Selective pressure during tumor promotion by phenobarbital leads to clonal outgrowth of β-catenin-mutated mouse liver tumors
Tumor promoters are non-mutagenic chemicals which increase the probability of cancer by accelerating the clonal expansion of cells transformed during tumor initiation. Phenobarbital (PB) is an antiepileptic drug which promotes hepatocarcinogenesis in rodents when administered subsequent to an initia...
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description | Tumor promoters are non-mutagenic chemicals which increase the probability of cancer by accelerating the clonal expansion of cells transformed during tumor initiation. Phenobarbital (PB) is an antiepileptic drug which promotes hepatocarcinogenesis in rodents when administered subsequent to an initiating carcinogen like diethylnitrosamine (DEN). Here we have investigated the prevalence and patterns of mutations in two genes, Ha-ras and beta-catenin, both known mutational targets in mouse hepatocarcinogenesis. Liver tumors were generated by a single administration of DEN to 6 week old mice followed by feeding of PB (0.05%) containing or control diet for 39 weeks. Mutations at Ha-ras codon 61 were screened by allele-specific oligonucleotide hybridization; beta-catenin mutations were detected by direct sequencing of PCR products spanning exon 2. In tumors from mice treated with DEN alone, the prevalence of Ha-ras mutations was approximately 30% (6/20), while no beta-catenin mutations (0/13) were detectable in tumors of this treatment group. By contrast, Ha-ras mutations were undetectable in tumors from mice treated with DEN/PB (0/32), while approximately 80% (37/46) of tumors from this group showed beta-catenin mutations. These results demonstrate that PB strongly affects the prevalence of mutations in the two cancer-related genes, presumably by positive and negative selection for cells harboring the respective mutation. |
doi_str_mv | 10.1038/sj.onc.1204982 |
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Phenobarbital (PB) is an antiepileptic drug which promotes hepatocarcinogenesis in rodents when administered subsequent to an initiating carcinogen like diethylnitrosamine (DEN). Here we have investigated the prevalence and patterns of mutations in two genes, Ha-ras and beta-catenin, both known mutational targets in mouse hepatocarcinogenesis. Liver tumors were generated by a single administration of DEN to 6 week old mice followed by feeding of PB (0.05%) containing or control diet for 39 weeks. Mutations at Ha-ras codon 61 were screened by allele-specific oligonucleotide hybridization; beta-catenin mutations were detected by direct sequencing of PCR products spanning exon 2. In tumors from mice treated with DEN alone, the prevalence of Ha-ras mutations was approximately 30% (6/20), while no beta-catenin mutations (0/13) were detectable in tumors of this treatment group. By contrast, Ha-ras mutations were undetectable in tumors from mice treated with DEN/PB (0/32), while approximately 80% (37/46) of tumors from this group showed beta-catenin mutations. These results demonstrate that PB strongly affects the prevalence of mutations in the two cancer-related genes, presumably by positive and negative selection for cells harboring the respective mutation.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1204982</identifier><identifier>PMID: 11753661</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Animals ; Antiepileptic agents ; b-catenin ; Base Sequence ; beta Catenin ; Biological and medical sciences ; Carcinogens ; Carcinogens - pharmacology ; Cell Division - drug effects ; Clone Cells - drug effects ; Clone Cells - metabolism ; Clone Cells - pathology ; Cytoskeletal Proteins - analysis ; Cytoskeletal Proteins - chemistry ; Cytoskeletal Proteins - genetics ; Diethylnitrosamine ; Diethylnitrosamine - pharmacology ; DNA Mutational Analysis ; DNA, Neoplasm - genetics ; Fundamental and applied biological sciences. Psychology ; Genes, ras - genetics ; Ha-ras gene ; Hybridization ; Immunohistochemistry ; Liver cancer ; Liver Neoplasms, Experimental - chemically induced ; Liver Neoplasms, Experimental - genetics ; Liver Neoplasms, Experimental - pathology ; Mice ; Mice, Knockout ; Molecular and cellular biology ; Molecular Sequence Data ; Mutagenesis - drug effects ; Mutagenesis - genetics ; Mutation ; Negative selection ; Oligonucleotides ; Phenobarbital ; Phenobarbital - pharmacology ; Polymerase Chain Reaction ; Selection, Genetic ; Trans-Activators ; Tumorigenesis ; Tumors ; β-Catenin</subject><ispartof>Oncogene, 2001-11, Vol.20 (53), p.7812-7816</ispartof><rights>2002 INIST-CNRS</rights><rights>COPYRIGHT 2001 Nature Publishing Group</rights><rights>Macmillan Publishers Limited 2001.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-873fd98f32a0b5f94377edca30adce0adb600cc678c423c76b2084fbf7d77d403</citedby><cites>FETCH-LOGICAL-c487t-873fd98f32a0b5f94377edca30adce0adb600cc678c423c76b2084fbf7d77d403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14159100$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11753661$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>AYDINLIK, Huriye</creatorcontrib><creatorcontrib>NGUYEN, Tri Dung</creatorcontrib><creatorcontrib>MOENNIKES, Oliver</creatorcontrib><creatorcontrib>BUCHMANN, Albrecht</creatorcontrib><creatorcontrib>SCHWARZ, Michael</creatorcontrib><title>Selective pressure during tumor promotion by phenobarbital leads to clonal outgrowth of β-catenin-mutated mouse liver tumors</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Tumor promoters are non-mutagenic chemicals which increase the probability of cancer by accelerating the clonal expansion of cells transformed during tumor initiation. Phenobarbital (PB) is an antiepileptic drug which promotes hepatocarcinogenesis in rodents when administered subsequent to an initiating carcinogen like diethylnitrosamine (DEN). Here we have investigated the prevalence and patterns of mutations in two genes, Ha-ras and beta-catenin, both known mutational targets in mouse hepatocarcinogenesis. Liver tumors were generated by a single administration of DEN to 6 week old mice followed by feeding of PB (0.05%) containing or control diet for 39 weeks. Mutations at Ha-ras codon 61 were screened by allele-specific oligonucleotide hybridization; beta-catenin mutations were detected by direct sequencing of PCR products spanning exon 2. In tumors from mice treated with DEN alone, the prevalence of Ha-ras mutations was approximately 30% (6/20), while no beta-catenin mutations (0/13) were detectable in tumors of this treatment group. By contrast, Ha-ras mutations were undetectable in tumors from mice treated with DEN/PB (0/32), while approximately 80% (37/46) of tumors from this group showed beta-catenin mutations. These results demonstrate that PB strongly affects the prevalence of mutations in the two cancer-related genes, presumably by positive and negative selection for cells harboring the respective mutation.</description><subject>Animals</subject><subject>Antiepileptic agents</subject><subject>b-catenin</subject><subject>Base Sequence</subject><subject>beta Catenin</subject><subject>Biological and medical sciences</subject><subject>Carcinogens</subject><subject>Carcinogens - pharmacology</subject><subject>Cell Division - drug effects</subject><subject>Clone Cells - drug effects</subject><subject>Clone Cells - metabolism</subject><subject>Clone Cells - pathology</subject><subject>Cytoskeletal Proteins - analysis</subject><subject>Cytoskeletal Proteins - chemistry</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Diethylnitrosamine</subject><subject>Diethylnitrosamine - pharmacology</subject><subject>DNA Mutational Analysis</subject><subject>DNA, Neoplasm - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genes, ras - genetics</subject><subject>Ha-ras gene</subject><subject>Hybridization</subject><subject>Immunohistochemistry</subject><subject>Liver cancer</subject><subject>Liver Neoplasms, Experimental - chemically induced</subject><subject>Liver Neoplasms, Experimental - genetics</subject><subject>Liver Neoplasms, Experimental - pathology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>Mutagenesis - drug effects</subject><subject>Mutagenesis - genetics</subject><subject>Mutation</subject><subject>Negative selection</subject><subject>Oligonucleotides</subject><subject>Phenobarbital</subject><subject>Phenobarbital - pharmacology</subject><subject>Polymerase Chain Reaction</subject><subject>Selection, Genetic</subject><subject>Trans-Activators</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>β-Catenin</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkcuKFDEUhoMoTju6dSkB0V21uVWlshwGbzDgQl2HVOqkJ00qaZOUMgtfygfxmUwzDQ0yBHI5fOc_5-RH6CUlW0r4-K7stynaLWVEqJE9Qhsq5ND1vRKP0YaonnSKcXaBnpWyJ4RIRdhTdEGp7Pkw0A36_RUC2Op_Aj5kKGXNgOc1-7jDdV1SbtG0pOpTxNMdPtxCTJPJk68m4ABmLrgmbEOK7Z3WusvpV73FyeG_fzprKkQfu2Wt7TbjJa0FcGi18r14eY6eOBMKvDidl-j7h_ffrj91N18-fr6-uumsGGXtRsndrEbHmSFT75TgUsJsDSdmttC2aSDE2kGOVjBu5TAxMgo3OTlLOQvCL9Hbe902zY8VStWLLxZCMBFaU5qOTCgyHMHX_4H7tOY2XNFsEJS3fx7EmdqZANpHl2o29iiprxghnEmuVKO2D1BtzbB4myI43-IPJdicSsng9CH7xeQ7TYk-uq3LXje39cntlvDq1O06LTCf8ZO9DXhzAkyxJrhsovXlzAnaK9rq_wPSrLUh</recordid><startdate>20011122</startdate><enddate>20011122</enddate><creator>AYDINLIK, Huriye</creator><creator>NGUYEN, Tri Dung</creator><creator>MOENNIKES, Oliver</creator><creator>BUCHMANN, Albrecht</creator><creator>SCHWARZ, Michael</creator><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</scope><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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20011122</creationdate><title>Selective pressure during tumor promotion by phenobarbital leads to clonal outgrowth of β-catenin-mutated mouse liver tumors</title><author>AYDINLIK, Huriye ; NGUYEN, Tri Dung ; MOENNIKES, Oliver ; BUCHMANN, Albrecht ; SCHWARZ, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-873fd98f32a0b5f94377edca30adce0adb600cc678c423c76b2084fbf7d77d403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Antiepileptic agents</topic><topic>b-catenin</topic><topic>Base Sequence</topic><topic>beta Catenin</topic><topic>Biological and medical sciences</topic><topic>Carcinogens</topic><topic>Carcinogens - pharmacology</topic><topic>Cell Division - drug effects</topic><topic>Clone Cells - drug effects</topic><topic>Clone Cells - metabolism</topic><topic>Clone Cells - pathology</topic><topic>Cytoskeletal Proteins - analysis</topic><topic>Cytoskeletal Proteins - chemistry</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Diethylnitrosamine</topic><topic>Diethylnitrosamine - pharmacology</topic><topic>DNA Mutational Analysis</topic><topic>DNA, Neoplasm - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genes, ras - genetics</topic><topic>Ha-ras gene</topic><topic>Hybridization</topic><topic>Immunohistochemistry</topic><topic>Liver cancer</topic><topic>Liver Neoplasms, Experimental - chemically induced</topic><topic>Liver Neoplasms, Experimental - genetics</topic><topic>Liver Neoplasms, Experimental - pathology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Molecular and cellular biology</topic><topic>Molecular Sequence Data</topic><topic>Mutagenesis - drug effects</topic><topic>Mutagenesis - genetics</topic><topic>Mutation</topic><topic>Negative selection</topic><topic>Oligonucleotides</topic><topic>Phenobarbital</topic><topic>Phenobarbital - pharmacology</topic><topic>Polymerase Chain Reaction</topic><topic>Selection, Genetic</topic><topic>Trans-Activators</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>AYDINLIK, Huriye</creatorcontrib><creatorcontrib>NGUYEN, Tri Dung</creatorcontrib><creatorcontrib>MOENNIKES, Oliver</creatorcontrib><creatorcontrib>BUCHMANN, Albrecht</creatorcontrib><creatorcontrib>SCHWARZ, Michael</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>AYDINLIK, Huriye</au><au>NGUYEN, Tri Dung</au><au>MOENNIKES, Oliver</au><au>BUCHMANN, Albrecht</au><au>SCHWARZ, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective pressure during tumor promotion by phenobarbital leads to clonal outgrowth of β-catenin-mutated mouse liver tumors</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>2001-11-22</date><risdate>2001</risdate><volume>20</volume><issue>53</issue><spage>7812</spage><epage>7816</epage><pages>7812-7816</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Tumor promoters are non-mutagenic chemicals which increase the probability of cancer by accelerating the clonal expansion of cells transformed during tumor initiation. Phenobarbital (PB) is an antiepileptic drug which promotes hepatocarcinogenesis in rodents when administered subsequent to an initiating carcinogen like diethylnitrosamine (DEN). Here we have investigated the prevalence and patterns of mutations in two genes, Ha-ras and beta-catenin, both known mutational targets in mouse hepatocarcinogenesis. Liver tumors were generated by a single administration of DEN to 6 week old mice followed by feeding of PB (0.05%) containing or control diet for 39 weeks. Mutations at Ha-ras codon 61 were screened by allele-specific oligonucleotide hybridization; beta-catenin mutations were detected by direct sequencing of PCR products spanning exon 2. In tumors from mice treated with DEN alone, the prevalence of Ha-ras mutations was approximately 30% (6/20), while no beta-catenin mutations (0/13) were detectable in tumors of this treatment group. By contrast, Ha-ras mutations were undetectable in tumors from mice treated with DEN/PB (0/32), while approximately 80% (37/46) of tumors from this group showed beta-catenin mutations. These results demonstrate that PB strongly affects the prevalence of mutations in the two cancer-related genes, presumably by positive and negative selection for cells harboring the respective mutation.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>11753661</pmid><doi>10.1038/sj.onc.1204982</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antiepileptic agents b-catenin Base Sequence beta Catenin Biological and medical sciences Carcinogens Carcinogens - pharmacology Cell Division - drug effects Clone Cells - drug effects Clone Cells - metabolism Clone Cells - pathology Cytoskeletal Proteins - analysis Cytoskeletal Proteins - chemistry Cytoskeletal Proteins - genetics Diethylnitrosamine Diethylnitrosamine - pharmacology DNA Mutational Analysis DNA, Neoplasm - genetics Fundamental and applied biological sciences. Psychology Genes, ras - genetics Ha-ras gene Hybridization Immunohistochemistry Liver cancer Liver Neoplasms, Experimental - chemically induced Liver Neoplasms, Experimental - genetics Liver Neoplasms, Experimental - pathology Mice Mice, Knockout Molecular and cellular biology Molecular Sequence Data Mutagenesis - drug effects Mutagenesis - genetics Mutation Negative selection Oligonucleotides Phenobarbital Phenobarbital - pharmacology Polymerase Chain Reaction Selection, Genetic Trans-Activators Tumorigenesis Tumors β-Catenin |
title | Selective pressure during tumor promotion by phenobarbital leads to clonal outgrowth of β-catenin-mutated mouse liver tumors |
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