Deletion and Single Nucleotide Polymorphisms in Common Glutathione-S Transferases Contribute to Colorectal Cancer Development
Glutathione-S transferases (GSTs) are xenobiotic-conjugation enzymes involved in the detoxification process of heterocyclic aromatic amines and polycyclic aromatic hydrocarbons, widely recognized risk factors of colorectal cancer (CRC) development. Polymorphism in GSTs often leads to alteration or c...
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| Veröffentlicht in: | Pathology oncology research 2019-10, Vol.25 (4), p.1579-1587 |
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| creator | Stojkovic Lalosevic, Milica Lj Coric, Vesna M. Pekmezovic, Tatjana D. Simic, Tatjana P. Pljesa Ercegovac, Marija S. Pavlovic Markovic, Aleksandra R. Krivokapic, Zoran V. |
| description | Glutathione-S transferases (GSTs) are xenobiotic-conjugation enzymes involved in the detoxification process of heterocyclic aromatic amines and polycyclic aromatic hydrocarbons, widely recognized risk factors of colorectal cancer (CRC) development. Polymorphism in GSTs often leads to alteration or complete lack of enzyme activity, which might have an effect on CRC carcinogenesis. Aim of this study was to investigate GST gene variants as risk factors in patients with CRC. A total of 523 CRC patients administered for surgical resection and 400 matched controls were included. Deletion polymorphism of GSTs M1 and T1 was investigated by polymerase chain reaction. Single nucleotide polymorphism of GST A1 and P1 was investigated by restriction fragment length polymorphism method. The association between GST genotype and risk of CRC development was found in carriers of GSTT1-null and GSTP1-variant genotypes individually (
p
= 0.050 and
p
= 0.016, respectively). Furthermore, statistically significant association was found when combination of GSTP1-variant genotype with any of other three common GST genotypes was analyzed with respect to CRC susceptibility. Additionally, patients with combined GSTM1-null/GSTT1-null/GSTA1 low-activity/GSTP1-variant genotype showed 2.71-fold increased risk of developing CRC (
p
= 0.037). This study supports hypothesis that GST polymorphisms might have an important role in the process of the CRC development. Additionally, GSTM1-null/ GSTT1-null/ GSTA1 low-activity/ GSTP1-variant genotype could be combination of GST genotypes whose carriers are more prone to CRC development. |
| doi_str_mv | 10.1007/s12253-019-00589-1 |
| format | Article |
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p
= 0.050 and
p
= 0.016, respectively). Furthermore, statistically significant association was found when combination of GSTP1-variant genotype with any of other three common GST genotypes was analyzed with respect to CRC susceptibility. Additionally, patients with combined GSTM1-null/GSTT1-null/GSTA1 low-activity/GSTP1-variant genotype showed 2.71-fold increased risk of developing CRC (
p
= 0.037). This study supports hypothesis that GST polymorphisms might have an important role in the process of the CRC development. Additionally, GSTM1-null/ GSTT1-null/ GSTA1 low-activity/ GSTP1-variant genotype could be combination of GST genotypes whose carriers are more prone to CRC development.</description><identifier>ISSN: 1219-4956</identifier><identifier>EISSN: 1532-2807</identifier><identifier>DOI: 10.1007/s12253-019-00589-1</identifier><identifier>PMID: 30694518</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Amines ; Biomarkers, Tumor - genetics ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Carcinogenesis ; Case-Control Studies ; Clonal deletion ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Detoxification ; Enzymatic activity ; Female ; Follow-Up Studies ; Gene deletion ; Gene polymorphism ; Genetic Predisposition to Disease ; Genotype ; Genotype & phenotype ; Genotypes ; Glutathione ; Glutathione S-Transferase pi - genetics ; Glutathione transferase ; Glutathione Transferase - genetics ; GSTM1 protein ; GSTT1 protein ; Health risks ; Humans ; Immunology ; Male ; Middle Aged ; Oncology ; Original Article ; Pathology ; Polycyclic aromatic hydrocarbons ; Polymerase chain reaction ; Polymorphism ; Polymorphism, Single Nucleotide ; Prognosis ; Restriction fragment length polymorphism ; Risk Factors ; Sequence Deletion ; Single-nucleotide polymorphism ; Statistical analysis</subject><ispartof>Pathology oncology research, 2019-10, Vol.25 (4), p.1579-1587</ispartof><rights>Arányi Lajos Foundation 2019</rights><rights>Pathology & Oncology Research is a copyright of Springer, (2019). All Rights Reserved.</rights><rights>Copyright Springer Nature B.V. 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c403t-84a85beace26383a4c7b7afb73cf02884cb9d0f9e57b2fb91f349270df546e003</citedby><cites>FETCH-LOGICAL-c403t-84a85beace26383a4c7b7afb73cf02884cb9d0f9e57b2fb91f349270df546e003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12253-019-00589-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12253-019-00589-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,782,786,27931,27932,41495,42564,51326</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30694518$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stojkovic Lalosevic, Milica Lj</creatorcontrib><creatorcontrib>Coric, Vesna M.</creatorcontrib><creatorcontrib>Pekmezovic, Tatjana D.</creatorcontrib><creatorcontrib>Simic, Tatjana P.</creatorcontrib><creatorcontrib>Pljesa Ercegovac, Marija S.</creatorcontrib><creatorcontrib>Pavlovic Markovic, Aleksandra R.</creatorcontrib><creatorcontrib>Krivokapic, Zoran V.</creatorcontrib><title>Deletion and Single Nucleotide Polymorphisms in Common Glutathione-S Transferases Contribute to Colorectal Cancer Development</title><title>Pathology oncology research</title><addtitle>Pathol. Oncol. Res</addtitle><addtitle>Pathol Oncol Res</addtitle><description>Glutathione-S transferases (GSTs) are xenobiotic-conjugation enzymes involved in the detoxification process of heterocyclic aromatic amines and polycyclic aromatic hydrocarbons, widely recognized risk factors of colorectal cancer (CRC) development. Polymorphism in GSTs often leads to alteration or complete lack of enzyme activity, which might have an effect on CRC carcinogenesis. Aim of this study was to investigate GST gene variants as risk factors in patients with CRC. A total of 523 CRC patients administered for surgical resection and 400 matched controls were included. Deletion polymorphism of GSTs M1 and T1 was investigated by polymerase chain reaction. Single nucleotide polymorphism of GST A1 and P1 was investigated by restriction fragment length polymorphism method. The association between GST genotype and risk of CRC development was found in carriers of GSTT1-null and GSTP1-variant genotypes individually (
p
= 0.050 and
p
= 0.016, respectively). Furthermore, statistically significant association was found when combination of GSTP1-variant genotype with any of other three common GST genotypes was analyzed with respect to CRC susceptibility. Additionally, patients with combined GSTM1-null/GSTT1-null/GSTA1 low-activity/GSTP1-variant genotype showed 2.71-fold increased risk of developing CRC (
p
= 0.037). This study supports hypothesis that GST polymorphisms might have an important role in the process of the CRC development. Additionally, GSTM1-null/ GSTT1-null/ GSTA1 low-activity/ GSTP1-variant genotype could be combination of GST genotypes whose carriers are more prone to CRC development.</description><subject>Amines</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinogenesis</subject><subject>Case-Control Studies</subject><subject>Clonal deletion</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Detoxification</subject><subject>Enzymatic activity</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gene deletion</subject><subject>Gene polymorphism</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Glutathione</subject><subject>Glutathione S-Transferase pi - genetics</subject><subject>Glutathione transferase</subject><subject>Glutathione Transferase - genetics</subject><subject>GSTM1 protein</subject><subject>GSTT1 protein</subject><subject>Health risks</subject><subject>Humans</subject><subject>Immunology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Polycyclic aromatic hydrocarbons</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prognosis</subject><subject>Restriction fragment length polymorphism</subject><subject>Risk Factors</subject><subject>Sequence Deletion</subject><subject>Single-nucleotide polymorphism</subject><subject>Statistical analysis</subject><issn>1219-4956</issn><issn>1532-2807</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kbtuFTEURUcIRB7wAxTIEvUEvx8luoGAFAFSQm15PMfJRB77YnuQUvDvGG6ALpWPddbep1jD8IrgM4KxelsJpYKNmJgRY6HNSJ4Mx0QwOlKN1dM-077iRsij4aTWO9xD0sjnwxHD0nBB9PHw8xwitCUn5NKMrpZ0EwF93nyE3JYZ0Ncc79dc9rdLXStaEtrlde30Rdyaa7c9COMVui4u1QDFVaidSK0s09YAtdx_MRfwzUW0c8lDQefwA2Ler5Dai-FZcLHCy4f3dPj24f317uN4-eXi0-7d5eg5Zm3U3GkxgfNAJdPMca8m5cKkmA-Yas39ZGYcDAg10TAZEhg3VOE5CC4BY3Y6vDn07kv-vkFt9i5vJfWTljKsjdRU6kcpoijXTEnRKXqgfMm1Fgh2X5bVlXtLsP3txR682O7F_vFiSQ-9fqjephXmf5G_IjrADkDtq3QD5f_tR2p_AVEGmd4</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Stojkovic Lalosevic, Milica Lj</creator><creator>Coric, Vesna M.</creator><creator>Pekmezovic, Tatjana D.</creator><creator>Simic, Tatjana P.</creator><creator>Pljesa Ercegovac, Marija S.</creator><creator>Pavlovic Markovic, Aleksandra R.</creator><creator>Krivokapic, Zoran V.</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20191001</creationdate><title>Deletion and Single Nucleotide Polymorphisms in Common Glutathione-S Transferases Contribute to Colorectal Cancer Development</title><author>Stojkovic Lalosevic, Milica Lj ; Coric, Vesna M. ; Pekmezovic, Tatjana D. ; Simic, Tatjana P. ; Pljesa Ercegovac, Marija S. ; Pavlovic Markovic, Aleksandra R. ; Krivokapic, Zoran V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c403t-84a85beace26383a4c7b7afb73cf02884cb9d0f9e57b2fb91f349270df546e003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Amines</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Carcinogenesis</topic><topic>Case-Control Studies</topic><topic>Clonal deletion</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Detoxification</topic><topic>Enzymatic activity</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gene deletion</topic><topic>Gene polymorphism</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Glutathione</topic><topic>Glutathione S-Transferase pi - genetics</topic><topic>Glutathione transferase</topic><topic>Glutathione Transferase - genetics</topic><topic>GSTM1 protein</topic><topic>GSTT1 protein</topic><topic>Health risks</topic><topic>Humans</topic><topic>Immunology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Polycyclic aromatic hydrocarbons</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prognosis</topic><topic>Restriction fragment length polymorphism</topic><topic>Risk Factors</topic><topic>Sequence Deletion</topic><topic>Single-nucleotide polymorphism</topic><topic>Statistical analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stojkovic Lalosevic, Milica Lj</creatorcontrib><creatorcontrib>Coric, Vesna M.</creatorcontrib><creatorcontrib>Pekmezovic, Tatjana D.</creatorcontrib><creatorcontrib>Simic, Tatjana P.</creatorcontrib><creatorcontrib>Pljesa Ercegovac, Marija S.</creatorcontrib><creatorcontrib>Pavlovic Markovic, Aleksandra R.</creatorcontrib><creatorcontrib>Krivokapic, Zoran V.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Pathology oncology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stojkovic Lalosevic, Milica Lj</au><au>Coric, Vesna M.</au><au>Pekmezovic, Tatjana D.</au><au>Simic, Tatjana P.</au><au>Pljesa Ercegovac, Marija S.</au><au>Pavlovic Markovic, Aleksandra R.</au><au>Krivokapic, Zoran V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deletion and Single Nucleotide Polymorphisms in Common Glutathione-S Transferases Contribute to Colorectal Cancer Development</atitle><jtitle>Pathology oncology research</jtitle><stitle>Pathol. Oncol. Res</stitle><addtitle>Pathol Oncol Res</addtitle><date>2019-10-01</date><risdate>2019</risdate><volume>25</volume><issue>4</issue><spage>1579</spage><epage>1587</epage><pages>1579-1587</pages><issn>1219-4956</issn><eissn>1532-2807</eissn><abstract>Glutathione-S transferases (GSTs) are xenobiotic-conjugation enzymes involved in the detoxification process of heterocyclic aromatic amines and polycyclic aromatic hydrocarbons, widely recognized risk factors of colorectal cancer (CRC) development. Polymorphism in GSTs often leads to alteration or complete lack of enzyme activity, which might have an effect on CRC carcinogenesis. Aim of this study was to investigate GST gene variants as risk factors in patients with CRC. A total of 523 CRC patients administered for surgical resection and 400 matched controls were included. Deletion polymorphism of GSTs M1 and T1 was investigated by polymerase chain reaction. Single nucleotide polymorphism of GST A1 and P1 was investigated by restriction fragment length polymorphism method. The association between GST genotype and risk of CRC development was found in carriers of GSTT1-null and GSTP1-variant genotypes individually (
p
= 0.050 and
p
= 0.016, respectively). Furthermore, statistically significant association was found when combination of GSTP1-variant genotype with any of other three common GST genotypes was analyzed with respect to CRC susceptibility. Additionally, patients with combined GSTM1-null/GSTT1-null/GSTA1 low-activity/GSTP1-variant genotype showed 2.71-fold increased risk of developing CRC (
p
= 0.037). This study supports hypothesis that GST polymorphisms might have an important role in the process of the CRC development. Additionally, GSTM1-null/ GSTT1-null/ GSTA1 low-activity/ GSTP1-variant genotype could be combination of GST genotypes whose carriers are more prone to CRC development.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>30694518</pmid><doi>10.1007/s12253-019-00589-1</doi><tpages>9</tpages></addata></record> |
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| subjects | Amines Biomarkers, Tumor - genetics Biomedical and Life Sciences Biomedicine Cancer Research Carcinogenesis Case-Control Studies Clonal deletion Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Detoxification Enzymatic activity Female Follow-Up Studies Gene deletion Gene polymorphism Genetic Predisposition to Disease Genotype Genotype & phenotype Genotypes Glutathione Glutathione S-Transferase pi - genetics Glutathione transferase Glutathione Transferase - genetics GSTM1 protein GSTT1 protein Health risks Humans Immunology Male Middle Aged Oncology Original Article Pathology Polycyclic aromatic hydrocarbons Polymerase chain reaction Polymorphism Polymorphism, Single Nucleotide Prognosis Restriction fragment length polymorphism Risk Factors Sequence Deletion Single-nucleotide polymorphism Statistical analysis |
| title | Deletion and Single Nucleotide Polymorphisms in Common Glutathione-S Transferases Contribute to Colorectal Cancer Development |
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