P53 alterations in bladder tumors from arsenic and tobacco exposed patients

Autores
Moore, Lee E.; Smith, Allan H.; Eng, Clarence; Devries, Sandy; Kalman, Dave; Bhargava, Vivek; Chew, Karen; Ferreccio, Catterina; Rey, Omar A.; Hopenhayn, Claudia; Biggs, Mary Lou; Bates, Michael N.
Año de publicación
2003
Idioma
español castellano
Tipo de recurso
artículo
Estado
versión aceptada
Descripción
Previous studies demonstrated that tobacco and arsenic exposure are risk factors for bladder cancer. A case-case study was conducted to compare p53 mutations in 147 bladder tumors from South American patients by tobacco and arsenic exposure. Information on residential history and lifestyle factors was collected. The prevalence of p53 mutations and protein expression was examined in relation to tumor stage, grade, patient age, gender, tobacco and arsenic exposure. Smokers were grouped as ever/never smokers and by pack years of exposure (0, 1-20, >20). Patients were also grouped into four arsenic exposure categories based on the average of the five highest years arsenic concentration in their drinking water: group 1, non-detectable to < 10 μg/l (n = 50); group 2, 10-99 μg/l (n = 31); group 3, 100-299 μg/l (n = 35); group 4, >300 μg/l (n = 30). The proportion of tumor samples with p53 mutations and P53 immunopositivity increased strongly with both stage and grade, but not with arsenic exposure or smoking. The prevalence of tumors containing mutational transitions increased markedly with tumor stage (from 14 to 52%, Ptrend = 0.005) and grade (from 11 to 48%, Ptrend = 0.004) and was higher in smokers than in non-smokers (34 versus 18%, respectively, P = 0.10). An increasing trend was observed with pack years of smoking (P = 0.09). The majority of mutations in tumors from both smokers and non-smokers were G → A transitions, however, in smokers a preference for G → A transitions at CpG sites was observed (P = 0.07, two-tailed) and a positive trend was observed with pack years of exposure (P = 0.04). A hotspot was found at codon 273 in 12% of the tumors from smokers but was not observed in never smokers (P = 0.05) and a positive trend was observed with pack years of tobacco exposure (P = 0.001). Neither stage nor grade demonstrated a preference for CpG site mutation, suggesting that these changes may be early exposure-related events in carcinogenesis and are not related to tumor progression. Arsenic exposure was not associated with an increased prevalence of p53 mutation or P53 immunopositivity and there was no evidence of interaction between arsenic and smoking with these outcome variables.
Fil: Moore, Lee E. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Smith, Allan H. University of Washington, Seattle, WA, United States
Fil: Eng, Clarence. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Devries, Sandy. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Kalman, Dave. University of Washington, Seattle, WA, United States
Fil: Bhargava, Vivek. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Chew, Karen. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Ferreccio, Catterina. Universidad Católica de Córdoba. Facultad de Ciencias de la Salud; Argentina
Fil: Rey, Omar A. Universidad Católica de Córdoba. Facultad de Ciencias de la Salud; Argentina
Fil: Hopenhayn, Claudia. University of Kentucky, Lexington, KY, United States
Fil: Biggs, Mary Lou. University of Washington, Seattle, WA, United States
Fil: Bates, Michael N. Arsenic Health Research Program, School of Public Health, University of California, Berkeley, CA 7360, 140 Warren Hall, United States
Fuente
Moore, Lee E., Smith, Allan H., Eng, Clarence, Devries, Sandy, Kalman, Dave, Bhargava, Vivek, Chew, Karen, Ferreccio, Catterina ORCID: https://orcid.org/0000-0001-6331-5534 , Rey, Omar A. ORCID: https://orcid.org/0000-0002-9232-1252 , Hopenhayn, Claudia, Biggs, Mary Lou and Bates, Michael N. (2003) P53 alterations in bladder tumors from arsenic and tobacco exposed patients. Carcinogenesis, 24 (11). 1785 -1791. ISSN 0143-3334
Materia
R Medicina (General)
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
Repositorio
Producción Académica (UCC)
Institución
Universidad Católica de Córdoba
OAI Identificador
oai:pa.bibdigital.uccor.edu.ar:3955

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network_acronym_str PAUCC
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network_name_str Producción Académica (UCC)
spelling P53 alterations in bladder tumors from arsenic and tobacco exposed patientsMoore, Lee E.Smith, Allan H.Eng, ClarenceDevries, SandyKalman, DaveBhargava, VivekChew, KarenFerreccio, CatterinaRey, Omar A.Hopenhayn, ClaudiaBiggs, Mary LouBates, Michael N.R Medicina (General)Previous studies demonstrated that tobacco and arsenic exposure are risk factors for bladder cancer. A case-case study was conducted to compare p53 mutations in 147 bladder tumors from South American patients by tobacco and arsenic exposure. Information on residential history and lifestyle factors was collected. The prevalence of p53 mutations and protein expression was examined in relation to tumor stage, grade, patient age, gender, tobacco and arsenic exposure. Smokers were grouped as ever/never smokers and by pack years of exposure (0, 1-20, >20). Patients were also grouped into four arsenic exposure categories based on the average of the five highest years arsenic concentration in their drinking water: group 1, non-detectable to < 10 μg/l (n = 50); group 2, 10-99 μg/l (n = 31); group 3, 100-299 μg/l (n = 35); group 4, >300 μg/l (n = 30). The proportion of tumor samples with p53 mutations and P53 immunopositivity increased strongly with both stage and grade, but not with arsenic exposure or smoking. The prevalence of tumors containing mutational transitions increased markedly with tumor stage (from 14 to 52%, Ptrend = 0.005) and grade (from 11 to 48%, Ptrend = 0.004) and was higher in smokers than in non-smokers (34 versus 18%, respectively, P = 0.10). An increasing trend was observed with pack years of smoking (P = 0.09). The majority of mutations in tumors from both smokers and non-smokers were G → A transitions, however, in smokers a preference for G → A transitions at CpG sites was observed (P = 0.07, two-tailed) and a positive trend was observed with pack years of exposure (P = 0.04). A hotspot was found at codon 273 in 12% of the tumors from smokers but was not observed in never smokers (P = 0.05) and a positive trend was observed with pack years of tobacco exposure (P = 0.001). Neither stage nor grade demonstrated a preference for CpG site mutation, suggesting that these changes may be early exposure-related events in carcinogenesis and are not related to tumor progression. Arsenic exposure was not associated with an increased prevalence of p53 mutation or P53 immunopositivity and there was no evidence of interaction between arsenic and smoking with these outcome variables.Fil: Moore, Lee E. University of California, San Francisco Cancer Center, San Francisco, CA, United StatesFil: Smith, Allan H. University of Washington, Seattle, WA, United StatesFil: Eng, Clarence. University of California, San Francisco Cancer Center, San Francisco, CA, United StatesFil: Devries, Sandy. University of California, San Francisco Cancer Center, San Francisco, CA, United StatesFil: Kalman, Dave. University of Washington, Seattle, WA, United StatesFil: Bhargava, Vivek. University of California, San Francisco Cancer Center, San Francisco, CA, United StatesFil: Chew, Karen. University of California, San Francisco Cancer Center, San Francisco, CA, United StatesFil: Ferreccio, Catterina. Universidad Católica de Córdoba. Facultad de Ciencias de la Salud; ArgentinaFil: Rey, Omar A. Universidad Católica de Córdoba. Facultad de Ciencias de la Salud; ArgentinaFil: Hopenhayn, Claudia. University of Kentucky, Lexington, KY, United StatesFil: Biggs, Mary Lou. University of Washington, Seattle, WA, United StatesFil: Bates, Michael N. Arsenic Health Research Program, School of Public Health, University of California, Berkeley, CA 7360, 140 Warren Hall, United States2003-12-31info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://pa.bibdigital.ucc.edu.ar/3955/1/A_Moore_Smith_Eng_DeVries_Kalman_Bhargava_Chew_Ferreccio_Rey_Hopenhayn_Biggs_Bates_Waldman.pdf Moore, Lee E., Smith, Allan H., Eng, Clarence, Devries, Sandy, Kalman, Dave, Bhargava, Vivek, Chew, Karen, Ferreccio, Catterina ORCID: https://orcid.org/0000-0001-6331-5534 <https://orcid.org/0000-0001-6331-5534>, Rey, Omar A. ORCID: https://orcid.org/0000-0002-9232-1252 <https://orcid.org/0000-0002-9232-1252>, Hopenhayn, Claudia, Biggs, Mary Lou and Bates, Michael N. (2003) P53 alterations in bladder tumors from arsenic and tobacco exposed patients. Carcinogenesis, 24 (11). 1785 -1791. ISSN 0143-3334 reponame:Producción Académica (UCC)instname:Universidad Católica de Córdobaspahttp://pa.bibdigital.ucc.edu.ar/3955/info:eu-repo/semantics/altIdentifier/doi/10.1093/carcin/bgg136info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es2025-09-29T14:29:44Zoai:pa.bibdigital.uccor.edu.ar:3955instacron:UCCInstitucionalhttp://pa.bibdigital.uccor.edu.ar/Universidad privadaNo correspondehttp://pa.bibdigital.uccor.edu.ar/cgi/oai2bibdir@uccor.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:27182025-09-29 14:29:44.304Producción Académica (UCC) - Universidad Católica de Córdobafalse
dc.title.none.fl_str_mv P53 alterations in bladder tumors from arsenic and tobacco exposed patients
title P53 alterations in bladder tumors from arsenic and tobacco exposed patients
spellingShingle P53 alterations in bladder tumors from arsenic and tobacco exposed patients
Moore, Lee E.
R Medicina (General)
title_short P53 alterations in bladder tumors from arsenic and tobacco exposed patients
title_full P53 alterations in bladder tumors from arsenic and tobacco exposed patients
title_fullStr P53 alterations in bladder tumors from arsenic and tobacco exposed patients
title_full_unstemmed P53 alterations in bladder tumors from arsenic and tobacco exposed patients
title_sort P53 alterations in bladder tumors from arsenic and tobacco exposed patients
dc.creator.none.fl_str_mv Moore, Lee E.
Smith, Allan H.
Eng, Clarence
Devries, Sandy
Kalman, Dave
Bhargava, Vivek
Chew, Karen
Ferreccio, Catterina
Rey, Omar A.
Hopenhayn, Claudia
Biggs, Mary Lou
Bates, Michael N.
author Moore, Lee E.
author_facet Moore, Lee E.
Smith, Allan H.
Eng, Clarence
Devries, Sandy
Kalman, Dave
Bhargava, Vivek
Chew, Karen
Ferreccio, Catterina
Rey, Omar A.
Hopenhayn, Claudia
Biggs, Mary Lou
Bates, Michael N.
author_role author
author2 Smith, Allan H.
Eng, Clarence
Devries, Sandy
Kalman, Dave
Bhargava, Vivek
Chew, Karen
Ferreccio, Catterina
Rey, Omar A.
Hopenhayn, Claudia
Biggs, Mary Lou
Bates, Michael N.
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv R Medicina (General)
topic R Medicina (General)
dc.description.none.fl_txt_mv Previous studies demonstrated that tobacco and arsenic exposure are risk factors for bladder cancer. A case-case study was conducted to compare p53 mutations in 147 bladder tumors from South American patients by tobacco and arsenic exposure. Information on residential history and lifestyle factors was collected. The prevalence of p53 mutations and protein expression was examined in relation to tumor stage, grade, patient age, gender, tobacco and arsenic exposure. Smokers were grouped as ever/never smokers and by pack years of exposure (0, 1-20, >20). Patients were also grouped into four arsenic exposure categories based on the average of the five highest years arsenic concentration in their drinking water: group 1, non-detectable to < 10 μg/l (n = 50); group 2, 10-99 μg/l (n = 31); group 3, 100-299 μg/l (n = 35); group 4, >300 μg/l (n = 30). The proportion of tumor samples with p53 mutations and P53 immunopositivity increased strongly with both stage and grade, but not with arsenic exposure or smoking. The prevalence of tumors containing mutational transitions increased markedly with tumor stage (from 14 to 52%, Ptrend = 0.005) and grade (from 11 to 48%, Ptrend = 0.004) and was higher in smokers than in non-smokers (34 versus 18%, respectively, P = 0.10). An increasing trend was observed with pack years of smoking (P = 0.09). The majority of mutations in tumors from both smokers and non-smokers were G → A transitions, however, in smokers a preference for G → A transitions at CpG sites was observed (P = 0.07, two-tailed) and a positive trend was observed with pack years of exposure (P = 0.04). A hotspot was found at codon 273 in 12% of the tumors from smokers but was not observed in never smokers (P = 0.05) and a positive trend was observed with pack years of tobacco exposure (P = 0.001). Neither stage nor grade demonstrated a preference for CpG site mutation, suggesting that these changes may be early exposure-related events in carcinogenesis and are not related to tumor progression. Arsenic exposure was not associated with an increased prevalence of p53 mutation or P53 immunopositivity and there was no evidence of interaction between arsenic and smoking with these outcome variables.
Fil: Moore, Lee E. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Smith, Allan H. University of Washington, Seattle, WA, United States
Fil: Eng, Clarence. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Devries, Sandy. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Kalman, Dave. University of Washington, Seattle, WA, United States
Fil: Bhargava, Vivek. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Chew, Karen. University of California, San Francisco Cancer Center, San Francisco, CA, United States
Fil: Ferreccio, Catterina. Universidad Católica de Córdoba. Facultad de Ciencias de la Salud; Argentina
Fil: Rey, Omar A. Universidad Católica de Córdoba. Facultad de Ciencias de la Salud; Argentina
Fil: Hopenhayn, Claudia. University of Kentucky, Lexington, KY, United States
Fil: Biggs, Mary Lou. University of Washington, Seattle, WA, United States
Fil: Bates, Michael N. Arsenic Health Research Program, School of Public Health, University of California, Berkeley, CA 7360, 140 Warren Hall, United States
description Previous studies demonstrated that tobacco and arsenic exposure are risk factors for bladder cancer. A case-case study was conducted to compare p53 mutations in 147 bladder tumors from South American patients by tobacco and arsenic exposure. Information on residential history and lifestyle factors was collected. The prevalence of p53 mutations and protein expression was examined in relation to tumor stage, grade, patient age, gender, tobacco and arsenic exposure. Smokers were grouped as ever/never smokers and by pack years of exposure (0, 1-20, >20). Patients were also grouped into four arsenic exposure categories based on the average of the five highest years arsenic concentration in their drinking water: group 1, non-detectable to < 10 μg/l (n = 50); group 2, 10-99 μg/l (n = 31); group 3, 100-299 μg/l (n = 35); group 4, >300 μg/l (n = 30). The proportion of tumor samples with p53 mutations and P53 immunopositivity increased strongly with both stage and grade, but not with arsenic exposure or smoking. The prevalence of tumors containing mutational transitions increased markedly with tumor stage (from 14 to 52%, Ptrend = 0.005) and grade (from 11 to 48%, Ptrend = 0.004) and was higher in smokers than in non-smokers (34 versus 18%, respectively, P = 0.10). An increasing trend was observed with pack years of smoking (P = 0.09). The majority of mutations in tumors from both smokers and non-smokers were G → A transitions, however, in smokers a preference for G → A transitions at CpG sites was observed (P = 0.07, two-tailed) and a positive trend was observed with pack years of exposure (P = 0.04). A hotspot was found at codon 273 in 12% of the tumors from smokers but was not observed in never smokers (P = 0.05) and a positive trend was observed with pack years of tobacco exposure (P = 0.001). Neither stage nor grade demonstrated a preference for CpG site mutation, suggesting that these changes may be early exposure-related events in carcinogenesis and are not related to tumor progression. Arsenic exposure was not associated with an increased prevalence of p53 mutation or P53 immunopositivity and there was no evidence of interaction between arsenic and smoking with these outcome variables.
publishDate 2003
dc.date.none.fl_str_mv 2003-12-31
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
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info:ar-repo/semantics/articulo
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv http://pa.bibdigital.ucc.edu.ar/3955/1/A_Moore_Smith_Eng_DeVries_Kalman_Bhargava_Chew_Ferreccio_Rey_Hopenhayn_Biggs_Bates_Waldman.pdf
url http://pa.bibdigital.ucc.edu.ar/3955/1/A_Moore_Smith_Eng_DeVries_Kalman_Bhargava_Chew_Ferreccio_Rey_Hopenhayn_Biggs_Bates_Waldman.pdf
dc.language.none.fl_str_mv spa
language spa
dc.relation.none.fl_str_mv http://pa.bibdigital.ucc.edu.ar/3955/
info:eu-repo/semantics/altIdentifier/doi/10.1093/carcin/bgg136
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https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv Moore, Lee E., Smith, Allan H., Eng, Clarence, Devries, Sandy, Kalman, Dave, Bhargava, Vivek, Chew, Karen, Ferreccio, Catterina ORCID: https://orcid.org/0000-0001-6331-5534 <https://orcid.org/0000-0001-6331-5534>, Rey, Omar A. ORCID: https://orcid.org/0000-0002-9232-1252 <https://orcid.org/0000-0002-9232-1252>, Hopenhayn, Claudia, Biggs, Mary Lou and Bates, Michael N. (2003) P53 alterations in bladder tumors from arsenic and tobacco exposed patients. Carcinogenesis, 24 (11). 1785 -1791. ISSN 0143-3334
reponame:Producción Académica (UCC)
instname:Universidad Católica de Córdoba
reponame_str Producción Académica (UCC)
collection Producción Académica (UCC)
instname_str Universidad Católica de Córdoba
repository.name.fl_str_mv Producción Académica (UCC) - Universidad Católica de Córdoba
repository.mail.fl_str_mv bibdir@uccor.edu.ar
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