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Loss of Heterozygosity and Nonsense Mutation in Apc in Azoxymethane-induced Colonic Tumours in Min Mice
C57BL/6J Min/+ mice, which carry a nonsense mutation in Apc, were injected twice neonatally with 5 mg azoxymethane (AOM) /kg body weight. AOM treatment in comparison with untreated Min mice increased the incidence and number of colonic tumours from 6/14 to 22/24 (incidence) and 0.64±0.9 to 4.0±3.5...
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| Published in: | Anticancer research 2004-09, Vol.24 (5A), p.2595-2599 |
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| container_title | Anticancer research |
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| creator | MØLLERSEN, Linda PAULSEN, Jan Erik ALEXANDER, Jan |
| description | C57BL/6J Min/+ mice, which carry a nonsense mutation in Apc, were injected twice neonatally with 5 mg azoxymethane (AOM) /kg
body weight. AOM treatment in comparison with untreated Min mice increased the incidence and number of colonic tumours from
6/14 to 22/24 (incidence) and 0.64±0.9 to 4.0±3.5 tumours per mice, respectively. Colonic tumours were analysed for loss of
heterozygosity (LOH) in Apc, and 32 of the samples showed LOH whereas 14 did not. In untreated Min mice, all 8 tumours had
LOH in Apc. All tumour samples from the AOM-treated Min mice were analysed for nonsense mutations between codons 686 and 1217
in the Apc gene, and one sample had a Gâ A transition mutation in codon 1047. No β-catenin mutations in the region coding
for phosphorylation sites important for degradation were found. In conclusion, the main mechanism for colonic tumour induction
in AOM-induced Min mice is LOH in Apc, but Apc nonsense mutations may also occur. |
| format | article |
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body weight. AOM treatment in comparison with untreated Min mice increased the incidence and number of colonic tumours from
6/14 to 22/24 (incidence) and 0.64±0.9 to 4.0±3.5 tumours per mice, respectively. Colonic tumours were analysed for loss of
heterozygosity (LOH) in Apc, and 32 of the samples showed LOH whereas 14 did not. In untreated Min mice, all 8 tumours had
LOH in Apc. All tumour samples from the AOM-treated Min mice were analysed for nonsense mutations between codons 686 and 1217
in the Apc gene, and one sample had a Gâ A transition mutation in codon 1047. No β-catenin mutations in the region coding
for phosphorylation sites important for degradation were found. In conclusion, the main mechanism for colonic tumour induction
in AOM-induced Min mice is LOH in Apc, but Apc nonsense mutations may also occur.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 15517863</identifier><language>eng</language><publisher>Attiki: International Institute of Anticancer Research</publisher><subject>Animals ; Azoxymethane ; beta Catenin ; Biological and medical sciences ; Carcinogens ; Cocarcinogenesis ; Codon, Nonsense ; Colonic Neoplasms - chemically induced ; Colonic Neoplasms - genetics ; Cytoskeletal Proteins - genetics ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Genes, APC - physiology ; Genetic Predisposition to Disease ; Loss of Heterozygosity ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Trans-Activators - genetics ; Tumors</subject><ispartof>Anticancer research, 2004-09, Vol.24 (5A), p.2595-2599</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16196295$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15517863$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MØLLERSEN, Linda</creatorcontrib><creatorcontrib>PAULSEN, Jan Erik</creatorcontrib><creatorcontrib>ALEXANDER, Jan</creatorcontrib><title>Loss of Heterozygosity and Nonsense Mutation in Apc in Azoxymethane-induced Colonic Tumours in Min Mice</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>C57BL/6J Min/+ mice, which carry a nonsense mutation in Apc, were injected twice neonatally with 5 mg azoxymethane (AOM) /kg
body weight. AOM treatment in comparison with untreated Min mice increased the incidence and number of colonic tumours from
6/14 to 22/24 (incidence) and 0.64±0.9 to 4.0±3.5 tumours per mice, respectively. Colonic tumours were analysed for loss of
heterozygosity (LOH) in Apc, and 32 of the samples showed LOH whereas 14 did not. In untreated Min mice, all 8 tumours had
LOH in Apc. All tumour samples from the AOM-treated Min mice were analysed for nonsense mutations between codons 686 and 1217
in the Apc gene, and one sample had a Gâ A transition mutation in codon 1047. No β-catenin mutations in the region coding
for phosphorylation sites important for degradation were found. In conclusion, the main mechanism for colonic tumour induction
in AOM-induced Min mice is LOH in Apc, but Apc nonsense mutations may also occur.</description><subject>Animals</subject><subject>Azoxymethane</subject><subject>beta Catenin</subject><subject>Biological and medical sciences</subject><subject>Carcinogens</subject><subject>Cocarcinogenesis</subject><subject>Codon, Nonsense</subject><subject>Colonic Neoplasms - chemically induced</subject><subject>Colonic Neoplasms - genetics</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genes, APC - physiology</subject><subject>Genetic Predisposition to Disease</subject><subject>Loss of Heterozygosity</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Trans-Activators - genetics</subject><subject>Tumors</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNpFz1FLwzAUBeAgipvTvyB50bdC0jRJ-ziGOmHTl_lcsvRmjbTJSFq0-_XWbSLcw3n5OHAv0JTKgiaSM3KJpiTlJJGE8Am6ifGTECGKnF2jCeWcylywKdqtfIzYG7yEDoI_DDsfbTdg5Sr85l2E8fC671RnvcPW4fleH-vgv4cWulo5SKyreg0VXvjGO6vxpm99H-KvWx-j4RZdGdVEuDv3DH08P20Wy2T1_vK6mK-SOhV5l3AJhTHVlnJZbRUYXkCWURCQ69woRonWNGOZKDhnhmmREp1zIgUtmMpSodkM3Z929_22harcB9uqMJR_H4_g4QxU1KoxQTlt478bp0Ra8NE9nlxtd_WXDVDGVjXNOMtKFdKs5PMy5SP8AaJpbaw</recordid><startdate>20040901</startdate><enddate>20040901</enddate><creator>MØLLERSEN, Linda</creator><creator>PAULSEN, Jan Erik</creator><creator>ALEXANDER, Jan</creator><general>International Institute of Anticancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20040901</creationdate><title>Loss of Heterozygosity and Nonsense Mutation in Apc in Azoxymethane-induced Colonic Tumours in Min Mice</title><author>MØLLERSEN, Linda ; PAULSEN, Jan Erik ; ALEXANDER, Jan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h268t-57e9ffdb157dbaef59e441e6e8c8fa310cc143469553f3c620c85076193a426c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Azoxymethane</topic><topic>beta Catenin</topic><topic>Biological and medical sciences</topic><topic>Carcinogens</topic><topic>Cocarcinogenesis</topic><topic>Codon, Nonsense</topic><topic>Colonic Neoplasms - chemically induced</topic><topic>Colonic Neoplasms - genetics</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genes, APC - physiology</topic><topic>Genetic Predisposition to Disease</topic><topic>Loss of Heterozygosity</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Trans-Activators - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MØLLERSEN, Linda</creatorcontrib><creatorcontrib>PAULSEN, Jan Erik</creatorcontrib><creatorcontrib>ALEXANDER, Jan</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MØLLERSEN, Linda</au><au>PAULSEN, Jan Erik</au><au>ALEXANDER, Jan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of Heterozygosity and Nonsense Mutation in Apc in Azoxymethane-induced Colonic Tumours in Min Mice</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2004-09-01</date><risdate>2004</risdate><volume>24</volume><issue>5A</issue><spage>2595</spage><epage>2599</epage><pages>2595-2599</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>C57BL/6J Min/+ mice, which carry a nonsense mutation in Apc, were injected twice neonatally with 5 mg azoxymethane (AOM) /kg
body weight. AOM treatment in comparison with untreated Min mice increased the incidence and number of colonic tumours from
6/14 to 22/24 (incidence) and 0.64±0.9 to 4.0±3.5 tumours per mice, respectively. Colonic tumours were analysed for loss of
heterozygosity (LOH) in Apc, and 32 of the samples showed LOH whereas 14 did not. In untreated Min mice, all 8 tumours had
LOH in Apc. All tumour samples from the AOM-treated Min mice were analysed for nonsense mutations between codons 686 and 1217
in the Apc gene, and one sample had a Gâ A transition mutation in codon 1047. No β-catenin mutations in the region coding
for phosphorylation sites important for degradation were found. In conclusion, the main mechanism for colonic tumour induction
in AOM-induced Min mice is LOH in Apc, but Apc nonsense mutations may also occur.</abstract><cop>Attiki</cop><pub>International Institute of Anticancer Research</pub><pmid>15517863</pmid><tpages>5</tpages></addata></record> |
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| subjects | Animals Azoxymethane beta Catenin Biological and medical sciences Carcinogens Cocarcinogenesis Codon, Nonsense Colonic Neoplasms - chemically induced Colonic Neoplasms - genetics Cytoskeletal Proteins - genetics Female Gastroenterology. Liver. Pancreas. Abdomen Genes, APC - physiology Genetic Predisposition to Disease Loss of Heterozygosity Male Medical sciences Mice Mice, Inbred C57BL Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Trans-Activators - genetics Tumors |
| title | Loss of Heterozygosity and Nonsense Mutation in Apc in Azoxymethane-induced Colonic Tumours in Min Mice |
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