The effect of copy number variation in the phase II detoxification genes UGT2B17 and UGT2B28 on colorectal cancer risk
BACKGROUND Genetic polymorphisms in combination with the Western‐style diet, physical inactivity, smoking, excessive alcohol consumption, and obesity have been hypothesized to affect colorectal cancer (CRC) risk. Metabolizers of environmental carcinogenic and endogenous compounds affecting CRC risk...
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| Veröffentlicht in: | Cancer 2013-07, Vol.119 (13), p.2477-2485 |
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| creator | Angstadt, Andrea Y. Berg, Arthur Zhu, Junjia Miller, Paige Hartman, Terryl J. Lesko, Samuel M. Muscat, Joshua E. Lazarus, Philip Gallagher, Carla J. |
| description | BACKGROUND
Genetic polymorphisms in combination with the Western‐style diet, physical inactivity, smoking, excessive alcohol consumption, and obesity have been hypothesized to affect colorectal cancer (CRC) risk. Metabolizers of environmental carcinogenic and endogenous compounds affecting CRC risk include the phase II detoxification UDP‐glucuronosyltransferase (UGT) enzymes UGT2B17 and UGT2B28, which are 2 of the most commonly deleted genes in the genome.
METHODS
To study the effect of UGT2B17 and UGT2B28 copy number variation (CNV) on CRC risk, 665 Caucasian CRC cases and 621 Caucasian controls were genotyped who had completed extensive demographics and lifestyle questionnaires.
RESULTS
A significant association between the UGT2B17 deletion genotype (0/0) and decreased CRC risk was found when the entire population was analyzed (P = .044). Stratification by sex yielded a decreased risk (P = .020) in men with the UGT2B17 deletion (0/0), but no association was observed in women (P = .724). A significant association between UGT2B17 (0/0) and decreased risk for rectal (P = .0065) but not colon cancer was found. No significant association was found between UGT2B28 CNV and CRC risk.
CONCLUSIONS
The UGT2B17 deletion genotype (0/0) was associated with a decreased CRC risk in a Caucasian population. After sex stratification, the association was observed in men but not in women, which is consistent with previous findings that men have higher UGT2B17 expression and activity than women. Because UGT2B17 metabolizes certain nonsteroidal anti‐inflammatory drugs and flavonoids with antioxidative properties, individuals with a gene deletion may have higher levels of these protective dietary components. Cancer 2013;119:2477‐2485. © 2013 American Cancer Society.
UGT2B17 and UGT2B28 are 2 of the most commonly deleted genes in the human genome and are metabolizers of environmental and endogenous compounds. This study found that the UGT2B17 gene deletion is associated with decreased colorectal cancer risk, suggesting a protective function for the UGT2B17 gene, because individuals without the gene may have higher circulating levels of flavonoids and nonsteroidal anti‐inflammatory drugs. |
| doi_str_mv | 10.1002/cncr.28009 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3686841</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1434013146</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5199-c45a97e02e437a400e936a5202a2f802e7060994b596c5ad722420ef8213c1a93</originalsourceid><addsrcrecordid>eNp9kV1rFDEUhoModlu98QdILkWYevI1mdwIdrF1oSjIFrwL2eyZbnQ2WZPZ1f33pk4teuNVTs778CTwEvKCwTkD4G989PmcdwDmEZkxMLoBJvljMgOArlFSfDkhp6V8rVfNlXhKTrhQWnWdnpHDcoMU-x79SFNPfdodadxvV5jpweXgxpAiDZGOFdttXEG6WNA1juln6IOf4luMWOjN1ZJfME1dXE8z72gNfRpSrnY3UO-ir94cyrdn5EnvhoLP788zcnP5fjn_0Fx_ulrM3103XjFjGi-VMxqBoxTaSQA0onWKA3e87-paQwvGyJUyrVdurTmXHLDvOBOeOSPOyNvJu9uvtrj2GMfsBrvLYevy0SYX7L9JDBt7mw5WtF3bSVYFr-4FOX3fYxntNhSPw-Aipn2xTAoJTDDZVvT1hPqcSsnYPzzDwN4VZe-Ksr-LqvDLvz_2gP5ppgJsAn6EAY__Udn5x_nnSfoLboidHg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1434013146</pqid></control><display><type>article</type><title>The effect of copy number variation in the phase II detoxification genes UGT2B17 and UGT2B28 on colorectal cancer risk</title><source>Wiley Free Content</source><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Angstadt, Andrea Y. ; Berg, Arthur ; Zhu, Junjia ; Miller, Paige ; Hartman, Terryl J. ; Lesko, Samuel M. ; Muscat, Joshua E. ; Lazarus, Philip ; Gallagher, Carla J.</creator><creatorcontrib>Angstadt, Andrea Y. ; Berg, Arthur ; Zhu, Junjia ; Miller, Paige ; Hartman, Terryl J. ; Lesko, Samuel M. ; Muscat, Joshua E. ; Lazarus, Philip ; Gallagher, Carla J.</creatorcontrib><description>BACKGROUND
Genetic polymorphisms in combination with the Western‐style diet, physical inactivity, smoking, excessive alcohol consumption, and obesity have been hypothesized to affect colorectal cancer (CRC) risk. Metabolizers of environmental carcinogenic and endogenous compounds affecting CRC risk include the phase II detoxification UDP‐glucuronosyltransferase (UGT) enzymes UGT2B17 and UGT2B28, which are 2 of the most commonly deleted genes in the genome.
METHODS
To study the effect of UGT2B17 and UGT2B28 copy number variation (CNV) on CRC risk, 665 Caucasian CRC cases and 621 Caucasian controls were genotyped who had completed extensive demographics and lifestyle questionnaires.
RESULTS
A significant association between the UGT2B17 deletion genotype (0/0) and decreased CRC risk was found when the entire population was analyzed (P = .044). Stratification by sex yielded a decreased risk (P = .020) in men with the UGT2B17 deletion (0/0), but no association was observed in women (P = .724). A significant association between UGT2B17 (0/0) and decreased risk for rectal (P = .0065) but not colon cancer was found. No significant association was found between UGT2B28 CNV and CRC risk.
CONCLUSIONS
The UGT2B17 deletion genotype (0/0) was associated with a decreased CRC risk in a Caucasian population. After sex stratification, the association was observed in men but not in women, which is consistent with previous findings that men have higher UGT2B17 expression and activity than women. Because UGT2B17 metabolizes certain nonsteroidal anti‐inflammatory drugs and flavonoids with antioxidative properties, individuals with a gene deletion may have higher levels of these protective dietary components. Cancer 2013;119:2477‐2485. © 2013 American Cancer Society.
UGT2B17 and UGT2B28 are 2 of the most commonly deleted genes in the human genome and are metabolizers of environmental and endogenous compounds. This study found that the UGT2B17 gene deletion is associated with decreased colorectal cancer risk, suggesting a protective function for the UGT2B17 gene, because individuals without the gene may have higher circulating levels of flavonoids and nonsteroidal anti‐inflammatory drugs.</description><identifier>ISSN: 0008-543X</identifier><identifier>EISSN: 1097-0142</identifier><identifier>DOI: 10.1002/cncr.28009</identifier><identifier>PMID: 23575887</identifier><language>eng</language><publisher>United States</publisher><subject>Adult ; Aged ; Antiinflammatory agents ; Case-Control Studies ; Colonic Neoplasms - genetics ; colorectal cancer risk ; Colorectal Neoplasms - enzymology ; Colorectal Neoplasms - epidemiology ; Colorectal Neoplasms - genetics ; copy number variation ; DNA Copy Number Variations ; European Continental Ancestry Group - genetics ; Female ; Gene Deletion ; Genetic Predisposition to Disease ; Genotype ; Glucuronosyltransferase - genetics ; Humans ; Male ; Meat - adverse effects ; Meat Products - adverse effects ; Metabolic Detoxication, Phase II - genetics ; Middle Aged ; Minor Histocompatibility Antigens ; Pennsylvania - epidemiology ; phase II detoxification ; Rectal Neoplasms - genetics ; Risk Factors ; Sex Factors ; Surveys and Questionnaires ; UGT2B17 ; UGT2B28</subject><ispartof>Cancer, 2013-07, Vol.119 (13), p.2477-2485</ispartof><rights>Copyright © 2013 American Cancer Society</rights><rights>Copyright © 2013 American Cancer Society.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5199-c45a97e02e437a400e936a5202a2f802e7060994b596c5ad722420ef8213c1a93</citedby><cites>FETCH-LOGICAL-c5199-c45a97e02e437a400e936a5202a2f802e7060994b596c5ad722420ef8213c1a93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcncr.28009$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcncr.28009$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23575887$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Angstadt, Andrea Y.</creatorcontrib><creatorcontrib>Berg, Arthur</creatorcontrib><creatorcontrib>Zhu, Junjia</creatorcontrib><creatorcontrib>Miller, Paige</creatorcontrib><creatorcontrib>Hartman, Terryl J.</creatorcontrib><creatorcontrib>Lesko, Samuel M.</creatorcontrib><creatorcontrib>Muscat, Joshua E.</creatorcontrib><creatorcontrib>Lazarus, Philip</creatorcontrib><creatorcontrib>Gallagher, Carla J.</creatorcontrib><title>The effect of copy number variation in the phase II detoxification genes UGT2B17 and UGT2B28 on colorectal cancer risk</title><title>Cancer</title><addtitle>Cancer</addtitle><description>BACKGROUND
Genetic polymorphisms in combination with the Western‐style diet, physical inactivity, smoking, excessive alcohol consumption, and obesity have been hypothesized to affect colorectal cancer (CRC) risk. Metabolizers of environmental carcinogenic and endogenous compounds affecting CRC risk include the phase II detoxification UDP‐glucuronosyltransferase (UGT) enzymes UGT2B17 and UGT2B28, which are 2 of the most commonly deleted genes in the genome.
METHODS
To study the effect of UGT2B17 and UGT2B28 copy number variation (CNV) on CRC risk, 665 Caucasian CRC cases and 621 Caucasian controls were genotyped who had completed extensive demographics and lifestyle questionnaires.
RESULTS
A significant association between the UGT2B17 deletion genotype (0/0) and decreased CRC risk was found when the entire population was analyzed (P = .044). Stratification by sex yielded a decreased risk (P = .020) in men with the UGT2B17 deletion (0/0), but no association was observed in women (P = .724). A significant association between UGT2B17 (0/0) and decreased risk for rectal (P = .0065) but not colon cancer was found. No significant association was found between UGT2B28 CNV and CRC risk.
CONCLUSIONS
The UGT2B17 deletion genotype (0/0) was associated with a decreased CRC risk in a Caucasian population. After sex stratification, the association was observed in men but not in women, which is consistent with previous findings that men have higher UGT2B17 expression and activity than women. Because UGT2B17 metabolizes certain nonsteroidal anti‐inflammatory drugs and flavonoids with antioxidative properties, individuals with a gene deletion may have higher levels of these protective dietary components. Cancer 2013;119:2477‐2485. © 2013 American Cancer Society.
UGT2B17 and UGT2B28 are 2 of the most commonly deleted genes in the human genome and are metabolizers of environmental and endogenous compounds. This study found that the UGT2B17 gene deletion is associated with decreased colorectal cancer risk, suggesting a protective function for the UGT2B17 gene, because individuals without the gene may have higher circulating levels of flavonoids and nonsteroidal anti‐inflammatory drugs.</description><subject>Adult</subject><subject>Aged</subject><subject>Antiinflammatory agents</subject><subject>Case-Control Studies</subject><subject>Colonic Neoplasms - genetics</subject><subject>colorectal cancer risk</subject><subject>Colorectal Neoplasms - enzymology</subject><subject>Colorectal Neoplasms - epidemiology</subject><subject>Colorectal Neoplasms - genetics</subject><subject>copy number variation</subject><subject>DNA Copy Number Variations</subject><subject>European Continental Ancestry Group - genetics</subject><subject>Female</subject><subject>Gene Deletion</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Glucuronosyltransferase - genetics</subject><subject>Humans</subject><subject>Male</subject><subject>Meat - adverse effects</subject><subject>Meat Products - adverse effects</subject><subject>Metabolic Detoxication, Phase II - genetics</subject><subject>Middle Aged</subject><subject>Minor Histocompatibility Antigens</subject><subject>Pennsylvania - epidemiology</subject><subject>phase II detoxification</subject><subject>Rectal Neoplasms - genetics</subject><subject>Risk Factors</subject><subject>Sex Factors</subject><subject>Surveys and Questionnaires</subject><subject>UGT2B17</subject><subject>UGT2B28</subject><issn>0008-543X</issn><issn>1097-0142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kV1rFDEUhoModlu98QdILkWYevI1mdwIdrF1oSjIFrwL2eyZbnQ2WZPZ1f33pk4teuNVTs778CTwEvKCwTkD4G989PmcdwDmEZkxMLoBJvljMgOArlFSfDkhp6V8rVfNlXhKTrhQWnWdnpHDcoMU-x79SFNPfdodadxvV5jpweXgxpAiDZGOFdttXEG6WNA1juln6IOf4luMWOjN1ZJfME1dXE8z72gNfRpSrnY3UO-ir94cyrdn5EnvhoLP788zcnP5fjn_0Fx_ulrM3103XjFjGi-VMxqBoxTaSQA0onWKA3e87-paQwvGyJUyrVdurTmXHLDvOBOeOSPOyNvJu9uvtrj2GMfsBrvLYevy0SYX7L9JDBt7mw5WtF3bSVYFr-4FOX3fYxntNhSPw-Aipn2xTAoJTDDZVvT1hPqcSsnYPzzDwN4VZe-Ksr-LqvDLvz_2gP5ppgJsAn6EAY__Udn5x_nnSfoLboidHg</recordid><startdate>20130701</startdate><enddate>20130701</enddate><creator>Angstadt, Andrea Y.</creator><creator>Berg, Arthur</creator><creator>Zhu, Junjia</creator><creator>Miller, Paige</creator><creator>Hartman, Terryl J.</creator><creator>Lesko, Samuel M.</creator><creator>Muscat, Joshua E.</creator><creator>Lazarus, Philip</creator><creator>Gallagher, Carla J.</creator><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>7U1</scope><scope>7U2</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20130701</creationdate><title>The effect of copy number variation in the phase II detoxification genes UGT2B17 and UGT2B28 on colorectal cancer risk</title><author>Angstadt, Andrea Y. ; Berg, Arthur ; Zhu, Junjia ; Miller, Paige ; Hartman, Terryl J. ; Lesko, Samuel M. ; Muscat, Joshua E. ; Lazarus, Philip ; Gallagher, Carla J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5199-c45a97e02e437a400e936a5202a2f802e7060994b596c5ad722420ef8213c1a93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antiinflammatory agents</topic><topic>Case-Control Studies</topic><topic>Colonic Neoplasms - genetics</topic><topic>colorectal cancer risk</topic><topic>Colorectal Neoplasms - enzymology</topic><topic>Colorectal Neoplasms - epidemiology</topic><topic>Colorectal Neoplasms - genetics</topic><topic>copy number variation</topic><topic>DNA Copy Number Variations</topic><topic>European Continental Ancestry Group - genetics</topic><topic>Female</topic><topic>Gene Deletion</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Glucuronosyltransferase - genetics</topic><topic>Humans</topic><topic>Male</topic><topic>Meat - adverse effects</topic><topic>Meat Products - adverse effects</topic><topic>Metabolic Detoxication, Phase II - genetics</topic><topic>Middle Aged</topic><topic>Minor Histocompatibility Antigens</topic><topic>Pennsylvania - epidemiology</topic><topic>phase II detoxification</topic><topic>Rectal Neoplasms - genetics</topic><topic>Risk Factors</topic><topic>Sex Factors</topic><topic>Surveys and Questionnaires</topic><topic>UGT2B17</topic><topic>UGT2B28</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Angstadt, Andrea Y.</creatorcontrib><creatorcontrib>Berg, Arthur</creatorcontrib><creatorcontrib>Zhu, Junjia</creatorcontrib><creatorcontrib>Miller, Paige</creatorcontrib><creatorcontrib>Hartman, Terryl J.</creatorcontrib><creatorcontrib>Lesko, Samuel M.</creatorcontrib><creatorcontrib>Muscat, Joshua E.</creatorcontrib><creatorcontrib>Lazarus, Philip</creatorcontrib><creatorcontrib>Gallagher, Carla J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Angstadt, Andrea Y.</au><au>Berg, Arthur</au><au>Zhu, Junjia</au><au>Miller, Paige</au><au>Hartman, Terryl J.</au><au>Lesko, Samuel M.</au><au>Muscat, Joshua E.</au><au>Lazarus, Philip</au><au>Gallagher, Carla J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effect of copy number variation in the phase II detoxification genes UGT2B17 and UGT2B28 on colorectal cancer risk</atitle><jtitle>Cancer</jtitle><addtitle>Cancer</addtitle><date>2013-07-01</date><risdate>2013</risdate><volume>119</volume><issue>13</issue><spage>2477</spage><epage>2485</epage><pages>2477-2485</pages><issn>0008-543X</issn><eissn>1097-0142</eissn><abstract>BACKGROUND
Genetic polymorphisms in combination with the Western‐style diet, physical inactivity, smoking, excessive alcohol consumption, and obesity have been hypothesized to affect colorectal cancer (CRC) risk. Metabolizers of environmental carcinogenic and endogenous compounds affecting CRC risk include the phase II detoxification UDP‐glucuronosyltransferase (UGT) enzymes UGT2B17 and UGT2B28, which are 2 of the most commonly deleted genes in the genome.
METHODS
To study the effect of UGT2B17 and UGT2B28 copy number variation (CNV) on CRC risk, 665 Caucasian CRC cases and 621 Caucasian controls were genotyped who had completed extensive demographics and lifestyle questionnaires.
RESULTS
A significant association between the UGT2B17 deletion genotype (0/0) and decreased CRC risk was found when the entire population was analyzed (P = .044). Stratification by sex yielded a decreased risk (P = .020) in men with the UGT2B17 deletion (0/0), but no association was observed in women (P = .724). A significant association between UGT2B17 (0/0) and decreased risk for rectal (P = .0065) but not colon cancer was found. No significant association was found between UGT2B28 CNV and CRC risk.
CONCLUSIONS
The UGT2B17 deletion genotype (0/0) was associated with a decreased CRC risk in a Caucasian population. After sex stratification, the association was observed in men but not in women, which is consistent with previous findings that men have higher UGT2B17 expression and activity than women. Because UGT2B17 metabolizes certain nonsteroidal anti‐inflammatory drugs and flavonoids with antioxidative properties, individuals with a gene deletion may have higher levels of these protective dietary components. Cancer 2013;119:2477‐2485. © 2013 American Cancer Society.
UGT2B17 and UGT2B28 are 2 of the most commonly deleted genes in the human genome and are metabolizers of environmental and endogenous compounds. This study found that the UGT2B17 gene deletion is associated with decreased colorectal cancer risk, suggesting a protective function for the UGT2B17 gene, because individuals without the gene may have higher circulating levels of flavonoids and nonsteroidal anti‐inflammatory drugs.</abstract><cop>United States</cop><pmid>23575887</pmid><doi>10.1002/cncr.28009</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adult Aged Antiinflammatory agents Case-Control Studies Colonic Neoplasms - genetics colorectal cancer risk Colorectal Neoplasms - enzymology Colorectal Neoplasms - epidemiology Colorectal Neoplasms - genetics copy number variation DNA Copy Number Variations European Continental Ancestry Group - genetics Female Gene Deletion Genetic Predisposition to Disease Genotype Glucuronosyltransferase - genetics Humans Male Meat - adverse effects Meat Products - adverse effects Metabolic Detoxication, Phase II - genetics Middle Aged Minor Histocompatibility Antigens Pennsylvania - epidemiology phase II detoxification Rectal Neoplasms - genetics Risk Factors Sex Factors Surveys and Questionnaires UGT2B17 UGT2B28 |
| title | The effect of copy number variation in the phase II detoxification genes UGT2B17 and UGT2B28 on colorectal cancer risk |
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