Arsenic-Related Chromosomal Alterations in Bladder Cancer
Background: Previous studies have demonstrated that ingestion of arsenic in drinking water is a strong risk factor for several forms of cancer, including bladder cancer. It is not known whether arsenic-related cancers are genetically similar to cancers in unexposed individuals or what mechanisms of...
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| creator | Moore, Lee E. Smith, Allan H. Eng, Clarence Kalman, David DeVries, Sandy Bhargava, Vivek Chew, Karen Moore II, Dan Ferreccio, Catterina Rey, Omar A. Waldman, Frederic M. |
| description | Background: Previous studies have demonstrated that ingestion of arsenic in drinking water is a strong risk factor for several forms of cancer, including bladder cancer. It is not known whether arsenic-related cancers are genetically similar to cancers in unexposed individuals or what mechanisms of carcinogenesis may underlie their formation. This study was designed to compare chromosomal alterations in bladder cancers of arsenic-exposed individuals to provide insight into the mechanism of how arsenic may induce or promote cancer. Methods: A case–case study was conducted in Argentina and Chile examining chromosomal alterations in bladder tumor DNA in 123 patients who had been exposed to arsenic in their drinking water. Patients were placed into one of four arsenic exposure categories according to their average 5-year peak arsenic exposure. Patients were also classified as ever smokers or never smokers. Comparative genomic hybridization was used to identify chromosomal alterations throughout the genome. All statistical tests were two-sided. Results: The total number of chromosomal alterations was higher in individuals exposed to higher arsenic levels (5.7 ± 5.1, 5.6 ± 5.1, 7.3 ± 7.4, and 9.1 ± 6.5 [mean ± standard deviation] chromosomal alterations per tumor with increasing arsenic exposure; Ptrend = .02, adjusted for stage and grade). The trend was stronger in high-grade (G2–G3) tumors (6.3 ± 5.5, 8.3 ± 4.7, 10.3 ± 7.8, and 10.5 ± 6.4 alterations per tumor; Ptrend = .01) than it was in low-grade (G1) tumors (3.5 ± 3.1, 1.1 ± 1.1, 2.5 ± 2.5, and 3.6 ± 3.2 alterations per tumor; Ptrend = .79). The mean number of chromosomal alterations also increased with tumor stage and grade (Ptrend |
| doi_str_mv | 10.1093/jnci/94.22.1688 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_18628129</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>249985371</sourcerecordid><originalsourceid>FETCH-LOGICAL-c526t-f259cbf6fcb0322329b4e31ff7330bedc686dabbafbba1948c12b8cb178f42f13</originalsourceid><addsrcrecordid>eNpd0EtLAzEQB_AgitbH2Zssgt62TSbZbHKsxRf4AB8gXkKSTXDrPjTZgn57U1oUHAhzyG-G4Y_QIcFjgiWdzDtbTyQbA4wJF2IDjQjjOAeCi000whjKXIiS7aDdGOc4lQS2jXYIMEYosBGS0xBdV9v8wTV6cFU2ewt928e-1U02bQYX9FD3XczqLjtrdFW5kM10Z13YR1teN9EdrPseer44f5pd5Tf3l9ez6U1uC-BD7qGQ1njurcEUgII0zFHifUkpNq6yXPBKG6N9ekQyYQkYYQ0phWfgCd1Dp6u9H6H_XLg4qLaO1jWN7ly_iIoIDoKATPD4H5z3i9Cl2xQAlqXkkic0WSEb-hiD8-oj1K0O34pgtYxULSNVkqUZtYw0TRyt1y5M66o_v84wgZM10NHqxocUTx3_HJOkYJQml69cHQf39fuvw7viJS0LdfXyqqR8ZOz1Vqo7-gPMG42e</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>220979696</pqid></control><display><type>article</type><title>Arsenic-Related Chromosomal Alterations in Bladder Cancer</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Oxford University Press Journals All Titles (1996-Current)</source><creator>Moore, Lee E. ; Smith, Allan H. ; Eng, Clarence ; Kalman, David ; DeVries, Sandy ; Bhargava, Vivek ; Chew, Karen ; Moore II, Dan ; Ferreccio, Catterina ; Rey, Omar A. ; Waldman, Frederic M.</creator><creatorcontrib>Moore, Lee E. ; Smith, Allan H. ; Eng, Clarence ; Kalman, David ; DeVries, Sandy ; Bhargava, Vivek ; Chew, Karen ; Moore II, Dan ; Ferreccio, Catterina ; Rey, Omar A. ; Waldman, Frederic M.</creatorcontrib><description>Background: Previous studies have demonstrated that ingestion of arsenic in drinking water is a strong risk factor for several forms of cancer, including bladder cancer. It is not known whether arsenic-related cancers are genetically similar to cancers in unexposed individuals or what mechanisms of carcinogenesis may underlie their formation. This study was designed to compare chromosomal alterations in bladder cancers of arsenic-exposed individuals to provide insight into the mechanism of how arsenic may induce or promote cancer. Methods: A case–case study was conducted in Argentina and Chile examining chromosomal alterations in bladder tumor DNA in 123 patients who had been exposed to arsenic in their drinking water. Patients were placed into one of four arsenic exposure categories according to their average 5-year peak arsenic exposure. Patients were also classified as ever smokers or never smokers. Comparative genomic hybridization was used to identify chromosomal alterations throughout the genome. All statistical tests were two-sided. Results: The total number of chromosomal alterations was higher in individuals exposed to higher arsenic levels (5.7 ± 5.1, 5.6 ± 5.1, 7.3 ± 7.4, and 9.1 ± 6.5 [mean ± standard deviation] chromosomal alterations per tumor with increasing arsenic exposure; Ptrend = .02, adjusted for stage and grade). The trend was stronger in high-grade (G2–G3) tumors (6.3 ± 5.5, 8.3 ± 4.7, 10.3 ± 7.8, and 10.5 ± 6.4 alterations per tumor; Ptrend = .01) than it was in low-grade (G1) tumors (3.5 ± 3.1, 1.1 ± 1.1, 2.5 ± 2.5, and 3.6 ± 3.2 alterations per tumor; Ptrend = .79). The mean number of chromosomal alterations also increased with tumor stage and grade (Ptrend<.001) independently of arsenic exposure but was not associated with smoking history. Deletion of part or all of chromosome 17p (Ptrend<.001) showed the strongest association with arsenic exposure. Conclusions: Bladder tumors in patients with higher levels of arsenic exposure showed higher levels of chromosomal instability. Most of the chromosomal alterations associated with arsenic exposure were also associated with tumor stage and grade, raising the possibility that bladder tumors from arsenic-exposed patients may behave more aggressively than tumors from unexposed patients.</description><identifier>ISSN: 0027-8874</identifier><identifier>ISSN: 1460-2105</identifier><identifier>EISSN: 1460-2105</identifier><identifier>DOI: 10.1093/jnci/94.22.1688</identifier><identifier>PMID: 12441324</identifier><identifier>CODEN: JNCIEQ</identifier><language>eng</language><publisher>Cary, NC: Oxford University Press</publisher><subject>Argentina ; Arsenic ; Arsenic - adverse effects ; Biological and medical sciences ; Bladder cancer ; Cancer ; Carcinogens - adverse effects ; Case-Control Studies ; Chile ; Chromosome Aberrations - chemically induced ; Dose-Response Relationship, Drug ; Excretory system ; Genes ; Humans ; Medical sciences ; Mutation ; Neoplasm Staging ; Nephrology. Urinary tract diseases ; Nucleic Acid Hybridization ; Risk Factors ; Severity of Illness Index ; Sex Factors ; Smoking - adverse effects ; Teratogens ; Tropical medicine ; Tumors of the urinary system ; Urinary Bladder Neoplasms - chemically induced ; Urinary Bladder Neoplasms - diagnosis ; Urinary Bladder Neoplasms - etiology ; Urinary Bladder Neoplasms - genetics ; Urinary tract. Prostate gland</subject><ispartof>JNCI : Journal of the National Cancer Institute, 2002-11, Vol.94 (22), p.1688-1696</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Nov 20, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-f259cbf6fcb0322329b4e31ff7330bedc686dabbafbba1948c12b8cb178f42f13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14915433$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12441324$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moore, Lee E.</creatorcontrib><creatorcontrib>Smith, Allan H.</creatorcontrib><creatorcontrib>Eng, Clarence</creatorcontrib><creatorcontrib>Kalman, David</creatorcontrib><creatorcontrib>DeVries, Sandy</creatorcontrib><creatorcontrib>Bhargava, Vivek</creatorcontrib><creatorcontrib>Chew, Karen</creatorcontrib><creatorcontrib>Moore II, Dan</creatorcontrib><creatorcontrib>Ferreccio, Catterina</creatorcontrib><creatorcontrib>Rey, Omar A.</creatorcontrib><creatorcontrib>Waldman, Frederic M.</creatorcontrib><title>Arsenic-Related Chromosomal Alterations in Bladder Cancer</title><title>JNCI : Journal of the National Cancer Institute</title><addtitle>JNCI J Natl Cancer Inst</addtitle><description>Background: Previous studies have demonstrated that ingestion of arsenic in drinking water is a strong risk factor for several forms of cancer, including bladder cancer. It is not known whether arsenic-related cancers are genetically similar to cancers in unexposed individuals or what mechanisms of carcinogenesis may underlie their formation. This study was designed to compare chromosomal alterations in bladder cancers of arsenic-exposed individuals to provide insight into the mechanism of how arsenic may induce or promote cancer. Methods: A case–case study was conducted in Argentina and Chile examining chromosomal alterations in bladder tumor DNA in 123 patients who had been exposed to arsenic in their drinking water. Patients were placed into one of four arsenic exposure categories according to their average 5-year peak arsenic exposure. Patients were also classified as ever smokers or never smokers. Comparative genomic hybridization was used to identify chromosomal alterations throughout the genome. All statistical tests were two-sided. Results: The total number of chromosomal alterations was higher in individuals exposed to higher arsenic levels (5.7 ± 5.1, 5.6 ± 5.1, 7.3 ± 7.4, and 9.1 ± 6.5 [mean ± standard deviation] chromosomal alterations per tumor with increasing arsenic exposure; Ptrend = .02, adjusted for stage and grade). The trend was stronger in high-grade (G2–G3) tumors (6.3 ± 5.5, 8.3 ± 4.7, 10.3 ± 7.8, and 10.5 ± 6.4 alterations per tumor; Ptrend = .01) than it was in low-grade (G1) tumors (3.5 ± 3.1, 1.1 ± 1.1, 2.5 ± 2.5, and 3.6 ± 3.2 alterations per tumor; Ptrend = .79). The mean number of chromosomal alterations also increased with tumor stage and grade (Ptrend<.001) independently of arsenic exposure but was not associated with smoking history. Deletion of part or all of chromosome 17p (Ptrend<.001) showed the strongest association with arsenic exposure. Conclusions: Bladder tumors in patients with higher levels of arsenic exposure showed higher levels of chromosomal instability. Most of the chromosomal alterations associated with arsenic exposure were also associated with tumor stage and grade, raising the possibility that bladder tumors from arsenic-exposed patients may behave more aggressively than tumors from unexposed patients.</description><subject>Argentina</subject><subject>Arsenic</subject><subject>Arsenic - adverse effects</subject><subject>Biological and medical sciences</subject><subject>Bladder cancer</subject><subject>Cancer</subject><subject>Carcinogens - adverse effects</subject><subject>Case-Control Studies</subject><subject>Chile</subject><subject>Chromosome Aberrations - chemically induced</subject><subject>Dose-Response Relationship, Drug</subject><subject>Excretory system</subject><subject>Genes</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mutation</subject><subject>Neoplasm Staging</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nucleic Acid Hybridization</subject><subject>Risk Factors</subject><subject>Severity of Illness Index</subject><subject>Sex Factors</subject><subject>Smoking - adverse effects</subject><subject>Teratogens</subject><subject>Tropical medicine</subject><subject>Tumors of the urinary system</subject><subject>Urinary Bladder Neoplasms - chemically induced</subject><subject>Urinary Bladder Neoplasms - diagnosis</subject><subject>Urinary Bladder Neoplasms - etiology</subject><subject>Urinary Bladder Neoplasms - genetics</subject><subject>Urinary tract. Prostate gland</subject><issn>0027-8874</issn><issn>1460-2105</issn><issn>1460-2105</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0EtLAzEQB_AgitbH2Zssgt62TSbZbHKsxRf4AB8gXkKSTXDrPjTZgn57U1oUHAhzyG-G4Y_QIcFjgiWdzDtbTyQbA4wJF2IDjQjjOAeCi000whjKXIiS7aDdGOc4lQS2jXYIMEYosBGS0xBdV9v8wTV6cFU2ewt928e-1U02bQYX9FD3XczqLjtrdFW5kM10Z13YR1teN9EdrPseer44f5pd5Tf3l9ez6U1uC-BD7qGQ1njurcEUgII0zFHifUkpNq6yXPBKG6N9ekQyYQkYYQ0phWfgCd1Dp6u9H6H_XLg4qLaO1jWN7ly_iIoIDoKATPD4H5z3i9Cl2xQAlqXkkic0WSEb-hiD8-oj1K0O34pgtYxULSNVkqUZtYw0TRyt1y5M66o_v84wgZM10NHqxocUTx3_HJOkYJQml69cHQf39fuvw7viJS0LdfXyqqR8ZOz1Vqo7-gPMG42e</recordid><startdate>20021120</startdate><enddate>20021120</enddate><creator>Moore, Lee E.</creator><creator>Smith, Allan H.</creator><creator>Eng, Clarence</creator><creator>Kalman, David</creator><creator>DeVries, Sandy</creator><creator>Bhargava, Vivek</creator><creator>Chew, Karen</creator><creator>Moore II, Dan</creator><creator>Ferreccio, Catterina</creator><creator>Rey, Omar A.</creator><creator>Waldman, Frederic M.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><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>7U7</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7T2</scope><scope>7TV</scope><scope>7U1</scope><scope>7U2</scope></search><sort><creationdate>20021120</creationdate><title>Arsenic-Related Chromosomal Alterations in Bladder Cancer</title><author>Moore, Lee E. ; Smith, Allan H. ; Eng, Clarence ; Kalman, David ; DeVries, Sandy ; Bhargava, Vivek ; Chew, Karen ; Moore II, Dan ; Ferreccio, Catterina ; Rey, Omar A. ; Waldman, Frederic M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-f259cbf6fcb0322329b4e31ff7330bedc686dabbafbba1948c12b8cb178f42f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Argentina</topic><topic>Arsenic</topic><topic>Arsenic - adverse effects</topic><topic>Biological and medical sciences</topic><topic>Bladder cancer</topic><topic>Cancer</topic><topic>Carcinogens - adverse effects</topic><topic>Case-Control Studies</topic><topic>Chile</topic><topic>Chromosome Aberrations - chemically induced</topic><topic>Dose-Response Relationship, Drug</topic><topic>Excretory system</topic><topic>Genes</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mutation</topic><topic>Neoplasm Staging</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nucleic Acid Hybridization</topic><topic>Risk Factors</topic><topic>Severity of Illness Index</topic><topic>Sex Factors</topic><topic>Smoking - adverse effects</topic><topic>Teratogens</topic><topic>Tropical medicine</topic><topic>Tumors of the urinary system</topic><topic>Urinary Bladder Neoplasms - chemically induced</topic><topic>Urinary Bladder Neoplasms - diagnosis</topic><topic>Urinary Bladder Neoplasms - etiology</topic><topic>Urinary Bladder Neoplasms - genetics</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moore, Lee E.</creatorcontrib><creatorcontrib>Smith, Allan H.</creatorcontrib><creatorcontrib>Eng, Clarence</creatorcontrib><creatorcontrib>Kalman, David</creatorcontrib><creatorcontrib>DeVries, Sandy</creatorcontrib><creatorcontrib>Bhargava, Vivek</creatorcontrib><creatorcontrib>Chew, Karen</creatorcontrib><creatorcontrib>Moore II, Dan</creatorcontrib><creatorcontrib>Ferreccio, Catterina</creatorcontrib><creatorcontrib>Rey, Omar A.</creatorcontrib><creatorcontrib>Waldman, Frederic M.</creatorcontrib><collection>Istex</collection><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>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Pollution Abstracts</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><jtitle>JNCI : Journal of the National Cancer Institute</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moore, Lee E.</au><au>Smith, Allan H.</au><au>Eng, Clarence</au><au>Kalman, David</au><au>DeVries, Sandy</au><au>Bhargava, Vivek</au><au>Chew, Karen</au><au>Moore II, Dan</au><au>Ferreccio, Catterina</au><au>Rey, Omar A.</au><au>Waldman, Frederic M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arsenic-Related Chromosomal Alterations in Bladder Cancer</atitle><jtitle>JNCI : Journal of the National Cancer Institute</jtitle><addtitle>JNCI J Natl Cancer Inst</addtitle><date>2002-11-20</date><risdate>2002</risdate><volume>94</volume><issue>22</issue><spage>1688</spage><epage>1696</epage><pages>1688-1696</pages><issn>0027-8874</issn><issn>1460-2105</issn><eissn>1460-2105</eissn><coden>JNCIEQ</coden><abstract>Background: Previous studies have demonstrated that ingestion of arsenic in drinking water is a strong risk factor for several forms of cancer, including bladder cancer. It is not known whether arsenic-related cancers are genetically similar to cancers in unexposed individuals or what mechanisms of carcinogenesis may underlie their formation. This study was designed to compare chromosomal alterations in bladder cancers of arsenic-exposed individuals to provide insight into the mechanism of how arsenic may induce or promote cancer. Methods: A case–case study was conducted in Argentina and Chile examining chromosomal alterations in bladder tumor DNA in 123 patients who had been exposed to arsenic in their drinking water. Patients were placed into one of four arsenic exposure categories according to their average 5-year peak arsenic exposure. Patients were also classified as ever smokers or never smokers. Comparative genomic hybridization was used to identify chromosomal alterations throughout the genome. All statistical tests were two-sided. Results: The total number of chromosomal alterations was higher in individuals exposed to higher arsenic levels (5.7 ± 5.1, 5.6 ± 5.1, 7.3 ± 7.4, and 9.1 ± 6.5 [mean ± standard deviation] chromosomal alterations per tumor with increasing arsenic exposure; Ptrend = .02, adjusted for stage and grade). The trend was stronger in high-grade (G2–G3) tumors (6.3 ± 5.5, 8.3 ± 4.7, 10.3 ± 7.8, and 10.5 ± 6.4 alterations per tumor; Ptrend = .01) than it was in low-grade (G1) tumors (3.5 ± 3.1, 1.1 ± 1.1, 2.5 ± 2.5, and 3.6 ± 3.2 alterations per tumor; Ptrend = .79). The mean number of chromosomal alterations also increased with tumor stage and grade (Ptrend<.001) independently of arsenic exposure but was not associated with smoking history. Deletion of part or all of chromosome 17p (Ptrend<.001) showed the strongest association with arsenic exposure. Conclusions: Bladder tumors in patients with higher levels of arsenic exposure showed higher levels of chromosomal instability. Most of the chromosomal alterations associated with arsenic exposure were also associated with tumor stage and grade, raising the possibility that bladder tumors from arsenic-exposed patients may behave more aggressively than tumors from unexposed patients.</abstract><cop>Cary, NC</cop><pub>Oxford University Press</pub><pmid>12441324</pmid><doi>10.1093/jnci/94.22.1688</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Argentina Arsenic Arsenic - adverse effects Biological and medical sciences Bladder cancer Cancer Carcinogens - adverse effects Case-Control Studies Chile Chromosome Aberrations - chemically induced Dose-Response Relationship, Drug Excretory system Genes Humans Medical sciences Mutation Neoplasm Staging Nephrology. Urinary tract diseases Nucleic Acid Hybridization Risk Factors Severity of Illness Index Sex Factors Smoking - adverse effects Teratogens Tropical medicine Tumors of the urinary system Urinary Bladder Neoplasms - chemically induced Urinary Bladder Neoplasms - diagnosis Urinary Bladder Neoplasms - etiology Urinary Bladder Neoplasms - genetics Urinary tract. Prostate gland |
| title | Arsenic-Related Chromosomal Alterations in Bladder Cancer |
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