Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype
Considerable rodent strain differences have been documented with regard to susceptibility to colon carcinogens. To clarify mechanisms, chimeras of susceptible strain C3H and relatively resistant strain C57BL/6N (B6) mice were exposed to a colonotropic carcinogen, 1,2-dimethylhydrazine (DMH) and tumo...
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| Veröffentlicht in: | Cancer letters 2006-08, Vol.239 (2), p.205-211 |
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| container_title | Cancer letters |
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| creator | Tsukamoto, Tetsuya Yamamoto, Masami Fukami, Hiroko Yoshikawa, Akemi Sakai, Hiroki Hirata, Akihiro Kusakabe, Moriaki Tatematsu, Masae |
| description | Considerable rodent strain differences have been documented with regard to susceptibility to colon carcinogens. To clarify mechanisms, chimeras of susceptible strain C3H and relatively resistant strain C57BL/6N (B6) mice were exposed to a colonotropic carcinogen, 1,2-dimethylhydrazine (DMH) and tumor incidence and multiplicity were assessed. In the chimeras, incidence was as high as the C3H level. Multiplicity of lesions of B6 cells was also increased (
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| doi_str_mv | 10.1016/j.canlet.2005.08.004 |
| format | Article |
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P<0.001), but maintenance of the strain difference. When tumor localization was analyzed, tumors of B6 genotype in chimeras demonstrated a greater spread of distribution than in the parental case. The chimeric environment may thus stimulate tumor initiation but cell autonomous suppressive factors may be retained.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2005.08.004</identifier><identifier>PMID: 16168562</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>1,2-dimethylhydrazine ; Animals ; Cancer ; Carcinogens ; Chimera ; Chimeric mouse ; Colon ; Colon carcinogenesis ; Colonic Neoplasms - genetics ; Colonic Neoplasms - pathology ; Disease Susceptibility ; Genotype ; Genotype & phenotype ; Immunohistochemistry ; Medical research ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Proteins ; Rodent strain differences ; Susceptibility ; Tumorigenesis ; Tumors</subject><ispartof>Cancer letters, 2006-08, Vol.239 (2), p.205-211</ispartof><rights>2005 Elsevier Ireland Ltd</rights><rights>Copyright Elsevier Limited Aug 8, 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-d829b16b4ed66d14242b6ddf9387afdcbd01b249a3fff730c86d7fce65e8e8f43</citedby><cites>FETCH-LOGICAL-c485t-d829b16b4ed66d14242b6ddf9387afdcbd01b249a3fff730c86d7fce65e8e8f43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2005.08.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16168562$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsukamoto, Tetsuya</creatorcontrib><creatorcontrib>Yamamoto, Masami</creatorcontrib><creatorcontrib>Fukami, Hiroko</creatorcontrib><creatorcontrib>Yoshikawa, Akemi</creatorcontrib><creatorcontrib>Sakai, Hiroki</creatorcontrib><creatorcontrib>Hirata, Akihiro</creatorcontrib><creatorcontrib>Kusakabe, Moriaki</creatorcontrib><creatorcontrib>Tatematsu, Masae</creatorcontrib><title>Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Considerable rodent strain differences have been documented with regard to susceptibility to colon carcinogens. To clarify mechanisms, chimeras of susceptible strain C3H and relatively resistant strain C57BL/6N (B6) mice were exposed to a colonotropic carcinogen, 1,2-dimethylhydrazine (DMH) and tumor incidence and multiplicity were assessed. In the chimeras, incidence was as high as the C3H level. Multiplicity of lesions of B6 cells was also increased (
P<0.001), but maintenance of the strain difference. When tumor localization was analyzed, tumors of B6 genotype in chimeras demonstrated a greater spread of distribution than in the parental case. The chimeric environment may thus stimulate tumor initiation but cell autonomous suppressive factors may be retained.</description><subject>1,2-dimethylhydrazine</subject><subject>Animals</subject><subject>Cancer</subject><subject>Carcinogens</subject><subject>Chimera</subject><subject>Chimeric mouse</subject><subject>Colon</subject><subject>Colon carcinogenesis</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - pathology</subject><subject>Disease Susceptibility</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Immunohistochemistry</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Proteins</subject><subject>Rodent strain differences</subject><subject>Susceptibility</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2KFDEURoMoTjv6BiIBwV3V5L9SG0EbdYQGF-o6VCW3nDRVSZukBvsFfAKf0CcxTTcILlxlkXO_5LsHoeeUtJRQdbNv7RBmKC0jRLZEt4SIB2hDdceartfkIdoQTkTDNZdX6EnOe1JB0cnH6IoqqrRUbIN-fF6zhUPxo599OeISsY1zDNgOyfoQv0GA7DP2AW_57e-fv7aye7u7Udje-QWSt3jxFnCCaQZbMh5jucPF57zC6SZFCPc-xbBAKHgIDtfAWI4HeIoeTcOc4dnlvEZf37_7sr1tdp8-fNy-2TVWaFkap1k_UjUKcEo5Kphgo3Ju6rnuhsnZ0RE6MtEPfJqmjhOrlesmC0qCBj0Jfo1enXMPKX5fIRez-Np4nocAcc2G9lp0jNEKvvwH3Mc1hfo3QyWRvBNE80qJM1Wr5Vxrm0Pyy5COhhJz8mL25uzFnLwYok31UsdeXMLXcQH3d-giogKvzwDUXdx7SCZbD8GC86ku1rjo___CH_jrowk</recordid><startdate>20060808</startdate><enddate>20060808</enddate><creator>Tsukamoto, Tetsuya</creator><creator>Yamamoto, Masami</creator><creator>Fukami, Hiroko</creator><creator>Yoshikawa, Akemi</creator><creator>Sakai, Hiroki</creator><creator>Hirata, Akihiro</creator><creator>Kusakabe, Moriaki</creator><creator>Tatematsu, Masae</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Limited</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20060808</creationdate><title>Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype</title><author>Tsukamoto, Tetsuya ; Yamamoto, Masami ; Fukami, Hiroko ; Yoshikawa, Akemi ; Sakai, Hiroki ; Hirata, Akihiro ; Kusakabe, Moriaki ; Tatematsu, Masae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-d829b16b4ed66d14242b6ddf9387afdcbd01b249a3fff730c86d7fce65e8e8f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>1,2-dimethylhydrazine</topic><topic>Animals</topic><topic>Cancer</topic><topic>Carcinogens</topic><topic>Chimera</topic><topic>Chimeric mouse</topic><topic>Colon</topic><topic>Colon carcinogenesis</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - pathology</topic><topic>Disease Susceptibility</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Immunohistochemistry</topic><topic>Medical research</topic><topic>Mice</topic><topic>Mice, Inbred C3H</topic><topic>Mice, Inbred C57BL</topic><topic>Proteins</topic><topic>Rodent strain differences</topic><topic>Susceptibility</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsukamoto, Tetsuya</creatorcontrib><creatorcontrib>Yamamoto, Masami</creatorcontrib><creatorcontrib>Fukami, Hiroko</creatorcontrib><creatorcontrib>Yoshikawa, Akemi</creatorcontrib><creatorcontrib>Sakai, Hiroki</creatorcontrib><creatorcontrib>Hirata, Akihiro</creatorcontrib><creatorcontrib>Kusakabe, Moriaki</creatorcontrib><creatorcontrib>Tatematsu, Masae</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsukamoto, Tetsuya</au><au>Yamamoto, Masami</au><au>Fukami, Hiroko</au><au>Yoshikawa, Akemi</au><au>Sakai, Hiroki</au><au>Hirata, Akihiro</au><au>Kusakabe, Moriaki</au><au>Tatematsu, Masae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2006-08-08</date><risdate>2006</risdate><volume>239</volume><issue>2</issue><spage>205</spage><epage>211</epage><pages>205-211</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Considerable rodent strain differences have been documented with regard to susceptibility to colon carcinogens. To clarify mechanisms, chimeras of susceptible strain C3H and relatively resistant strain C57BL/6N (B6) mice were exposed to a colonotropic carcinogen, 1,2-dimethylhydrazine (DMH) and tumor incidence and multiplicity were assessed. In the chimeras, incidence was as high as the C3H level. Multiplicity of lesions of B6 cells was also increased (
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| fulltext | fulltext |
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| ispartof | Cancer letters, 2006-08, Vol.239 (2), p.205-211 |
| issn | 0304-3835 1872-7980 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | 1,2-dimethylhydrazine Animals Cancer Carcinogens Chimera Chimeric mouse Colon Colon carcinogenesis Colonic Neoplasms - genetics Colonic Neoplasms - pathology Disease Susceptibility Genotype Genotype & phenotype Immunohistochemistry Medical research Mice Mice, Inbred C3H Mice, Inbred C57BL Proteins Rodent strain differences Susceptibility Tumorigenesis Tumors |
| title | Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype |
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