Loading…
EGF gene polymorphism and the risk of incident primary Melanoma
Overexpression of the epidermal growth factor (EGF) pathway has been implicated in melanoma pathogenesis, and a recent case-control study identified a single nucleotide polymorphism (G to A) in the EGF gene where the G allele was associated with increased EGF expression and an increased risk of mela...
Saved in:
Published in: | Cancer research (Chicago, Ill.) Ill.), 2004-04, Vol.64 (8), p.2668-2672 |
---|---|
Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c446t-5ffcea2319c28c0da1c0e15433ff20be1c729290994c2124f294a91ea4e7887f3 |
---|---|
cites | cdi_FETCH-LOGICAL-c446t-5ffcea2319c28c0da1c0e15433ff20be1c729290994c2124f294a91ea4e7887f3 |
container_end_page | 2672 |
container_issue | 8 |
container_start_page | 2668 |
container_title | Cancer research (Chicago, Ill.) |
container_volume | 64 |
creator | AMEND, Kandace L ELDER, James T TOMSHO, Lynn P BONNER, Joseph D JOHNSON, Timothy M SCHWARTZ, Jennifer BERWICK, Marianne GRUBER, Stephen B |
description | Overexpression of the epidermal growth factor (EGF) pathway has been implicated in melanoma pathogenesis, and a recent case-control study identified a single nucleotide polymorphism (G to A) in the EGF gene where the G allele was associated with increased EGF expression and an increased risk of melanoma. To further evaluate this association, we conducted a case-control analysis from the Genes, Environment, and Melanoma study at the University of Michigan site using two different study designs. Incident cases of histopathologically confirmed first primary melanoma that were diagnosed between January 1, 2000 and December 31, 2000 from the University of Michigan Melanoma Clinic (n = 330) were compared with the following two different sources of nonmelanoma controls: spouse/friend controls (n = 84) and healthy volunteer controls from a case-control study of psoriasis (n = 148). Using a second analytic design, comparisons between multiple primary melanoma cases (n = 62) and single primary melanoma cases (n = 330) were also evaluated to estimate odds ratios (ORs). Genotyping for the single nucleotide substitution (G to A) at position 61 in the 5' untranslated region of the EGF gene was performed from genomic DNA, and epidemiological risk factors were assessed through a telephone interview. When EGF genotypes were compared between incident primary melanoma cases and the nonmelanoma controls, the risk associated with the homozygous G/G genotype was not statistically significantly associated with an increased risk for incident primary melanoma compared with the homozygous A/A genotype [OR, 1.09; 95% confidence interval (CI); 0.65-1.85]. No strong associations with EGF G/G genotype were observed in comparisons of multiple primary and single primary melanoma cases (OR, 0.66; 95% CI; 0.25-1.73). Case subjects with tumors >/=3.5 mm compared with those |
doi_str_mv | 10.1158/0008-5472.CAN-03-3855 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71835251</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71835251</sourcerecordid><originalsourceid>FETCH-LOGICAL-c446t-5ffcea2319c28c0da1c0e15433ff20be1c729290994c2124f294a91ea4e7887f3</originalsourceid><addsrcrecordid>eNqFkLtOwzAUhi0EoqXwCCAvsAV8O7E9oapqC1KBBWbLdWwayKXE6dC3J1EjYGM6OtL3n8uH0CUlt5SCuiOEqASEZLez6XNCeMIVwBEaU-AqkULAMRr_MCN0FuNH1wIlcIpGFIiSXKZjdD9fLvC7rzze1sW-rJvtJo8ltlWG243HTR4_cR1wXrk881WLt01e2maPn3xhq7q05-gk2CL6i6FO0Nti_jp7SFYvy8fZdJU4IdI2gRCct4xT7ZhyJLPUEU9BcB4CI2tPnWSaaaK1cIwyEZgWVlNvhZdKycAn6OYwd9vUXzsfW1Pm0fmiu8LXu2gkVRwY0H9BKmWqCOgOhAPomjrGxgcz_GYoMb1i0-szvT7TKTaEm15xl7saFuzWpc9-U4PTDrgeABudLUJjO3nxD5dK4Kni3-hLgrE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17768059</pqid></control><display><type>article</type><title>EGF gene polymorphism and the risk of incident primary Melanoma</title><source>EZB Electronic Journals Library</source><creator>AMEND, Kandace L ; ELDER, James T ; TOMSHO, Lynn P ; BONNER, Joseph D ; JOHNSON, Timothy M ; SCHWARTZ, Jennifer ; BERWICK, Marianne ; GRUBER, Stephen B</creator><creatorcontrib>AMEND, Kandace L ; ELDER, James T ; TOMSHO, Lynn P ; BONNER, Joseph D ; JOHNSON, Timothy M ; SCHWARTZ, Jennifer ; BERWICK, Marianne ; GRUBER, Stephen B</creatorcontrib><description>Overexpression of the epidermal growth factor (EGF) pathway has been implicated in melanoma pathogenesis, and a recent case-control study identified a single nucleotide polymorphism (G to A) in the EGF gene where the G allele was associated with increased EGF expression and an increased risk of melanoma. To further evaluate this association, we conducted a case-control analysis from the Genes, Environment, and Melanoma study at the University of Michigan site using two different study designs. Incident cases of histopathologically confirmed first primary melanoma that were diagnosed between January 1, 2000 and December 31, 2000 from the University of Michigan Melanoma Clinic (n = 330) were compared with the following two different sources of nonmelanoma controls: spouse/friend controls (n = 84) and healthy volunteer controls from a case-control study of psoriasis (n = 148). Using a second analytic design, comparisons between multiple primary melanoma cases (n = 62) and single primary melanoma cases (n = 330) were also evaluated to estimate odds ratios (ORs). Genotyping for the single nucleotide substitution (G to A) at position 61 in the 5' untranslated region of the EGF gene was performed from genomic DNA, and epidemiological risk factors were assessed through a telephone interview. When EGF genotypes were compared between incident primary melanoma cases and the nonmelanoma controls, the risk associated with the homozygous G/G genotype was not statistically significantly associated with an increased risk for incident primary melanoma compared with the homozygous A/A genotype [OR, 1.09; 95% confidence interval (CI); 0.65-1.85]. No strong associations with EGF G/G genotype were observed in comparisons of multiple primary and single primary melanoma cases (OR, 0.66; 95% CI; 0.25-1.73). Case subjects with tumors >/=3.5 mm compared with those <3.5 mm were not significantly associated with the G/G genotype (OR, 0.54; 95% CI; 0.12-2.35). Our data do not support a significant association between melanoma and the EGF 61*G allele or the homozygous G/G genotype. The EGF polymorphism is not a reproducible risk factor for melanoma or thick melanoma in our data. The two analytic approaches used in the study provide evidence against a strong association between EGF 61*G and melanoma and demonstrate the potential utility of case-case designs for evaluating the role of single nucleotide polymorphisms and cancer. Additional independent studies will be required to elucidate relationships between genetic variation in the EGF gene and risk of melanoma.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-03-3855</identifier><identifier>PMID: 15087376</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Alleles ; Antineoplastic agents ; Biological and medical sciences ; Case-Control Studies ; Epidermal Growth Factor - genetics ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Medical sciences ; Melanoma - genetics ; Melanoma - pathology ; Middle Aged ; Neoplasm Invasiveness ; Pharmacology. Drug treatments ; Polymorphism, Genetic ; Sex Factors ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 2004-04, Vol.64 (8), p.2668-2672</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-5ffcea2319c28c0da1c0e15433ff20be1c729290994c2124f294a91ea4e7887f3</citedby><cites>FETCH-LOGICAL-c446t-5ffcea2319c28c0da1c0e15433ff20be1c729290994c2124f294a91ea4e7887f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15675368$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15087376$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>AMEND, Kandace L</creatorcontrib><creatorcontrib>ELDER, James T</creatorcontrib><creatorcontrib>TOMSHO, Lynn P</creatorcontrib><creatorcontrib>BONNER, Joseph D</creatorcontrib><creatorcontrib>JOHNSON, Timothy M</creatorcontrib><creatorcontrib>SCHWARTZ, Jennifer</creatorcontrib><creatorcontrib>BERWICK, Marianne</creatorcontrib><creatorcontrib>GRUBER, Stephen B</creatorcontrib><title>EGF gene polymorphism and the risk of incident primary Melanoma</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Overexpression of the epidermal growth factor (EGF) pathway has been implicated in melanoma pathogenesis, and a recent case-control study identified a single nucleotide polymorphism (G to A) in the EGF gene where the G allele was associated with increased EGF expression and an increased risk of melanoma. To further evaluate this association, we conducted a case-control analysis from the Genes, Environment, and Melanoma study at the University of Michigan site using two different study designs. Incident cases of histopathologically confirmed first primary melanoma that were diagnosed between January 1, 2000 and December 31, 2000 from the University of Michigan Melanoma Clinic (n = 330) were compared with the following two different sources of nonmelanoma controls: spouse/friend controls (n = 84) and healthy volunteer controls from a case-control study of psoriasis (n = 148). Using a second analytic design, comparisons between multiple primary melanoma cases (n = 62) and single primary melanoma cases (n = 330) were also evaluated to estimate odds ratios (ORs). Genotyping for the single nucleotide substitution (G to A) at position 61 in the 5' untranslated region of the EGF gene was performed from genomic DNA, and epidemiological risk factors were assessed through a telephone interview. When EGF genotypes were compared between incident primary melanoma cases and the nonmelanoma controls, the risk associated with the homozygous G/G genotype was not statistically significantly associated with an increased risk for incident primary melanoma compared with the homozygous A/A genotype [OR, 1.09; 95% confidence interval (CI); 0.65-1.85]. No strong associations with EGF G/G genotype were observed in comparisons of multiple primary and single primary melanoma cases (OR, 0.66; 95% CI; 0.25-1.73). Case subjects with tumors >/=3.5 mm compared with those <3.5 mm were not significantly associated with the G/G genotype (OR, 0.54; 95% CI; 0.12-2.35). Our data do not support a significant association between melanoma and the EGF 61*G allele or the homozygous G/G genotype. The EGF polymorphism is not a reproducible risk factor for melanoma or thick melanoma in our data. The two analytic approaches used in the study provide evidence against a strong association between EGF 61*G and melanoma and demonstrate the potential utility of case-case designs for evaluating the role of single nucleotide polymorphisms and cancer. Additional independent studies will be required to elucidate relationships between genetic variation in the EGF gene and risk of melanoma.</description><subject>Alleles</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Epidermal Growth Factor - genetics</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Melanoma - genetics</subject><subject>Melanoma - pathology</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymorphism, Genetic</subject><subject>Sex Factors</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqFkLtOwzAUhi0EoqXwCCAvsAV8O7E9oapqC1KBBWbLdWwayKXE6dC3J1EjYGM6OtL3n8uH0CUlt5SCuiOEqASEZLez6XNCeMIVwBEaU-AqkULAMRr_MCN0FuNH1wIlcIpGFIiSXKZjdD9fLvC7rzze1sW-rJvtJo8ltlWG243HTR4_cR1wXrk881WLt01e2maPn3xhq7q05-gk2CL6i6FO0Nti_jp7SFYvy8fZdJU4IdI2gRCct4xT7ZhyJLPUEU9BcB4CI2tPnWSaaaK1cIwyEZgWVlNvhZdKycAn6OYwd9vUXzsfW1Pm0fmiu8LXu2gkVRwY0H9BKmWqCOgOhAPomjrGxgcz_GYoMb1i0-szvT7TKTaEm15xl7saFuzWpc9-U4PTDrgeABudLUJjO3nxD5dK4Kni3-hLgrE</recordid><startdate>20040415</startdate><enddate>20040415</enddate><creator>AMEND, Kandace L</creator><creator>ELDER, James T</creator><creator>TOMSHO, Lynn P</creator><creator>BONNER, Joseph D</creator><creator>JOHNSON, Timothy M</creator><creator>SCHWARTZ, Jennifer</creator><creator>BERWICK, Marianne</creator><creator>GRUBER, Stephen B</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><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>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20040415</creationdate><title>EGF gene polymorphism and the risk of incident primary Melanoma</title><author>AMEND, Kandace L ; ELDER, James T ; TOMSHO, Lynn P ; BONNER, Joseph D ; JOHNSON, Timothy M ; SCHWARTZ, Jennifer ; BERWICK, Marianne ; GRUBER, Stephen B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-5ffcea2319c28c0da1c0e15433ff20be1c729290994c2124f294a91ea4e7887f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Alleles</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Epidermal Growth Factor - genetics</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Melanoma - genetics</topic><topic>Melanoma - pathology</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymorphism, Genetic</topic><topic>Sex Factors</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>AMEND, Kandace L</creatorcontrib><creatorcontrib>ELDER, James T</creatorcontrib><creatorcontrib>TOMSHO, Lynn P</creatorcontrib><creatorcontrib>BONNER, Joseph D</creatorcontrib><creatorcontrib>JOHNSON, Timothy M</creatorcontrib><creatorcontrib>SCHWARTZ, Jennifer</creatorcontrib><creatorcontrib>BERWICK, Marianne</creatorcontrib><creatorcontrib>GRUBER, Stephen B</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>AMEND, Kandace L</au><au>ELDER, James T</au><au>TOMSHO, Lynn P</au><au>BONNER, Joseph D</au><au>JOHNSON, Timothy M</au><au>SCHWARTZ, Jennifer</au><au>BERWICK, Marianne</au><au>GRUBER, Stephen B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EGF gene polymorphism and the risk of incident primary Melanoma</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2004-04-15</date><risdate>2004</risdate><volume>64</volume><issue>8</issue><spage>2668</spage><epage>2672</epage><pages>2668-2672</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Overexpression of the epidermal growth factor (EGF) pathway has been implicated in melanoma pathogenesis, and a recent case-control study identified a single nucleotide polymorphism (G to A) in the EGF gene where the G allele was associated with increased EGF expression and an increased risk of melanoma. To further evaluate this association, we conducted a case-control analysis from the Genes, Environment, and Melanoma study at the University of Michigan site using two different study designs. Incident cases of histopathologically confirmed first primary melanoma that were diagnosed between January 1, 2000 and December 31, 2000 from the University of Michigan Melanoma Clinic (n = 330) were compared with the following two different sources of nonmelanoma controls: spouse/friend controls (n = 84) and healthy volunteer controls from a case-control study of psoriasis (n = 148). Using a second analytic design, comparisons between multiple primary melanoma cases (n = 62) and single primary melanoma cases (n = 330) were also evaluated to estimate odds ratios (ORs). Genotyping for the single nucleotide substitution (G to A) at position 61 in the 5' untranslated region of the EGF gene was performed from genomic DNA, and epidemiological risk factors were assessed through a telephone interview. When EGF genotypes were compared between incident primary melanoma cases and the nonmelanoma controls, the risk associated with the homozygous G/G genotype was not statistically significantly associated with an increased risk for incident primary melanoma compared with the homozygous A/A genotype [OR, 1.09; 95% confidence interval (CI); 0.65-1.85]. No strong associations with EGF G/G genotype were observed in comparisons of multiple primary and single primary melanoma cases (OR, 0.66; 95% CI; 0.25-1.73). Case subjects with tumors >/=3.5 mm compared with those <3.5 mm were not significantly associated with the G/G genotype (OR, 0.54; 95% CI; 0.12-2.35). Our data do not support a significant association between melanoma and the EGF 61*G allele or the homozygous G/G genotype. The EGF polymorphism is not a reproducible risk factor for melanoma or thick melanoma in our data. The two analytic approaches used in the study provide evidence against a strong association between EGF 61*G and melanoma and demonstrate the potential utility of case-case designs for evaluating the role of single nucleotide polymorphisms and cancer. Additional independent studies will be required to elucidate relationships between genetic variation in the EGF gene and risk of melanoma.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>15087376</pmid><doi>10.1158/0008-5472.CAN-03-3855</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0008-5472 |
ispartof | Cancer research (Chicago, Ill.), 2004-04, Vol.64 (8), p.2668-2672 |
issn | 0008-5472 1538-7445 |
language | eng |
recordid | cdi_proquest_miscellaneous_71835251 |
source | EZB Electronic Journals Library |
subjects | Alleles Antineoplastic agents Biological and medical sciences Case-Control Studies Epidermal Growth Factor - genetics Female Genetic Predisposition to Disease Genotype Humans Male Medical sciences Melanoma - genetics Melanoma - pathology Middle Aged Neoplasm Invasiveness Pharmacology. Drug treatments Polymorphism, Genetic Sex Factors Tumors |
title | EGF gene polymorphism and the risk of incident primary Melanoma |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T14%3A51%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=EGF%20gene%20polymorphism%20and%20the%20risk%20of%20incident%20primary%20Melanoma&rft.jtitle=Cancer%20research%20(Chicago,%20Ill.)&rft.au=AMEND,%20Kandace%20L&rft.date=2004-04-15&rft.volume=64&rft.issue=8&rft.spage=2668&rft.epage=2672&rft.pages=2668-2672&rft.issn=0008-5472&rft.eissn=1538-7445&rft.coden=CNREA8&rft_id=info:doi/10.1158/0008-5472.CAN-03-3855&rft_dat=%3Cproquest_cross%3E71835251%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c446t-5ffcea2319c28c0da1c0e15433ff20be1c729290994c2124f294a91ea4e7887f3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=17768059&rft_id=info:pmid/15087376&rfr_iscdi=true |