PPAR-alpha L162V polymorphism in human hepatocellular carcinoma
Several lines of evidence suggest that peroxisome proliferator-activated receptor alpha may be involved in hepatocarcinogenesis. L162V polymorphism of the peroxisome proliferator-activated receptor alpha gene enhances the transactivation activity of this transcription factor. The aim of this study w...
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| Veröffentlicht in: | The Turkish journal of gastroenterology 2008-12, Vol.19 (4), p.245-249 |
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| creator | Koytak, Elif Sare Mizrak, Dilşa Bektaş, Mehmet Verdi, Hasibe Arslan Ergül, Ayça Idilman, Ramazan Cinar, Kubilay Yurdaydin, Cihan Ersõz, Sadik Karayalçin, Kaan Uzunalimoğlu, Ozden Bozkaya, Hakan |
| description | Several lines of evidence suggest that peroxisome proliferator-activated receptor alpha may be involved in hepatocarcinogenesis. L162V polymorphism of the peroxisome proliferator-activated receptor alpha gene enhances the transactivation activity of this transcription factor. The aim of this study was to determine the frequency and clinical correlates of peroxisome proliferator-activated receptor alpha L162V polymorphism in hepatitis virus-induced hepatocellular carcinoma.
90 hepatocellular carcinoma patients diagnosed at Ankara University Gastroenterology Clinic between January 2002 and July 2003 and 80 healthy controls with normal body mass index, blood chemistry and with negative viral serology were included. peroxisome proliferator-activated receptor alpha L162V polymorphism was determined by PCR-RFLP.
hepatocellular carcinoma etiologies were as follows: 56 HBV, 12 HBV+HDV, 22 HCV. Eighty-seven patients (97%) were cirrhotic, and 60 patients (67.5%) had advanced tumors. In 83 (92%) of 90 hepatocellular carcinoma patients, gene segment including polymorphic region could be amplified by PCR (50 HBV, 12 HBV+HDV, 21 HCV) and 6 of them (7.2%, all infected with HBV) had L162V polymorphism, while 2 (2.5%) of 80 controls had this polymorphism (p=0.162). This trend became more remarkable when only HBV (HBV+HDV)-infected patients were compared with controls (6/62, 9.7% vs. 2/80, 2.5%, respectively, p=0.071). Five of 6 patients with L162V had advanced disease.
Peroxisome proliferator-activated receptor alpha L162V polymorphism tends to occur in HBV-induced hepatocellular carcinoma and is absent in HCV-related hepatocellular carcinoma. These findings may show clues for the existence of different carcinogenesis mechanisms in these two common etiologies. Frequent occurrence of advanced disease in patients with L162V polymorphism suggests a role for this polymorphism in tumor progression. |
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| fullrecord | <record><control><sourceid>pubmed_ulakb</sourceid><recordid>TN_cdi_ulakbim_primary_97276</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19119483</sourcerecordid><originalsourceid>FETCH-LOGICAL-p230t-8467b0e3002b2c3c908a50b025ee912f2b19d5e656ffd040ffdd6aeba301030c3</originalsourceid><addsrcrecordid>eNo9j11LwzAUhoMork7_gUj-QOAkadPmSsbwCwoO2bwdJ2lKq8ka2vVi_97A1JvnwHngPee9IJngecUKBeUlybgEYLnOqwW5maYvAFlxJa7JgmvO01pm5HGzWX0w9LFDWif5SePgT2EYY9dPgfYH2s0BE13E42Cd97PHkVocbX8YAt6Sqxb95O5-55Lsnp-261dWv7-8rVc1i0LCkVW5Kg249I8wwkqrocICDIjCOc1FKwzXTeFUodq2gRwSG4XOoAQOEqxckvtzbjr_bfqwj2MfcDztdSlKlfTDWcfZBNf827-i8gc1P06y</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>PPAR-alpha L162V polymorphism in human hepatocellular carcinoma</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Koytak, Elif Sare ; Mizrak, Dilşa ; Bektaş, Mehmet ; Verdi, Hasibe ; Arslan Ergül, Ayça ; Idilman, Ramazan ; Cinar, Kubilay ; Yurdaydin, Cihan ; Ersõz, Sadik ; Karayalçin, Kaan ; Uzunalimoğlu, Ozden ; Bozkaya, Hakan</creator><creatorcontrib>Koytak, Elif Sare ; Mizrak, Dilşa ; Bektaş, Mehmet ; Verdi, Hasibe ; Arslan Ergül, Ayça ; Idilman, Ramazan ; Cinar, Kubilay ; Yurdaydin, Cihan ; Ersõz, Sadik ; Karayalçin, Kaan ; Uzunalimoğlu, Ozden ; Bozkaya, Hakan</creatorcontrib><description>Several lines of evidence suggest that peroxisome proliferator-activated receptor alpha may be involved in hepatocarcinogenesis. L162V polymorphism of the peroxisome proliferator-activated receptor alpha gene enhances the transactivation activity of this transcription factor. The aim of this study was to determine the frequency and clinical correlates of peroxisome proliferator-activated receptor alpha L162V polymorphism in hepatitis virus-induced hepatocellular carcinoma.
90 hepatocellular carcinoma patients diagnosed at Ankara University Gastroenterology Clinic between January 2002 and July 2003 and 80 healthy controls with normal body mass index, blood chemistry and with negative viral serology were included. peroxisome proliferator-activated receptor alpha L162V polymorphism was determined by PCR-RFLP.
hepatocellular carcinoma etiologies were as follows: 56 HBV, 12 HBV+HDV, 22 HCV. Eighty-seven patients (97%) were cirrhotic, and 60 patients (67.5%) had advanced tumors. In 83 (92%) of 90 hepatocellular carcinoma patients, gene segment including polymorphic region could be amplified by PCR (50 HBV, 12 HBV+HDV, 21 HCV) and 6 of them (7.2%, all infected with HBV) had L162V polymorphism, while 2 (2.5%) of 80 controls had this polymorphism (p=0.162). This trend became more remarkable when only HBV (HBV+HDV)-infected patients were compared with controls (6/62, 9.7% vs. 2/80, 2.5%, respectively, p=0.071). Five of 6 patients with L162V had advanced disease.
Peroxisome proliferator-activated receptor alpha L162V polymorphism tends to occur in HBV-induced hepatocellular carcinoma and is absent in HCV-related hepatocellular carcinoma. These findings may show clues for the existence of different carcinogenesis mechanisms in these two common etiologies. Frequent occurrence of advanced disease in patients with L162V polymorphism suggests a role for this polymorphism in tumor progression.</description><identifier>ISSN: 1300-4948</identifier><identifier>EISSN: 2148-5607</identifier><identifier>PMID: 19119483</identifier><language>eng</language><publisher>Turkey: Türk Gastroenteroloji Vakfı</publisher><subject>Carcinoma, Hepatocellular ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - virology ; Case-Control Studies ; Digestive system diseases ; Female ; Hepatit B, kronik ; Hepatit C, kronik ; Hepatitis B, Chronic ; Hepatitis B, Chronic - complications ; Hepatitis C, Chronic ; Hepatitis C, Chronic - complications ; Humans ; Karaciğer neoplazmları ; Karsinom, hepatosellüler ; Liver Neoplasms ; Liver Neoplasms - genetics ; Liver Neoplasms - virology ; Male ; Neoplasms ; Neoplazmlar ; Olgu-kontrol çalışmaları ; Peroksizom prolifetör-aktive reseptörler ; Peroxisome Proliferator-Activated Receptors ; Peroxisome Proliferator-Activated Receptors - genetics ; Polimeraz zincir reaksiyonu ; Polimorfizm, genetik ; Polimorfizm, kesim parçacığı uzunluk ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Sindirim sistemi hastalıkları ; Virus diseases ; Virüs hastalıkları</subject><ispartof>The Turkish journal of gastroenterology, 2008-12, Vol.19 (4), p.245-249</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19119483$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koytak, Elif Sare</creatorcontrib><creatorcontrib>Mizrak, Dilşa</creatorcontrib><creatorcontrib>Bektaş, Mehmet</creatorcontrib><creatorcontrib>Verdi, Hasibe</creatorcontrib><creatorcontrib>Arslan Ergül, Ayça</creatorcontrib><creatorcontrib>Idilman, Ramazan</creatorcontrib><creatorcontrib>Cinar, Kubilay</creatorcontrib><creatorcontrib>Yurdaydin, Cihan</creatorcontrib><creatorcontrib>Ersõz, Sadik</creatorcontrib><creatorcontrib>Karayalçin, Kaan</creatorcontrib><creatorcontrib>Uzunalimoğlu, Ozden</creatorcontrib><creatorcontrib>Bozkaya, Hakan</creatorcontrib><title>PPAR-alpha L162V polymorphism in human hepatocellular carcinoma</title><title>The Turkish journal of gastroenterology</title><addtitle>Turk J Gastroenterol</addtitle><description>Several lines of evidence suggest that peroxisome proliferator-activated receptor alpha may be involved in hepatocarcinogenesis. L162V polymorphism of the peroxisome proliferator-activated receptor alpha gene enhances the transactivation activity of this transcription factor. The aim of this study was to determine the frequency and clinical correlates of peroxisome proliferator-activated receptor alpha L162V polymorphism in hepatitis virus-induced hepatocellular carcinoma.
90 hepatocellular carcinoma patients diagnosed at Ankara University Gastroenterology Clinic between January 2002 and July 2003 and 80 healthy controls with normal body mass index, blood chemistry and with negative viral serology were included. peroxisome proliferator-activated receptor alpha L162V polymorphism was determined by PCR-RFLP.
hepatocellular carcinoma etiologies were as follows: 56 HBV, 12 HBV+HDV, 22 HCV. Eighty-seven patients (97%) were cirrhotic, and 60 patients (67.5%) had advanced tumors. In 83 (92%) of 90 hepatocellular carcinoma patients, gene segment including polymorphic region could be amplified by PCR (50 HBV, 12 HBV+HDV, 21 HCV) and 6 of them (7.2%, all infected with HBV) had L162V polymorphism, while 2 (2.5%) of 80 controls had this polymorphism (p=0.162). This trend became more remarkable when only HBV (HBV+HDV)-infected patients were compared with controls (6/62, 9.7% vs. 2/80, 2.5%, respectively, p=0.071). Five of 6 patients with L162V had advanced disease.
Peroxisome proliferator-activated receptor alpha L162V polymorphism tends to occur in HBV-induced hepatocellular carcinoma and is absent in HCV-related hepatocellular carcinoma. These findings may show clues for the existence of different carcinogenesis mechanisms in these two common etiologies. Frequent occurrence of advanced disease in patients with L162V polymorphism suggests a role for this polymorphism in tumor progression.</description><subject>Carcinoma, Hepatocellular</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - virology</subject><subject>Case-Control Studies</subject><subject>Digestive system diseases</subject><subject>Female</subject><subject>Hepatit B, kronik</subject><subject>Hepatit C, kronik</subject><subject>Hepatitis B, Chronic</subject><subject>Hepatitis B, Chronic - complications</subject><subject>Hepatitis C, Chronic</subject><subject>Hepatitis C, Chronic - complications</subject><subject>Humans</subject><subject>Karaciğer neoplazmları</subject><subject>Karsinom, hepatosellüler</subject><subject>Liver Neoplasms</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - virology</subject><subject>Male</subject><subject>Neoplasms</subject><subject>Neoplazmlar</subject><subject>Olgu-kontrol çalışmaları</subject><subject>Peroksizom prolifetör-aktive reseptörler</subject><subject>Peroxisome Proliferator-Activated Receptors</subject><subject>Peroxisome Proliferator-Activated Receptors - genetics</subject><subject>Polimeraz zincir reaksiyonu</subject><subject>Polimorfizm, genetik</subject><subject>Polimorfizm, kesim parçacığı uzunluk</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Sindirim sistemi hastalıkları</subject><subject>Virus diseases</subject><subject>Virüs hastalıkları</subject><issn>1300-4948</issn><issn>2148-5607</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9j11LwzAUhoMork7_gUj-QOAkadPmSsbwCwoO2bwdJ2lKq8ka2vVi_97A1JvnwHngPee9IJngecUKBeUlybgEYLnOqwW5maYvAFlxJa7JgmvO01pm5HGzWX0w9LFDWif5SePgT2EYY9dPgfYH2s0BE13E42Cd97PHkVocbX8YAt6Sqxb95O5-55Lsnp-261dWv7-8rVc1i0LCkVW5Kg249I8wwkqrocICDIjCOc1FKwzXTeFUodq2gRwSG4XOoAQOEqxckvtzbjr_bfqwj2MfcDztdSlKlfTDWcfZBNf827-i8gc1P06y</recordid><startdate>20081201</startdate><enddate>20081201</enddate><creator>Koytak, Elif Sare</creator><creator>Mizrak, Dilşa</creator><creator>Bektaş, Mehmet</creator><creator>Verdi, Hasibe</creator><creator>Arslan Ergül, Ayça</creator><creator>Idilman, Ramazan</creator><creator>Cinar, Kubilay</creator><creator>Yurdaydin, Cihan</creator><creator>Ersõz, Sadik</creator><creator>Karayalçin, Kaan</creator><creator>Uzunalimoğlu, Ozden</creator><creator>Bozkaya, Hakan</creator><general>Türk Gastroenteroloji Vakfı</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>GIY</scope><scope>GIZ</scope><scope>GJA</scope><scope>GJB</scope></search><sort><creationdate>20081201</creationdate><title>PPAR-alpha L162V polymorphism in human hepatocellular carcinoma</title><author>Koytak, Elif Sare ; Mizrak, Dilşa ; Bektaş, Mehmet ; Verdi, Hasibe ; Arslan Ergül, Ayça ; Idilman, Ramazan ; Cinar, Kubilay ; Yurdaydin, Cihan ; Ersõz, Sadik ; Karayalçin, Kaan ; Uzunalimoğlu, Ozden ; Bozkaya, Hakan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p230t-8467b0e3002b2c3c908a50b025ee912f2b19d5e656ffd040ffdd6aeba301030c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Carcinoma, Hepatocellular</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - virology</topic><topic>Case-Control Studies</topic><topic>Digestive system diseases</topic><topic>Female</topic><topic>Hepatit B, kronik</topic><topic>Hepatit C, kronik</topic><topic>Hepatitis B, Chronic</topic><topic>Hepatitis B, Chronic - complications</topic><topic>Hepatitis C, Chronic</topic><topic>Hepatitis C, Chronic - complications</topic><topic>Humans</topic><topic>Karaciğer neoplazmları</topic><topic>Karsinom, hepatosellüler</topic><topic>Liver Neoplasms</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - virology</topic><topic>Male</topic><topic>Neoplasms</topic><topic>Neoplazmlar</topic><topic>Olgu-kontrol çalışmaları</topic><topic>Peroksizom prolifetör-aktive reseptörler</topic><topic>Peroxisome Proliferator-Activated Receptors</topic><topic>Peroxisome Proliferator-Activated Receptors - genetics</topic><topic>Polimeraz zincir reaksiyonu</topic><topic>Polimorfizm, genetik</topic><topic>Polimorfizm, kesim parçacığı uzunluk</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Genetic</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Sindirim sistemi hastalıkları</topic><topic>Virus diseases</topic><topic>Virüs hastalıkları</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koytak, Elif Sare</creatorcontrib><creatorcontrib>Mizrak, Dilşa</creatorcontrib><creatorcontrib>Bektaş, Mehmet</creatorcontrib><creatorcontrib>Verdi, Hasibe</creatorcontrib><creatorcontrib>Arslan Ergül, Ayça</creatorcontrib><creatorcontrib>Idilman, Ramazan</creatorcontrib><creatorcontrib>Cinar, Kubilay</creatorcontrib><creatorcontrib>Yurdaydin, Cihan</creatorcontrib><creatorcontrib>Ersõz, Sadik</creatorcontrib><creatorcontrib>Karayalçin, Kaan</creatorcontrib><creatorcontrib>Uzunalimoğlu, Ozden</creatorcontrib><creatorcontrib>Bozkaya, Hakan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ULAKBIM - Mühendislik ve Temel Bilimler Veri Tabani</collection><collection>ULAKBIM - Yaşam Bilimleri Veri Tabani</collection><collection>ULAKBIM - Turk Sosyal Bilimler Veri Tabani</collection><collection>ULAKBIM - Türk Tıp Veri Tabani</collection><jtitle>The Turkish journal of gastroenterology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koytak, Elif Sare</au><au>Mizrak, Dilşa</au><au>Bektaş, Mehmet</au><au>Verdi, Hasibe</au><au>Arslan Ergül, Ayça</au><au>Idilman, Ramazan</au><au>Cinar, Kubilay</au><au>Yurdaydin, Cihan</au><au>Ersõz, Sadik</au><au>Karayalçin, Kaan</au><au>Uzunalimoğlu, Ozden</au><au>Bozkaya, Hakan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PPAR-alpha L162V polymorphism in human hepatocellular carcinoma</atitle><jtitle>The Turkish journal of gastroenterology</jtitle><addtitle>Turk J Gastroenterol</addtitle><date>2008-12-01</date><risdate>2008</risdate><volume>19</volume><issue>4</issue><spage>245</spage><epage>249</epage><pages>245-249</pages><issn>1300-4948</issn><eissn>2148-5607</eissn><abstract>Several lines of evidence suggest that peroxisome proliferator-activated receptor alpha may be involved in hepatocarcinogenesis. L162V polymorphism of the peroxisome proliferator-activated receptor alpha gene enhances the transactivation activity of this transcription factor. The aim of this study was to determine the frequency and clinical correlates of peroxisome proliferator-activated receptor alpha L162V polymorphism in hepatitis virus-induced hepatocellular carcinoma.
90 hepatocellular carcinoma patients diagnosed at Ankara University Gastroenterology Clinic between January 2002 and July 2003 and 80 healthy controls with normal body mass index, blood chemistry and with negative viral serology were included. peroxisome proliferator-activated receptor alpha L162V polymorphism was determined by PCR-RFLP.
hepatocellular carcinoma etiologies were as follows: 56 HBV, 12 HBV+HDV, 22 HCV. Eighty-seven patients (97%) were cirrhotic, and 60 patients (67.5%) had advanced tumors. In 83 (92%) of 90 hepatocellular carcinoma patients, gene segment including polymorphic region could be amplified by PCR (50 HBV, 12 HBV+HDV, 21 HCV) and 6 of them (7.2%, all infected with HBV) had L162V polymorphism, while 2 (2.5%) of 80 controls had this polymorphism (p=0.162). This trend became more remarkable when only HBV (HBV+HDV)-infected patients were compared with controls (6/62, 9.7% vs. 2/80, 2.5%, respectively, p=0.071). Five of 6 patients with L162V had advanced disease.
Peroxisome proliferator-activated receptor alpha L162V polymorphism tends to occur in HBV-induced hepatocellular carcinoma and is absent in HCV-related hepatocellular carcinoma. These findings may show clues for the existence of different carcinogenesis mechanisms in these two common etiologies. Frequent occurrence of advanced disease in patients with L162V polymorphism suggests a role for this polymorphism in tumor progression.</abstract><cop>Turkey</cop><pub>Türk Gastroenteroloji Vakfı</pub><pmid>19119483</pmid><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Carcinoma, Hepatocellular Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - virology Case-Control Studies Digestive system diseases Female Hepatit B, kronik Hepatit C, kronik Hepatitis B, Chronic Hepatitis B, Chronic - complications Hepatitis C, Chronic Hepatitis C, Chronic - complications Humans Karaciğer neoplazmları Karsinom, hepatosellüler Liver Neoplasms Liver Neoplasms - genetics Liver Neoplasms - virology Male Neoplasms Neoplazmlar Olgu-kontrol çalışmaları Peroksizom prolifetör-aktive reseptörler Peroxisome Proliferator-Activated Receptors Peroxisome Proliferator-Activated Receptors - genetics Polimeraz zincir reaksiyonu Polimorfizm, genetik Polimorfizm, kesim parçacığı uzunluk Polymerase Chain Reaction Polymorphism, Genetic Polymorphism, Restriction Fragment Length Sindirim sistemi hastalıkları Virus diseases Virüs hastalıkları |
| title | PPAR-alpha L162V polymorphism in human hepatocellular carcinoma |
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