Loss of insulin-like growth factor-II imprinting and the presence of screen-detected colorectal adenomas in women
Loss of imprinting (LOI) of insulin-like growth factor-II (IGF-II) may be an inherited epigenetic trait that is polymorphic in the population, and its presence may predispose an individual to the development of colorectal cancer. We evaluated the association between LOI of IGF-II in normal colonic m...
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description | Loss of imprinting (LOI) of insulin-like growth factor-II (IGF-II) may be an inherited epigenetic trait that is polymorphic in the population, and its presence may predispose an individual to the development of colorectal cancer. We evaluated the association between LOI of IGF-II in normal colonic mucosal samples and adenomas in women participating in a colonoscopy screening study. Among 40 participants, 11 (27.5%) had LOI of IGF-II in their normal colonic mucosal tissue. After adjusting for body mass index and family history of colorectal cancer, LOI status was associated with a fivefold increased risk of adenoma formation (odds ratio = 5.2, 95% confidence interval = 1.0 to 26.7). On average, IGF-II expression was more than threefold higher among women with LOI of IGF-II than among women with normal imprinting status. Our findings support the hypothesis that LOI of IGF-II is an epigenetic trait polymorphic in the population and suggest that LOI of IGF-II may play a role in colorectal cancer. These findings are intriguing and need to be confirmed in larger studies. |
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We evaluated the association between LOI of IGF-II in normal colonic mucosal samples and adenomas in women participating in a colonoscopy screening study. Among 40 participants, 11 (27.5%) had LOI of IGF-II in their normal colonic mucosal tissue. After adjusting for body mass index and family history of colorectal cancer, LOI status was associated with a fivefold increased risk of adenoma formation (odds ratio = 5.2, 95% confidence interval = 1.0 to 26.7). On average, IGF-II expression was more than threefold higher among women with LOI of IGF-II than among women with normal imprinting status. Our findings support the hypothesis that LOI of IGF-II is an epigenetic trait polymorphic in the population and suggest that LOI of IGF-II may play a role in colorectal cancer. These findings are intriguing and need to be confirmed in larger studies.</description><identifier>ISSN: 0027-8874</identifier><identifier>EISSN: 1460-2105</identifier><identifier>DOI: 10.1093/jnci/djh042</identifier><identifier>PMID: 14996863</identifier><identifier>CODEN: JNCIEQ</identifier><language>eng</language><publisher>Cary, NC: Oxford University Press</publisher><subject>Actins - metabolism ; Adenoma - genetics ; Adult ; Aged ; Biological and medical sciences ; Clinical trials ; Colon ; Colonoscopy ; Colorectal cancer ; Colorectal Neoplasms - genetics ; DNA Methylation ; DNA, Complementary - metabolism ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; Genetics ; Genomic Imprinting ; Humans ; Incidence ; Insulin-Like Growth Factor II - genetics ; Intestinal Mucosa - metabolism ; Mass Screening - methods ; Medical sciences ; Middle Aged ; Odds Ratio ; Risk Assessment ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors ; Up-Regulation ; Women</subject><ispartof>JNCI : Journal of the National Cancer Institute, 2004-03, Vol.96 (5), p.407-410</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Mar 3, 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c410t-9f9e66f5a7a9b474296a90a5d435eea7e8588703321f2b4552b85f026a565a813</citedby><cites>FETCH-LOGICAL-c410t-9f9e66f5a7a9b474296a90a5d435eea7e8588703321f2b4552b85f026a565a813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15927541$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14996863$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WOODSON, Karen</creatorcontrib><creatorcontrib>FLOOD, Andrew</creatorcontrib><creatorcontrib>GREEN, Lisa</creatorcontrib><creatorcontrib>TANGREA, Joseph A</creatorcontrib><creatorcontrib>HANSON, Jeffrey</creatorcontrib><creatorcontrib>CASH, Brooks</creatorcontrib><creatorcontrib>SCHATZKIN, Arthur</creatorcontrib><creatorcontrib>SCHOENFELD, Phillip</creatorcontrib><title>Loss of insulin-like growth factor-II imprinting and the presence of screen-detected colorectal adenomas in women</title><title>JNCI : Journal of the National Cancer Institute</title><addtitle>J Natl Cancer Inst</addtitle><description>Loss of imprinting (LOI) of insulin-like growth factor-II (IGF-II) may be an inherited epigenetic trait that is polymorphic in the population, and its presence may predispose an individual to the development of colorectal cancer. We evaluated the association between LOI of IGF-II in normal colonic mucosal samples and adenomas in women participating in a colonoscopy screening study. Among 40 participants, 11 (27.5%) had LOI of IGF-II in their normal colonic mucosal tissue. After adjusting for body mass index and family history of colorectal cancer, LOI status was associated with a fivefold increased risk of adenoma formation (odds ratio = 5.2, 95% confidence interval = 1.0 to 26.7). On average, IGF-II expression was more than threefold higher among women with LOI of IGF-II than among women with normal imprinting status. Our findings support the hypothesis that LOI of IGF-II is an epigenetic trait polymorphic in the population and suggest that LOI of IGF-II may play a role in colorectal cancer. These findings are intriguing and need to be confirmed in larger studies.</description><subject>Actins - metabolism</subject><subject>Adenoma - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Clinical trials</subject><subject>Colon</subject><subject>Colonoscopy</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - genetics</subject><subject>DNA Methylation</subject><subject>DNA, Complementary - metabolism</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetics</subject><subject>Genomic Imprinting</subject><subject>Humans</subject><subject>Incidence</subject><subject>Insulin-Like Growth Factor II - genetics</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Mass Screening - methods</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>Risk Assessment</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetics</topic><topic>Genomic Imprinting</topic><topic>Humans</topic><topic>Incidence</topic><topic>Insulin-Like Growth Factor II - genetics</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Mass Screening - methods</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>Risk Assessment</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><topic>Up-Regulation</topic><topic>Women</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WOODSON, Karen</creatorcontrib><creatorcontrib>FLOOD, Andrew</creatorcontrib><creatorcontrib>GREEN, Lisa</creatorcontrib><creatorcontrib>TANGREA, Joseph A</creatorcontrib><creatorcontrib>HANSON, Jeffrey</creatorcontrib><creatorcontrib>CASH, Brooks</creatorcontrib><creatorcontrib>SCHATZKIN, Arthur</creatorcontrib><creatorcontrib>SCHOENFELD, Phillip</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>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>JNCI : Journal of the National Cancer Institute</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WOODSON, Karen</au><au>FLOOD, Andrew</au><au>GREEN, Lisa</au><au>TANGREA, Joseph A</au><au>HANSON, Jeffrey</au><au>CASH, Brooks</au><au>SCHATZKIN, Arthur</au><au>SCHOENFELD, Phillip</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of insulin-like growth factor-II imprinting and the presence of screen-detected colorectal adenomas in women</atitle><jtitle>JNCI : Journal of the National Cancer Institute</jtitle><addtitle>J Natl Cancer Inst</addtitle><date>2004-03-03</date><risdate>2004</risdate><volume>96</volume><issue>5</issue><spage>407</spage><epage>410</epage><pages>407-410</pages><issn>0027-8874</issn><eissn>1460-2105</eissn><coden>JNCIEQ</coden><abstract>Loss of imprinting (LOI) of insulin-like growth factor-II (IGF-II) may be an inherited epigenetic trait that is polymorphic in the population, and its presence may predispose an individual to the development of colorectal cancer. We evaluated the association between LOI of IGF-II in normal colonic mucosal samples and adenomas in women participating in a colonoscopy screening study. Among 40 participants, 11 (27.5%) had LOI of IGF-II in their normal colonic mucosal tissue. After adjusting for body mass index and family history of colorectal cancer, LOI status was associated with a fivefold increased risk of adenoma formation (odds ratio = 5.2, 95% confidence interval = 1.0 to 26.7). On average, IGF-II expression was more than threefold higher among women with LOI of IGF-II than among women with normal imprinting status. Our findings support the hypothesis that LOI of IGF-II is an epigenetic trait polymorphic in the population and suggest that LOI of IGF-II may play a role in colorectal cancer. These findings are intriguing and need to be confirmed in larger studies.</abstract><cop>Cary, NC</cop><pub>Oxford University Press</pub><pmid>14996863</pmid><doi>10.1093/jnci/djh042</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Actins - metabolism Adenoma - genetics Adult Aged Biological and medical sciences Clinical trials Colon Colonoscopy Colorectal cancer Colorectal Neoplasms - genetics DNA Methylation DNA, Complementary - metabolism Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Genetics Genomic Imprinting Humans Incidence Insulin-Like Growth Factor II - genetics Intestinal Mucosa - metabolism Mass Screening - methods Medical sciences Middle Aged Odds Ratio Risk Assessment Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors Up-Regulation Women |
title | Loss of insulin-like growth factor-II imprinting and the presence of screen-detected colorectal adenomas in women |
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