BIOMAT Database Logo BIOMAT Database Logo

Activation of protooncogenes in spontaneously occurring non-liver tumors from C57BL/6 x C3H F1 mice. 1991

U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.

The C57BL/6 x C3H F1 (hereafter called B6C3F1) mouse is an important animal model for long-term carcinogenesis studies. Maintained under normal laboratory conditions, these mice develop various types of spontaneous tumors during their lifetime. Activated Ha-ras genes have been detected in 66% of spontaneous hepatocellular tumors in the B6C3F1 mouse [Reynolds et al., Science (Washington DC), 237:1309, 1988]. In this study 49 spontaneous non-liver tumors were investigated for oncogene activation by DNA transfection techniques. Of the 49 tumor DNAs analyzed, only 5 yielded multiple foci in the NIH 3T3 focus assay: 2 of 10 pulmonary adenocarcinomas; 0 of 25 lymphomas; 2 of 2 Harderian gland adenomas; 0 of 1 adenocarcinoma of the small intestine; 1 of 6 malignant skin tumors; 0 of 4 hemangiosarcomas; and 0 of 1 lung metastasis of a hepatocellular carcinoma. DNA from six lymphomas which were negative in the NIH 3T3 focus assay were further analyzed for transforming genes by the nude mouse tumorigenicity assay. One of the five lymphomas tested positive with this assay. Southern blot analysis identified five activated ras genes: H-ras in two Harderian gland adenomas; K-ras in one pulmonary adenocarcinoma and in one s.c. adenocarcinoma; and N-ras in one lymphoma. The mutations involved were CG to AT and AT to TA in codon 61 of the Ha-ras genes, GC to AT or TA in codon 12 of the K-ras genes, and a GC to AT mutation in codon 12 of the N-ras gene. Transformant DNA from a pulmonary adenocarcinoma which yielded multiple foci in the transfection assay did not hybridize to DNA probes specific for the K-, H-, and N-ras, raf, neu, and met genes. Thirteen additional tumor DNAs yielded a single focus in the NIH 3T3 transfection assay. The transformant DNAs retransmitted in a second cycle transfection assay. Rearranged and/or amplified raf genes were detected in six of the transformant DNAs. At present we do not know whether these activated raf genes were present in the original tumor DNA. The other seven transformant DNAs did not hybridize with any of the above mentioned specific DNA probes utilized in Southern blot analysis. Unlike liver tumors, the activation of ras protooncogenes is not a frequent event in the development of spontaneous non-liver tumors of the B6C3F1 mouse. The results from this study should aid in understanding the neoplastic development associated with exposure to chemical carcinogens in the B6C3F1 mouse.

UI MeSH Term Description Entries
D007414 Intestinal Neoplasms Tumors or cancer of the INTESTINES. Cancer of Intestines,Intestinal Cancer,Cancer of the Intestines,Intestines Cancer,Intestines Neoplasms,Neoplasms, Intestinal,Cancer, Intestinal,Cancer, Intestines,Cancers, Intestinal,Cancers, Intestines,Intestinal Cancers,Intestinal Neoplasm,Intestines Cancers,Intestines Neoplasm,Neoplasm, Intestinal,Neoplasm, Intestines,Neoplasms, Intestines
D008113 Liver Neoplasms Tumors or cancer of the LIVER. Cancer of Liver,Hepatic Cancer,Liver Cancer,Cancer of the Liver,Cancer, Hepatocellular,Hepatic Neoplasms,Hepatocellular Cancer,Neoplasms, Hepatic,Neoplasms, Liver,Cancer, Hepatic,Cancer, Liver,Cancers, Hepatic,Cancers, Hepatocellular,Cancers, Liver,Hepatic Cancers,Hepatic Neoplasm,Hepatocellular Cancers,Liver Cancers,Liver Neoplasm,Neoplasm, Hepatic,Neoplasm, Liver
D008175 Lung Neoplasms Tumors or cancer of the LUNG. Cancer of Lung,Lung Cancer,Pulmonary Cancer,Pulmonary Neoplasms,Cancer of the Lung,Neoplasms, Lung,Neoplasms, Pulmonary,Cancer, Lung,Cancer, Pulmonary,Cancers, Lung,Cancers, Pulmonary,Lung Cancers,Lung Neoplasm,Neoplasm, Lung,Neoplasm, Pulmonary,Pulmonary Cancers,Pulmonary Neoplasm
D008223 Lymphoma A general term for various neoplastic diseases of the lymphoid tissue. Germinoblastoma,Lymphoma, Malignant,Reticulolymphosarcoma,Sarcoma, Germinoblastic,Germinoblastic Sarcoma,Germinoblastic Sarcomas,Germinoblastomas,Lymphomas,Lymphomas, Malignant,Malignant Lymphoma,Malignant Lymphomas,Reticulolymphosarcomas,Sarcomas, Germinoblastic
D008969 Molecular Sequence Data Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories. Sequence Data, Molecular,Molecular Sequencing Data,Data, Molecular Sequence,Data, Molecular Sequencing,Sequencing Data, Molecular
D009154 Mutation Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations. Mutations
D009374 Neoplasms, Experimental Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms. Experimental Neoplasms,Experimental Neoplasm,Neoplasm, Experimental
D009693 Nucleic Acid Hybridization Widely used technique which exploits the ability of complementary sequences in single-stranded DNAs or RNAs to pair with each other to form a double helix. Hybridization can take place between two complimentary DNA sequences, between a single-stranded DNA and a complementary RNA, or between two RNA sequences. The technique is used to detect and isolate specific sequences, measure homology, or define other characteristics of one or both strands. (Kendrew, Encyclopedia of Molecular Biology, 1994, p503) Genomic Hybridization,Acid Hybridization, Nucleic,Acid Hybridizations, Nucleic,Genomic Hybridizations,Hybridization, Genomic,Hybridization, Nucleic Acid,Hybridizations, Genomic,Hybridizations, Nucleic Acid,Nucleic Acid Hybridizations
D011519 Proto-Oncogenes Normal cellular genes homologous to viral oncogenes. The products of proto-oncogenes are important regulators of biological processes and appear to be involved in the events that serve to maintain the ordered procession through the cell cycle. Proto-oncogenes have names of the form c-onc. Proto-Oncogene,Proto Oncogene,Proto Oncogenes
D002471 Cell Transformation, Neoplastic Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill. Neoplastic Transformation, Cell,Neoplastic Cell Transformation,Transformation, Neoplastic Cell,Tumorigenic Transformation,Cell Neoplastic Transformation,Cell Neoplastic Transformations,Cell Transformations, Neoplastic,Neoplastic Cell Transformations,Neoplastic Transformations, Cell,Transformation, Cell Neoplastic,Transformation, Tumorigenic,Transformations, Cell Neoplastic,Transformations, Neoplastic Cell,Transformations, Tumorigenic,Tumorigenic Transformations

Related Publications

U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Carcinogenicity of bucetin in (C57BL/6 X C3H)F1 mice.
November 1987, Journal of the National Cancer Institute,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Carcinogenicity of dipyrone in (C57BL/6 X C3H)F1 mice.
December 1983, Journal of the National Cancer Institute,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Histopathologic differences between liver tumors in untreated (C57BL/6 X C3H)F1 (B6C3F1) mice and Nitrofen-fed mice.
November 1980, Journal of the National Cancer Institute,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Lack of carcinogenicity of phenytoin in (C57BL/6 x C3H)F1 mice.
January 1988, Journal of toxicology and environmental health,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Spontaneous tumors in aging (C57BL/6N x C3H/HeN)F1 (B6C3F1) mice.
January 1988, Toxicologic pathology,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Histopathology of liver carcinomas in (C57BL/6N X C3H/HeN)F1 mice ingesting chlordane.
July 1979, Journal of the National Cancer Institute,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Relative susceptibilities of C57BL/6, (C57BL/6 x C3H/He)F1, and C3H/He mice to acute toxicity and carcinogenicity of nickel subsulfide.
February 1996, Toxicology,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Carcinogenicity of 1,3-butadiene in C57BL/6 x C3H F1 mice at low exposure concentrations.
October 1990, Cancer research,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
Carcinogenic effect of carbazole in the liver of (C57BL/6N x C3H/HeN)F1 mice.
December 1982, Journal of the National Cancer Institute,
U Candrian, and M You, and T Goodrow, and R R Maronpot, and S H Reynolds, and M W Anderson
The immune response of (C57BL/6 X C3H)F1 mice to the endogenous AKR-MuLV.
January 1977, Medical microbiology and immunology,
Copied contents to your clipboard!