thioguanine-anhydrous has been researched along with Carcinoma--Hepatocellular* in 3 studies
3 other study(ies) available for thioguanine-anhydrous and Carcinoma--Hepatocellular
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Isolation and characterization of HPRT-deficient human hepatoma cells.
Human hepatoma cells deficient in HPRT activity were isolated by challenging HepG2 cells with 6-thioguanine (6TG). Three 6TG-resistant isolates were plated in selective media, and each clonal line displayed an 8-azaguanine-resistant, HAT-sensitive phenotype. The HPRT-deficient phenotype of one of these clones, H30-1, was confirmed in genetic tests: the HAT-sensitivity of H30-1 cells was complemented by fusion by HPRT+ (Ltk-) but not HPRT- (A9) cells. Furthermore, transfection of the bacterial xanthine-guanine phosphoribosyl transferase (gpt) gene into H30-1 cells rendered them HAT-resistant. H30-1 cells maintained the differentiated morphology, growth characteristics, fusion properties, and transfection efficiencies typical of parental HepG2 cells, and they expressed several liver-specific genes. Finally, the H30-1 cell line contained a modal number of 50 chromosomes. Therefore, H30-1 cells represent an HPRT-deficient HepG2 derivative that retains its differentiated phenotype in vitro. Topics: Carcinoma, Hepatocellular; Cell Fusion; Gene Expression; Genetic Complementation Test; Humans; Hybrid Cells; Hypoxanthine Phosphoribosyltransferase; Karyotyping; Liver Neoplasms; Phenotype; Thioguanine; Transfection; Tumor Cells, Cultured | 1996 |
Use of an established human hepatoma cell line with endogenous bioactivation for gene mutation studies.
Genetic toxicology assays that rely on S9 microsomal mixes are subject to artifacts related to the generation of mutagenic metabolites by acidic pHs, variation in individual isolations of microsomes and the failure of subcellular fractions to faithfully produce metabolites generated in intact cells. We have developed a gene mutation assay utilizing the human hepatoma cell line HepG2, which has been shown to metabolize a broad spectrum of promutagens. Optimal conditions for assaying the induction of 6-thioguanine-resistant mutants in this cell line include: 1) growth of colonies for three weeks on lethally irradiated feeder layers of 10(6) thioguanine-resistant HepG2 cells (average plating efficiency = 60-80%); 2) a thioguanine concentration in selection dishes of 10(-4) M with a maximum seeding density of 2.5 x 10(5) cells per 100 mm culture dish; and 3) a minimum expression time of 6 days. In addition to ultraviolet light C (254 nm), a cytochrome P450 (cyclophosphamide)-dependent and a cytochrome P448 (aflatoxin B1)-dependent promutagen were shown to induce cytotoxicity and mutations in this test system. The present studies, therefore, suggest that the HepG2 cell line may be useful for a variety of assays in genetic toxicology. Topics: Aflatoxins; Biotransformation; Carcinoma, Hepatocellular; Cell Line; Cyclophosphamide; Drug Resistance; Evaluation Studies as Topic; Humans; Liver Neoplasms; Mutagenicity Tests; Thioguanine; Ultraviolet Rays | 1988 |
GROWTH INHIBITION OF A SPECTRUM OF TRANSPLANTED MOUSE TUMORS BY COMBINATIONS OF INHIBITORS OF NUCLEIC ACID BIOSYNTHESIS AND ALKYLATING AGENTS.
Topics: Alkylating Agents; Animals; Antineoplastic Agents; Azaguanine; Azaserine; Carcinoma, Ehrlich Tumor; Carcinoma, Hepatocellular; DNA; DNA, Neoplasm; Fluorouracil; Idoxuridine; Liver Neoplasms; Lymphoma; Lymphoma, Non-Hodgkin; Mercaptopurine; Mice; Neoplasms, Experimental; Nitrogen Mustard Compounds; Nucleosides; Nucleotides; Purines; Research; RNA; RNA, Neoplasm; Sarcoma 180; Thioguanine; Uracil Mustard | 1963 |