The genetic background modifies the spontaneous and X-ray-induced tumor spectrum in the Apc1638N mouse model
The effect of the genetic background on the tumor spectrum of Apc1638N, a mouse model for attenuated familial adenomatous polyposis (FAP), has been investigated in X‐irradiated and untreated F1 hybrids between C57BL/6JIco‐Apc1638N (B6) and A/JCrlBR (A/J), BALB/cByJIco (C) or C3H/HeOuJIco (C3). Simil...
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| Veröffentlicht in: | Genes chromosomes & cancer 1999-03, Vol.24 (3), p.191-198 |
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| creator | van der Houven van Oordt, C. Willemien Smits, Ron Schouten, Theo G. Houwing-Duistermaat, Jeanine J. Williamson, Sophia L.H. Luz, Arne Khan, P. Meera van der Eb, Alex J. Breuer, Marco L. Fodde, Riccardo |
| description | The effect of the genetic background on the tumor spectrum of Apc1638N, a mouse model for attenuated familial adenomatous polyposis (FAP), has been investigated in X‐irradiated and untreated F1 hybrids between C57BL/6JIco‐Apc1638N (B6) and A/JCrlBR (A/J), BALB/cByJIco (C) or C3H/HeOuJIco (C3). Similar to the ApcMin model, the Apc1638N intestinal tumor multiplicity seems to be modulated by Mom1. Moreover, several additional (X‐ray–responsive) modifier loci appear also to affect the Apc1638N intestinal tumor number. The genetic background did not significantly influence the number of spontaneous desmoids and cutaneous cysts in Apc1638N. In general, X‐irradiation increased the desmoid multiplicity in Apc1638N females but had no effect in males. The opposite was noted for the cyst multiplicity after X‐rays. Surprisingly, X‐irradiated CB6F1‐Apc1638N females were highly susceptible to the development of ovarian tumors, which displayed clear loss of the wild‐type Apc allele. Genes Chromosomes Cancer 24:191–198, 1999. © 1999 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/(SICI)1098-2264(199903)24:3<191::AID-GCC3>3.0.CO;2-L |
| format | Article |
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Willemien ; Smits, Ron ; Schouten, Theo G. ; Houwing-Duistermaat, Jeanine J. ; Williamson, Sophia L.H. ; Luz, Arne ; Khan, P. Meera ; van der Eb, Alex J. ; Breuer, Marco L. ; Fodde, Riccardo</creator><creatorcontrib>van der Houven van Oordt, C. Willemien ; Smits, Ron ; Schouten, Theo G. ; Houwing-Duistermaat, Jeanine J. ; Williamson, Sophia L.H. ; Luz, Arne ; Khan, P. Meera ; van der Eb, Alex J. ; Breuer, Marco L. ; Fodde, Riccardo</creatorcontrib><description>The effect of the genetic background on the tumor spectrum of Apc1638N, a mouse model for attenuated familial adenomatous polyposis (FAP), has been investigated in X‐irradiated and untreated F1 hybrids between C57BL/6JIco‐Apc1638N (B6) and A/JCrlBR (A/J), BALB/cByJIco (C) or C3H/HeOuJIco (C3). Similar to the ApcMin model, the Apc1638N intestinal tumor multiplicity seems to be modulated by Mom1. Moreover, several additional (X‐ray–responsive) modifier loci appear also to affect the Apc1638N intestinal tumor number. The genetic background did not significantly influence the number of spontaneous desmoids and cutaneous cysts in Apc1638N. In general, X‐irradiation increased the desmoid multiplicity in Apc1638N females but had no effect in males. The opposite was noted for the cyst multiplicity after X‐rays. Surprisingly, X‐irradiated CB6F1‐Apc1638N females were highly susceptible to the development of ovarian tumors, which displayed clear loss of the wild‐type Apc allele. Genes Chromosomes Cancer 24:191–198, 1999. © 1999 Wiley‐Liss, Inc.</description><identifier>ISSN: 1045-2257</identifier><identifier>EISSN: 1098-2264</identifier><identifier>DOI: 10.1002/(SICI)1098-2264(199903)24:3<191::AID-GCC3>3.0.CO;2-L</identifier><identifier>PMID: 10451698</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Adenomatous Polyposis Coli - genetics ; Animals ; Epidermal Cyst - genetics ; Female ; Fibromatosis, Aggressive - genetics ; Gastrointestinal Neoplasms - genetics ; Genetic Predisposition to Disease - genetics ; Loss of Heterozygosity - genetics ; Male ; Mammary Neoplasms, Animal - genetics ; Mice ; Mice, Inbred A ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Neoplasms, Multiple Primary - genetics ; Neoplasms, Radiation-Induced - genetics ; Ovarian Neoplasms - genetics ; Skin Neoplasms - genetics ; X-Rays</subject><ispartof>Genes chromosomes & cancer, 1999-03, Vol.24 (3), p.191-198</ispartof><rights>Copyright © 1999 Wiley‐Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291098-2264%28199903%2924%3A3%3C191%3A%3AAID-GCC3%3E3.0.CO%3B2-L$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291098-2264%28199903%2924%3A3%3C191%3A%3AAID-GCC3%3E3.0.CO%3B2-L$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27926,27927,45576,45577</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10451698$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van der Houven van Oordt, C. Willemien</creatorcontrib><creatorcontrib>Smits, Ron</creatorcontrib><creatorcontrib>Schouten, Theo G.</creatorcontrib><creatorcontrib>Houwing-Duistermaat, Jeanine J.</creatorcontrib><creatorcontrib>Williamson, Sophia L.H.</creatorcontrib><creatorcontrib>Luz, Arne</creatorcontrib><creatorcontrib>Khan, P. Meera</creatorcontrib><creatorcontrib>van der Eb, Alex J.</creatorcontrib><creatorcontrib>Breuer, Marco L.</creatorcontrib><creatorcontrib>Fodde, Riccardo</creatorcontrib><title>The genetic background modifies the spontaneous and X-ray-induced tumor spectrum in the Apc1638N mouse model</title><title>Genes chromosomes & cancer</title><addtitle>Genes Chromosom. Cancer</addtitle><description>The effect of the genetic background on the tumor spectrum of Apc1638N, a mouse model for attenuated familial adenomatous polyposis (FAP), has been investigated in X‐irradiated and untreated F1 hybrids between C57BL/6JIco‐Apc1638N (B6) and A/JCrlBR (A/J), BALB/cByJIco (C) or C3H/HeOuJIco (C3). Similar to the ApcMin model, the Apc1638N intestinal tumor multiplicity seems to be modulated by Mom1. Moreover, several additional (X‐ray–responsive) modifier loci appear also to affect the Apc1638N intestinal tumor number. The genetic background did not significantly influence the number of spontaneous desmoids and cutaneous cysts in Apc1638N. In general, X‐irradiation increased the desmoid multiplicity in Apc1638N females but had no effect in males. The opposite was noted for the cyst multiplicity after X‐rays. Surprisingly, X‐irradiated CB6F1‐Apc1638N females were highly susceptible to the development of ovarian tumors, which displayed clear loss of the wild‐type Apc allele. Genes Chromosomes Cancer 24:191–198, 1999. © 1999 Wiley‐Liss, Inc.</description><subject>Adenomatous Polyposis Coli - genetics</subject><subject>Animals</subject><subject>Epidermal Cyst - genetics</subject><subject>Female</subject><subject>Fibromatosis, Aggressive - genetics</subject><subject>Gastrointestinal Neoplasms - genetics</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Loss of Heterozygosity - genetics</subject><subject>Male</subject><subject>Mammary Neoplasms, Animal - genetics</subject><subject>Mice</subject><subject>Mice, Inbred A</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Mutant Strains</subject><subject>Neoplasms, Multiple Primary - genetics</subject><subject>Neoplasms, Radiation-Induced - genetics</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Skin Neoplasms - genetics</subject><subject>X-Rays</subject><issn>1045-2257</issn><issn>1098-2264</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkMtu2zAQRYmiRZKm-YVCy2RBhy9RohsEMNTWduHYi7iP3YCiRikbSzL0QOu_DxW3QVe8gztzAB5CbjibcMbE9eX9MltecWZSKoRWl9wYw-SVUFN5ww2fTmfLj3SeZfJWTtgk23wQdPWKnL0cvB6zikOOk1Pytut-Mca0NPEJOR0Lrk16Rnbbnxg9YI29d1Fu3eND2wx1EVVN4UuPXdSHvts3dW9rbIYusqH8QVt7oL4uBodF1A9V04YddH07VJGvn29me8e1TNeBNHQ48nD3jrwp7a7Di7_vOfn6-dM2W9DVZr7MZivqhUwkdSkapbnKtYmtVbo0wmluhUydzJEpwbTQNjastCJHzJUWsTB5KRKpEIWT5-T9kbsf8goL2Le-su0B_n07LGyPC7_9Dg__9TCqh9E8jCJhFAlH8yAUyJA5BPEwig8jg2wDAlbPc8DSI9Z3Pf55wdr2EXQikxi-r-dwt75nX-6-LWAhnwBMk4oe</recordid><startdate>199903</startdate><enddate>199903</enddate><creator>van der Houven van Oordt, C. 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Willemien</au><au>Smits, Ron</au><au>Schouten, Theo G.</au><au>Houwing-Duistermaat, Jeanine J.</au><au>Williamson, Sophia L.H.</au><au>Luz, Arne</au><au>Khan, P. Meera</au><au>van der Eb, Alex J.</au><au>Breuer, Marco L.</au><au>Fodde, Riccardo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The genetic background modifies the spontaneous and X-ray-induced tumor spectrum in the Apc1638N mouse model</atitle><jtitle>Genes chromosomes & cancer</jtitle><addtitle>Genes Chromosom. Cancer</addtitle><date>1999-03</date><risdate>1999</risdate><volume>24</volume><issue>3</issue><spage>191</spage><epage>198</epage><pages>191-198</pages><issn>1045-2257</issn><eissn>1098-2264</eissn><abstract>The effect of the genetic background on the tumor spectrum of Apc1638N, a mouse model for attenuated familial adenomatous polyposis (FAP), has been investigated in X‐irradiated and untreated F1 hybrids between C57BL/6JIco‐Apc1638N (B6) and A/JCrlBR (A/J), BALB/cByJIco (C) or C3H/HeOuJIco (C3). Similar to the ApcMin model, the Apc1638N intestinal tumor multiplicity seems to be modulated by Mom1. Moreover, several additional (X‐ray–responsive) modifier loci appear also to affect the Apc1638N intestinal tumor number. The genetic background did not significantly influence the number of spontaneous desmoids and cutaneous cysts in Apc1638N. In general, X‐irradiation increased the desmoid multiplicity in Apc1638N females but had no effect in males. The opposite was noted for the cyst multiplicity after X‐rays. Surprisingly, X‐irradiated CB6F1‐Apc1638N females were highly susceptible to the development of ovarian tumors, which displayed clear loss of the wild‐type Apc allele. Genes Chromosomes Cancer 24:191–198, 1999. © 1999 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>10451698</pmid><doi>10.1002/(SICI)1098-2264(199903)24:3<191::AID-GCC3>3.0.CO;2-L</doi><tpages>8</tpages></addata></record> |
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| ispartof | Genes chromosomes & cancer, 1999-03, Vol.24 (3), p.191-198 |
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| subjects | Adenomatous Polyposis Coli - genetics Animals Epidermal Cyst - genetics Female Fibromatosis, Aggressive - genetics Gastrointestinal Neoplasms - genetics Genetic Predisposition to Disease - genetics Loss of Heterozygosity - genetics Male Mammary Neoplasms, Animal - genetics Mice Mice, Inbred A Mice, Inbred BALB C Mice, Inbred C3H Mice, Inbred C57BL Mice, Mutant Strains Neoplasms, Multiple Primary - genetics Neoplasms, Radiation-Induced - genetics Ovarian Neoplasms - genetics Skin Neoplasms - genetics X-Rays |
| title | The genetic background modifies the spontaneous and X-ray-induced tumor spectrum in the Apc1638N mouse model |
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