methylnitronitrosoguanidine and Retinoblastoma
methylnitronitrosoguanidine has been researched along with Retinoblastoma* in 5 studies
Other Studies
5 other study(ies) available for methylnitronitrosoguanidine and Retinoblastoma
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The study of multi-stage carcinogenesis in retinoblastoma and familial polyposis coli patient-derived skin fibroblast cell culture systems.
Carcinogenesis is considered to be a multi-step process comprising 'initiation', 'promotion' and 'conversion' events. Skin fibroblasts from patients with hereditary retinoblastoma (RB) and familial polyposis coli (FPC) were chosen for study since their predisposition to the tumour may be due to an inherited 'initiation' event which is present in every cell. Experiments involving skin fibroblasts from FPC patients showed certain of these cells to grow in semi-solid medium following treatment with the complete carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) alone. When tested prior to the commencement of the experiments the FPC patient cell populations had shown no strong predisposition to malignant transformation as assessed by increased saturation densities, reduced serum requirements, altered migration patterns in collagen gels, anchorage-independent growth and tumourigenicity in nude mice. Following carcinogen or promoter treatment, apart from exhibiting low-level frequencies of anchorage-independent growth, the cells appeared no more transformed than they were before. Parallel cytogenetic studies showed TPA to increase both tetraploidy and the chromosome-aberration frequency during the course of these transformation studies. However, the FPC cell clones induced by TPA to grow in semi-solid medium were, at best, considered to be only partially transformed when their properties were compared with those of tumour-derived cell lines. Topics: Adenomatous Polyposis Coli; Cell Adhesion; Cell Division; Cell Transformation, Neoplastic; Cells, Cultured; Chromosome Aberrations; Eye Neoplasms; Female; Fibroblasts; Humans; Male; Methylnitronitrosoguanidine; Ploidies; Retinoblastoma; Skin | 1988 |
Analysis of spontaneous, carcinogen-induced and promoter-induced chromosomal instability in patients with hereditary retinoblastoma.
Skin fibroblasts from patients with hereditary retinoblastoma (RB cells) were examined since predisposition to the tumour might be expected to involve some degree of chromosomal instability, as has been noted for several cancer-prone conditions. Spontaneous and N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced aberration frequencies were measured, the cytogenetic effects of long-term treatment with 12-O-tetradecanoyl-phorbol-13acetate (TPA) were examined and also the spontaneous and TPA-induced sister chromatid exchange (SCE) frequencies. In all the studies the RB cells behaved in a similar fashion to normal human skin fibroblasts. Topics: Cells, Cultured; Chromosome Aberrations; Chromosome Deletion; Eye Neoplasms; Humans; Methylnitronitrosoguanidine; Ploidies; Retinoblastoma; Sister Chromatid Exchange; Skin; Tetradecanoylphorbol Acetate; Time Factors | 1983 |
In vitro studies of the possible mechanisms whereby tumour promoters mediate their responses.
Carcinogenesis is commonly considered to be a multi-step process, comprising "initiation" and "promotion" events. Skin fibroblasts from patients with hereditary retinoblastoma (RB) and familial polyposis coli (FPC) were chosen for study since their predisposition to the tumour may be due to an inherited "initiation" event which is present in every somatic cell. Thus, one might predict that skin fibroblasts from these patients might exhibit an increased susceptibility to in vitro transformation, by either tumour promoters alone or by the complete carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). In the case of skin fibroblasts from RB patients, transformation as measured by the ability of cells to grow in semi-solid medium and their migration in collagen gels, did not occur with either class of agent. However, experiments involving skin fibroblasts from FPC patients, showed these cells to grow in semi-solid medium following treatment with the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) alone, although their pattern of migration in collagen gels was unchanged and they were non-tumorigenic in nude mice. The clones which grew in semi-solid medium were also unaltered in terms of their migration in collagen gels and tumorigenicity in nude mice and were considered not to be completely transformed. These results are discussed in relation to theories that tumour promoters are only involved in cell selection and clonal expansion of initiated cells a second "mutational" event being required for complete transformation. Topics: Carcinogens; Cell Movement; Cell Transformation, Neoplastic; Cells, Cultured; Chromosome Aberrations; Colonic Neoplasms; Eye Neoplasms; Fibroblasts; Humans; Methylnitronitrosoguanidine; Mutation; Retinoblastoma; Skin; Tetradecanoylphorbol Acetate | 1983 |
SCE and UDS studies in a family with retinoblastoma: a case study.
The frequencies of both spontaneous and mitomycin C (MMC)-induced sister chromatid exchanges (SCE) were analyzed in mixed lymphocyte cultures from a kindred with retinoblastoma. Both the affected daughter and male proband, as well as two normal controls, were studied. No differences were observed in the spontaneous or in the MMC-induced SCE frequencies obtained from the peripheral lymphocytes of these patients compared to the normal controls. Unscheduled DNA synthesis (UDS) was observed in the lymphocytes treated with varying concentrations of both MMC and M-methyl-N-nitro-N-nitrosoguanidine (MNNG). Whereas no differences were observed in the rate of [3H]thymidine incorporation in the retinoblastoma-derived lymphocytes exposed to MMC when compared to the controls, differences were seen in the response to MNNG. Our data suggest that cells from these retinoblastoma patients respond like normal cells to damage induced by MMC, but that they are unable to repair damage induced by MNNG. Topics: Crossing Over, Genetic; DNA Repair; DNA, Neoplasm; Eye Neoplasms; Female; Humans; Infant, Newborn; Methylnitronitrosoguanidine; Mitomycins; Retinoblastoma; Sister Chromatid Exchange | 1982 |
Survival of hereditary retinoblastoma human skin fibroblasts after treatment with DNA-damaging chemicals.
Topics: 4-Nitroquinoline-1-oxide; Alkylating Agents; Cell Survival; Cells, Cultured; Ethyl Methanesulfonate; Eye Neoplasms; Fibroblasts; Humans; Methyl Methanesulfonate; Methylnitronitrosoguanidine; Retinoblastoma; Skin | 1982 |