated in vitro have been shown to possess common antigens to which lymphocytes from neuroblastoma patients react. Whether it is possible to augment the immune reactivity of patients with neuroblastoma to these common antigens and, if so, whether this heightened immune reactivity would have clinically beneficial effects are as yet unknown. These reactions are complex, involving both cellular and humoral mechanisms. The fact that one type of immune response can be detected to one type of antigen present in a tumor in vitro does not necessarily mean that the immune response is effective in vivo. Responses to other tumor antigens may be deficient, or the immune response may be depressed. This may be due to active suppression of and/or selective deficiencies in critical cell populations required for an augmented immune response; this possibility may be evaluated with techniques allowing for in vitro sensitization to tumor antigens.

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