Activation of Cellular Oncogenes by Chemical Carcinogens in Syrian Hamster Embryo Fibroblasts
Carcinogen-induced point mutations resulting in activation of ras oncogenes have been demonstrated in various experimental systems such as skin carcinogenesis, mammary, and liver carcinogenesis. In many cases, the data support the conclusion that these point mutations are critical changes in the ini...
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| Veröffentlicht in: | Environmental health perspectives 1990-08, Vol.88, p.175-178 |
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| creator | Ebert, Rolf Barrett, J. Carl Wiseman, Roger W. Pechan, Reinhard Reiss, Eva Röllich, Günther Schiffmann, Dietmar |
| description | Carcinogen-induced point mutations resulting in activation of ras oncogenes have been demonstrated in various experimental systems such as skin carcinogenesis, mammary, and liver carcinogenesis. In many cases, the data support the conclusion that these point mutations are critical changes in the initiation of these tumors. The Syrian hamster embryo (SHE) cell transformation model system has been widely used to study the multistep process of chemically induced neoplastic transformation. Recent data suggest that activation of the Ha-ras gene via point mutation is one of the crucial events in the transformation of these cells. We have now cloned the c-Ha-ras proto-oncogene from SHE cDNA-libraries, and we have performed polymerase chain reaction and direct sequencing to analyze tumor cell lines induced by different chemical carcinogens for the presence of point mutations. No changes were detectable at codons 12, 13, 59, 61, and 117 or adjacent regions in tumor cell lines induced by diethylstilbestrol, asbestos, benzo(a)pyrene, trenbolone, or aflatoxin B1. Thus, it is not known whether point mutations in the Ha-ras proto-oncogene are essential for the acquisition of the neoplastic phenotype of SHE cells. Activation of other oncogenes or inactivation of tumor suppressor genes may be responsible for the neoplastic progression of these cells. However, in SHE cells neoplastically transformed by diethylstilbestrol or trenbolone, a significant elevation of the c-Ha-ras expression was observed. Enhanced expression of c-myc was detected in SHE cells transformed by benzo(a)pyrene or trenbolone. |
| doi_str_mv | 10.1289/ehp.9088175 |
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Carl ; Wiseman, Roger W. ; Pechan, Reinhard ; Reiss, Eva ; Röllich, Günther ; Schiffmann, Dietmar</creator><creatorcontrib>Ebert, Rolf ; Barrett, J. Carl ; Wiseman, Roger W. ; Pechan, Reinhard ; Reiss, Eva ; Röllich, Günther ; Schiffmann, Dietmar</creatorcontrib><description>Carcinogen-induced point mutations resulting in activation of ras oncogenes have been demonstrated in various experimental systems such as skin carcinogenesis, mammary, and liver carcinogenesis. In many cases, the data support the conclusion that these point mutations are critical changes in the initiation of these tumors. The Syrian hamster embryo (SHE) cell transformation model system has been widely used to study the multistep process of chemically induced neoplastic transformation. Recent data suggest that activation of the Ha-ras gene via point mutation is one of the crucial events in the transformation of these cells. We have now cloned the c-Ha-ras proto-oncogene from SHE cDNA-libraries, and we have performed polymerase chain reaction and direct sequencing to analyze tumor cell lines induced by different chemical carcinogens for the presence of point mutations. No changes were detectable at codons 12, 13, 59, 61, and 117 or adjacent regions in tumor cell lines induced by diethylstilbestrol, asbestos, benzo(a)pyrene, trenbolone, or aflatoxin B1. Thus, it is not known whether point mutations in the Ha-ras proto-oncogene are essential for the acquisition of the neoplastic phenotype of SHE cells. Activation of other oncogenes or inactivation of tumor suppressor genes may be responsible for the neoplastic progression of these cells. However, in SHE cells neoplastically transformed by diethylstilbestrol or trenbolone, a significant elevation of the c-Ha-ras expression was observed. Enhanced expression of c-myc was detected in SHE cells transformed by benzo(a)pyrene or trenbolone.</description><identifier>ISSN: 0091-6765</identifier><identifier>EISSN: 1552-9924</identifier><identifier>DOI: 10.1289/ehp.9088175</identifier><identifier>PMID: 2272311</identifier><language>eng</language><publisher>United States: National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health, Education and Welfare</publisher><subject>560300 - Chemicals Metabolism & Toxicology ; AFLATOXINS ; ANIMAL CELLS ; ANIMALS ; ANTIGENS ; ASBESTOS ; BIOLOGICAL EFFECTS ; BODY ; CARBONIC ACID DERIVATIVES ; CARCINOGENESIS ; CARCINOGENS ; Carcinogens - toxicity ; Cell lines ; Cell Transformation, Neoplastic ; CELL TRANSFORMATIONS ; CHEMICAL ACTIVATION ; CONNECTIVE TISSUE CELLS ; Cricetinae ; DNA ; DNA - genetics ; DNA - metabolism ; Embryo, Mammalian ; EMBRYONIC CELLS ; FIBROBLASTS ; Gene Expression Regulation - drug effects ; GENE MUTATIONS ; GENES ; GENETIC EFFECTS ; HAMSTERS ; MAMMALS ; MATERIALS ; Mesocricetus ; METHYL NITROSOUREA ; Methylation ; Molecular and Cellular Aspects of Transformation and Differentiation ; MUTAGENS ; Mutation ; MUTATIONS ; Neoplastic cell transformation ; NITROSO COMPOUNDS ; ONCOGENES ; ONCOGENIC TRANSFORMATIONS ; ORGANIC COMPOUNDS ; ORGANIC NITROGEN COMPOUNDS ; ORGANS ; PATHOGENESIS ; Point mutation ; Proto-Oncogenes - drug effects ; RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT ; RODENTS ; SKIN ; SOMATIC CELLS ; TOXIC MATERIALS ; TOXINS ; Transformed cell line ; Tumor cell line ; Tumors ; VERTEBRATES</subject><ispartof>Environmental health perspectives, 1990-08, Vol.88, p.175-178</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3785-7c1e26ca60c584ecb3fddf3ec106de9f443b898fb338a6743a58a309be2b96e83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3431070$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3431070$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,864,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2272311$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/5840171$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Ebert, Rolf</creatorcontrib><creatorcontrib>Barrett, J. Carl</creatorcontrib><creatorcontrib>Wiseman, Roger W.</creatorcontrib><creatorcontrib>Pechan, Reinhard</creatorcontrib><creatorcontrib>Reiss, Eva</creatorcontrib><creatorcontrib>Röllich, Günther</creatorcontrib><creatorcontrib>Schiffmann, Dietmar</creatorcontrib><title>Activation of Cellular Oncogenes by Chemical Carcinogens in Syrian Hamster Embryo Fibroblasts</title><title>Environmental health perspectives</title><addtitle>Environ Health Perspect</addtitle><description>Carcinogen-induced point mutations resulting in activation of ras oncogenes have been demonstrated in various experimental systems such as skin carcinogenesis, mammary, and liver carcinogenesis. In many cases, the data support the conclusion that these point mutations are critical changes in the initiation of these tumors. The Syrian hamster embryo (SHE) cell transformation model system has been widely used to study the multistep process of chemically induced neoplastic transformation. Recent data suggest that activation of the Ha-ras gene via point mutation is one of the crucial events in the transformation of these cells. We have now cloned the c-Ha-ras proto-oncogene from SHE cDNA-libraries, and we have performed polymerase chain reaction and direct sequencing to analyze tumor cell lines induced by different chemical carcinogens for the presence of point mutations. No changes were detectable at codons 12, 13, 59, 61, and 117 or adjacent regions in tumor cell lines induced by diethylstilbestrol, asbestos, benzo(a)pyrene, trenbolone, or aflatoxin B1. Thus, it is not known whether point mutations in the Ha-ras proto-oncogene are essential for the acquisition of the neoplastic phenotype of SHE cells. Activation of other oncogenes or inactivation of tumor suppressor genes may be responsible for the neoplastic progression of these cells. However, in SHE cells neoplastically transformed by diethylstilbestrol or trenbolone, a significant elevation of the c-Ha-ras expression was observed. Enhanced expression of c-myc was detected in SHE cells transformed by benzo(a)pyrene or trenbolone.</description><subject>560300 - Chemicals Metabolism & Toxicology</subject><subject>AFLATOXINS</subject><subject>ANIMAL CELLS</subject><subject>ANIMALS</subject><subject>ANTIGENS</subject><subject>ASBESTOS</subject><subject>BIOLOGICAL EFFECTS</subject><subject>BODY</subject><subject>CARBONIC ACID DERIVATIVES</subject><subject>CARCINOGENESIS</subject><subject>CARCINOGENS</subject><subject>Carcinogens - toxicity</subject><subject>Cell lines</subject><subject>Cell Transformation, Neoplastic</subject><subject>CELL TRANSFORMATIONS</subject><subject>CHEMICAL ACTIVATION</subject><subject>CONNECTIVE TISSUE CELLS</subject><subject>Cricetinae</subject><subject>DNA</subject><subject>DNA - genetics</subject><subject>DNA - metabolism</subject><subject>Embryo, Mammalian</subject><subject>EMBRYONIC CELLS</subject><subject>FIBROBLASTS</subject><subject>Gene Expression Regulation - drug effects</subject><subject>GENE MUTATIONS</subject><subject>GENES</subject><subject>GENETIC EFFECTS</subject><subject>HAMSTERS</subject><subject>MAMMALS</subject><subject>MATERIALS</subject><subject>Mesocricetus</subject><subject>METHYL NITROSOUREA</subject><subject>Methylation</subject><subject>Molecular and Cellular Aspects of Transformation and Differentiation</subject><subject>MUTAGENS</subject><subject>Mutation</subject><subject>MUTATIONS</subject><subject>Neoplastic cell transformation</subject><subject>NITROSO COMPOUNDS</subject><subject>ONCOGENES</subject><subject>ONCOGENIC TRANSFORMATIONS</subject><subject>ORGANIC COMPOUNDS</subject><subject>ORGANIC NITROGEN COMPOUNDS</subject><subject>ORGANS</subject><subject>PATHOGENESIS</subject><subject>Point mutation</subject><subject>Proto-Oncogenes - drug effects</subject><subject>RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT</subject><subject>RODENTS</subject><subject>SKIN</subject><subject>SOMATIC CELLS</subject><subject>TOXIC MATERIALS</subject><subject>TOXINS</subject><subject>Transformed cell line</subject><subject>Tumor cell line</subject><subject>Tumors</subject><subject>VERTEBRATES</subject><issn>0091-6765</issn><issn>1552-9924</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1rVDEUxYModayuXAtBxI28mo-Xr41QHq0VCl2oSwlJ5r5OynvJmGQK89_7hhlKvZu7OIffPdyD0HtKLijT5itstheGaE2VeIFWVAjWGcP6l2hFiKGdVFK8Rm9qfSCEUC3lGTpjTDFO6Qr9uQwtProWc8J5xANM025yBd-lkO8hQcV-j4cNzDG4CQ-uhJgOQsUx4Z_7El3CN26uDQq-mn3ZZ3wdfcl-crXVt-jV6KYK7077HP2-vvo13HS3d99_DJe3XeBKi04FCkwGJ0kQuofg-bhejxwCJXINZux77rXRo-dcO6l67oR2nBgPzBsJmp-jb0fududnWAdIrbjJbkucXdnb7KL9X0lxY-_zo6VCakLNAvh4BOTaoq0hNgibkFOC0OySiVBFF9Pn05WS_-6gNjvHGpaPuQR5Vy2Vgi1zoH05GkPJtRYYn5JQYg-V2aUye6pscX94Hv7Je-po0T8d9YfacnmOYpwoy3tOiSL8H5HKnrg</recordid><startdate>19900801</startdate><enddate>19900801</enddate><creator>Ebert, Rolf</creator><creator>Barrett, J. Carl</creator><creator>Wiseman, Roger W.</creator><creator>Pechan, Reinhard</creator><creator>Reiss, Eva</creator><creator>Röllich, Günther</creator><creator>Schiffmann, Dietmar</creator><general>National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health, Education and Welfare</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope><scope>OTOTI</scope><scope>5PM</scope></search><sort><creationdate>19900801</creationdate><title>Activation of Cellular Oncogenes by Chemical Carcinogens in Syrian Hamster Embryo Fibroblasts</title><author>Ebert, Rolf ; Barrett, J. Carl ; Wiseman, Roger W. ; Pechan, Reinhard ; Reiss, Eva ; Röllich, Günther ; Schiffmann, Dietmar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3785-7c1e26ca60c584ecb3fddf3ec106de9f443b898fb338a6743a58a309be2b96e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>560300 - Chemicals Metabolism & Toxicology</topic><topic>AFLATOXINS</topic><topic>ANIMAL CELLS</topic><topic>ANIMALS</topic><topic>ANTIGENS</topic><topic>ASBESTOS</topic><topic>BIOLOGICAL EFFECTS</topic><topic>BODY</topic><topic>CARBONIC ACID DERIVATIVES</topic><topic>CARCINOGENESIS</topic><topic>CARCINOGENS</topic><topic>Carcinogens - toxicity</topic><topic>Cell lines</topic><topic>Cell Transformation, Neoplastic</topic><topic>CELL TRANSFORMATIONS</topic><topic>CHEMICAL ACTIVATION</topic><topic>CONNECTIVE TISSUE CELLS</topic><topic>Cricetinae</topic><topic>DNA</topic><topic>DNA - genetics</topic><topic>DNA - metabolism</topic><topic>Embryo, Mammalian</topic><topic>EMBRYONIC CELLS</topic><topic>FIBROBLASTS</topic><topic>Gene Expression Regulation - drug effects</topic><topic>GENE MUTATIONS</topic><topic>GENES</topic><topic>GENETIC EFFECTS</topic><topic>HAMSTERS</topic><topic>MAMMALS</topic><topic>MATERIALS</topic><topic>Mesocricetus</topic><topic>METHYL NITROSOUREA</topic><topic>Methylation</topic><topic>Molecular and Cellular Aspects of Transformation and Differentiation</topic><topic>MUTAGENS</topic><topic>Mutation</topic><topic>MUTATIONS</topic><topic>Neoplastic cell transformation</topic><topic>NITROSO COMPOUNDS</topic><topic>ONCOGENES</topic><topic>ONCOGENIC TRANSFORMATIONS</topic><topic>ORGANIC COMPOUNDS</topic><topic>ORGANIC NITROGEN COMPOUNDS</topic><topic>ORGANS</topic><topic>PATHOGENESIS</topic><topic>Point mutation</topic><topic>Proto-Oncogenes - drug effects</topic><topic>RADIATION, THERMAL, AND OTHER ENVIRON. 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Carl</creatorcontrib><creatorcontrib>Wiseman, Roger W.</creatorcontrib><creatorcontrib>Pechan, Reinhard</creatorcontrib><creatorcontrib>Reiss, Eva</creatorcontrib><creatorcontrib>Röllich, Günther</creatorcontrib><creatorcontrib>Schiffmann, Dietmar</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>OSTI.GOV</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Environmental health perspectives</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ebert, Rolf</au><au>Barrett, J. Carl</au><au>Wiseman, Roger W.</au><au>Pechan, Reinhard</au><au>Reiss, Eva</au><au>Röllich, Günther</au><au>Schiffmann, Dietmar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of Cellular Oncogenes by Chemical Carcinogens in Syrian Hamster Embryo Fibroblasts</atitle><jtitle>Environmental health perspectives</jtitle><addtitle>Environ Health Perspect</addtitle><date>1990-08-01</date><risdate>1990</risdate><volume>88</volume><spage>175</spage><epage>178</epage><pages>175-178</pages><issn>0091-6765</issn><eissn>1552-9924</eissn><abstract>Carcinogen-induced point mutations resulting in activation of ras oncogenes have been demonstrated in various experimental systems such as skin carcinogenesis, mammary, and liver carcinogenesis. In many cases, the data support the conclusion that these point mutations are critical changes in the initiation of these tumors. The Syrian hamster embryo (SHE) cell transformation model system has been widely used to study the multistep process of chemically induced neoplastic transformation. Recent data suggest that activation of the Ha-ras gene via point mutation is one of the crucial events in the transformation of these cells. We have now cloned the c-Ha-ras proto-oncogene from SHE cDNA-libraries, and we have performed polymerase chain reaction and direct sequencing to analyze tumor cell lines induced by different chemical carcinogens for the presence of point mutations. No changes were detectable at codons 12, 13, 59, 61, and 117 or adjacent regions in tumor cell lines induced by diethylstilbestrol, asbestos, benzo(a)pyrene, trenbolone, or aflatoxin B1. Thus, it is not known whether point mutations in the Ha-ras proto-oncogene are essential for the acquisition of the neoplastic phenotype of SHE cells. Activation of other oncogenes or inactivation of tumor suppressor genes may be responsible for the neoplastic progression of these cells. However, in SHE cells neoplastically transformed by diethylstilbestrol or trenbolone, a significant elevation of the c-Ha-ras expression was observed. Enhanced expression of c-myc was detected in SHE cells transformed by benzo(a)pyrene or trenbolone.</abstract><cop>United States</cop><pub>National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health, Education and Welfare</pub><pmid>2272311</pmid><doi>10.1289/ehp.9088175</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; PubMed Central Open Access; JSTOR Archive Collection A-Z Listing; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | 560300 - Chemicals Metabolism & Toxicology AFLATOXINS ANIMAL CELLS ANIMALS ANTIGENS ASBESTOS BIOLOGICAL EFFECTS BODY CARBONIC ACID DERIVATIVES CARCINOGENESIS CARCINOGENS Carcinogens - toxicity Cell lines Cell Transformation, Neoplastic CELL TRANSFORMATIONS CHEMICAL ACTIVATION CONNECTIVE TISSUE CELLS Cricetinae DNA DNA - genetics DNA - metabolism Embryo, Mammalian EMBRYONIC CELLS FIBROBLASTS Gene Expression Regulation - drug effects GENE MUTATIONS GENES GENETIC EFFECTS HAMSTERS MAMMALS MATERIALS Mesocricetus METHYL NITROSOUREA Methylation Molecular and Cellular Aspects of Transformation and Differentiation MUTAGENS Mutation MUTATIONS Neoplastic cell transformation NITROSO COMPOUNDS ONCOGENES ONCOGENIC TRANSFORMATIONS ORGANIC COMPOUNDS ORGANIC NITROGEN COMPOUNDS ORGANS PATHOGENESIS Point mutation Proto-Oncogenes - drug effects RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT RODENTS SKIN SOMATIC CELLS TOXIC MATERIALS TOXINS Transformed cell line Tumor cell line Tumors VERTEBRATES |
| title | Activation of Cellular Oncogenes by Chemical Carcinogens in Syrian Hamster Embryo Fibroblasts |
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