Cancer and Molecular Biomarkers of Phase 2
Associations between genotypes of phase 2 enzymes and cancer risk are extracted from epidemiological studies, namely case–control studies. Variant alleles in glutathione S‐transferase (GST), UDP‐glucuronosyltransferase (UGT), sulfotransferase (SULT), and N‐acetyltransferase (NAT) have been used as m...
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Veröffentlicht in: | Methods in Enzymology 2005, Vol.400, p.618-627 |
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creator | Dalhoff, Kim Buus Jensen, Kaspar Enghusen Poulsen, Henrik |
description | Associations between genotypes of phase 2 enzymes and cancer risk are extracted from epidemiological studies, namely case–control studies. Variant alleles in glutathione
S‐transferase (GST), UDP‐glucuronosyltransferase (UGT), sulfotransferase (SULT), and
N‐acetyltransferase (NAT) have been used as molecular genetic biomarkers of risk. GSTM(my)1 has been associated with an increased risk of colorectal cancer, lung cancer, and bladder cancer and GSTP(pi)1 with prostate cancer. UGT1A1*28 and *37 are both associated with an increased risk of breast cancer as is SULT1A1*2. The presence of UGT1A1*28 results in an increased risk of ovarian cancer and NAT2 of colorectal and lung cancer. A high frequency of SULT1A1*1 has been identified in patients with breast cancer; the role in colorectal cancer is more controversial. This chapter discusses the balance between carcinogen activation and detoxification in relation to phase 2 enzymes. |
doi_str_mv | 10.1016/S0076-6879(05)00035-2 |
format | Article |
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N‐acetyltransferase (NAT) have been used as molecular genetic biomarkers of risk. GSTM(my)1 has been associated with an increased risk of colorectal cancer, lung cancer, and bladder cancer and GSTP(pi)1 with prostate cancer. UGT1A1*28 and *37 are both associated with an increased risk of breast cancer as is SULT1A1*2. The presence of UGT1A1*28 results in an increased risk of ovarian cancer and NAT2 of colorectal and lung cancer. A high frequency of SULT1A1*1 has been identified in patients with breast cancer; the role in colorectal cancer is more controversial. This chapter discusses the balance between carcinogen activation and detoxification in relation to phase 2 enzymes.</description><identifier>ISSN: 0076-6879</identifier><identifier>ISBN: 0121828050</identifier><identifier>ISBN: 9780121828059</identifier><identifier>EISSN: 1557-7988</identifier><identifier>DOI: 10.1016/S0076-6879(05)00035-2</identifier><identifier>PMID: 16399374</identifier><language>eng</language><publisher>United States: Elsevier Science & Technology</publisher><subject>Acetyltransferases - genetics ; Acetyltransferases - metabolism ; Biomarkers, Tumor ; Genetic Predisposition to Disease ; Glucuronosyltransferase - genetics ; Glucuronosyltransferase - metabolism ; Glutathione Transferase - genetics ; Glutathione Transferase - metabolism ; Humans ; Inactivation, Metabolic ; Neoplasms - genetics ; Odds Ratio ; Polymorphism, Genetic ; Sulfotransferases - genetics ; Sulfotransferases - metabolism ; Transferases - genetics ; Transferases - metabolism</subject><ispartof>Methods in Enzymology, 2005, Vol.400, p.618-627</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c317t-47597006fafcfd233aad3d0cc7427e1ab8b5f77242b721afe62781640cc722683</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0076-6879(05)00035-2$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,779,780,784,793,3459,3550,4024,11288,27923,27924,27925,45810,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16399374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dalhoff, Kim</creatorcontrib><creatorcontrib>Buus Jensen, Kaspar</creatorcontrib><creatorcontrib>Enghusen Poulsen, Henrik</creatorcontrib><title>Cancer and Molecular Biomarkers of Phase 2</title><title>Methods in Enzymology</title><addtitle>Methods Enzymol</addtitle><description>Associations between genotypes of phase 2 enzymes and cancer risk are extracted from epidemiological studies, namely case–control studies. Variant alleles in glutathione
S‐transferase (GST), UDP‐glucuronosyltransferase (UGT), sulfotransferase (SULT), and
N‐acetyltransferase (NAT) have been used as molecular genetic biomarkers of risk. GSTM(my)1 has been associated with an increased risk of colorectal cancer, lung cancer, and bladder cancer and GSTP(pi)1 with prostate cancer. UGT1A1*28 and *37 are both associated with an increased risk of breast cancer as is SULT1A1*2. The presence of UGT1A1*28 results in an increased risk of ovarian cancer and NAT2 of colorectal and lung cancer. A high frequency of SULT1A1*1 has been identified in patients with breast cancer; the role in colorectal cancer is more controversial. This chapter discusses the balance between carcinogen activation and detoxification in relation to phase 2 enzymes.</description><subject>Acetyltransferases - genetics</subject><subject>Acetyltransferases - metabolism</subject><subject>Biomarkers, Tumor</subject><subject>Genetic Predisposition to Disease</subject><subject>Glucuronosyltransferase - genetics</subject><subject>Glucuronosyltransferase - metabolism</subject><subject>Glutathione Transferase - genetics</subject><subject>Glutathione Transferase - metabolism</subject><subject>Humans</subject><subject>Inactivation, Metabolic</subject><subject>Neoplasms - genetics</subject><subject>Odds Ratio</subject><subject>Polymorphism, Genetic</subject><subject>Sulfotransferases - genetics</subject><subject>Sulfotransferases - metabolism</subject><subject>Transferases - genetics</subject><subject>Transferases - metabolism</subject><issn>0076-6879</issn><issn>1557-7988</issn><isbn>0121828050</isbn><isbn>9780121828059</isbn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kFtLAzEQRoMX7EV_grKPKqzOJJtM9qlo8QYVBfU5ZHPB1bZbsq3gv3fbqk_zchjOdxg7RrhAQHX5AkAqV5rKU5BnACBkzndYH6WknEqtd9kAkKPmGiTssf4_32ODtv0A4KRLPGA9VKIsBRV9dj62cxdSZuc-e2ymwa2mNmXXdTOz6TOkNmti9vxu25DxQ7Yf7bQNR793yN5ub17H9_nk6e5hfDXJnUBa5gXJkgBUtNFFz4Ww1gsPzlHBKaCtdCUjES94RRxtDKqzQlWsCc6VFkN2sv27WFWz4M0i1Z3Mt_mT7oDRFgidxVcdkmldHboZvk7BLY1vaoNg1s3MpplZNzAgzaaZ4eIHIu1YuQ</recordid><startdate>2005</startdate><enddate>2005</enddate><creator>Dalhoff, Kim</creator><creator>Buus Jensen, Kaspar</creator><creator>Enghusen Poulsen, Henrik</creator><general>Elsevier Science & Technology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>2005</creationdate><title>Cancer and Molecular Biomarkers of Phase 2</title><author>Dalhoff, Kim ; Buus Jensen, Kaspar ; Enghusen Poulsen, Henrik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c317t-47597006fafcfd233aad3d0cc7427e1ab8b5f77242b721afe62781640cc722683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acetyltransferases - genetics</topic><topic>Acetyltransferases - metabolism</topic><topic>Biomarkers, Tumor</topic><topic>Genetic Predisposition to Disease</topic><topic>Glucuronosyltransferase - genetics</topic><topic>Glucuronosyltransferase - metabolism</topic><topic>Glutathione Transferase - genetics</topic><topic>Glutathione Transferase - metabolism</topic><topic>Humans</topic><topic>Inactivation, Metabolic</topic><topic>Neoplasms - genetics</topic><topic>Odds Ratio</topic><topic>Polymorphism, Genetic</topic><topic>Sulfotransferases - genetics</topic><topic>Sulfotransferases - metabolism</topic><topic>Transferases - genetics</topic><topic>Transferases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dalhoff, Kim</creatorcontrib><creatorcontrib>Buus Jensen, Kaspar</creatorcontrib><creatorcontrib>Enghusen Poulsen, Henrik</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Methods in Enzymology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dalhoff, Kim</au><au>Buus Jensen, Kaspar</au><au>Enghusen Poulsen, Henrik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer and Molecular Biomarkers of Phase 2</atitle><jtitle>Methods in Enzymology</jtitle><addtitle>Methods Enzymol</addtitle><date>2005</date><risdate>2005</risdate><volume>400</volume><spage>618</spage><epage>627</epage><pages>618-627</pages><issn>0076-6879</issn><eissn>1557-7988</eissn><isbn>0121828050</isbn><isbn>9780121828059</isbn><abstract>Associations between genotypes of phase 2 enzymes and cancer risk are extracted from epidemiological studies, namely case–control studies. Variant alleles in glutathione
S‐transferase (GST), UDP‐glucuronosyltransferase (UGT), sulfotransferase (SULT), and
N‐acetyltransferase (NAT) have been used as molecular genetic biomarkers of risk. GSTM(my)1 has been associated with an increased risk of colorectal cancer, lung cancer, and bladder cancer and GSTP(pi)1 with prostate cancer. UGT1A1*28 and *37 are both associated with an increased risk of breast cancer as is SULT1A1*2. The presence of UGT1A1*28 results in an increased risk of ovarian cancer and NAT2 of colorectal and lung cancer. A high frequency of SULT1A1*1 has been identified in patients with breast cancer; the role in colorectal cancer is more controversial. This chapter discusses the balance between carcinogen activation and detoxification in relation to phase 2 enzymes.</abstract><cop>United States</cop><pub>Elsevier Science & Technology</pub><pmid>16399374</pmid><doi>10.1016/S0076-6879(05)00035-2</doi><tpages>10</tpages></addata></record> |
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subjects | Acetyltransferases - genetics Acetyltransferases - metabolism Biomarkers, Tumor Genetic Predisposition to Disease Glucuronosyltransferase - genetics Glucuronosyltransferase - metabolism Glutathione Transferase - genetics Glutathione Transferase - metabolism Humans Inactivation, Metabolic Neoplasms - genetics Odds Ratio Polymorphism, Genetic Sulfotransferases - genetics Sulfotransferases - metabolism Transferases - genetics Transferases - metabolism |
title | Cancer and Molecular Biomarkers of Phase 2 |
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