Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer
Juan Alguacil, Miquel Porta, Timo Kauppinen, Núria Malats, Manolis Kogevinas, Alfredo Carrato
Department of Paediatrics, Obstetrics and Gynaecology and Preventive Medicine and Public Health
ras genes are known critical DNA targets for chemical carcinogens. Exocrine pancreatic cancer (EPC) is the human tumor with the highest prevalence of K-ras mutations at diagnosis. We analyzed the relationship between past occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons (PAHs) and other agents and mutations in codon 12 of the K-ras gene in 107 incident cases of EPC. Information on occupational and life-style factors was obtained from personal interviews conducted during hospital stay. Occupational exposures were examined using industrial hygienists (IH) assessment and the Finnish job-exposure matrix (Finjem). Specific occupational exposures among K-ras mutated EPC cases (n = 83) were compared to those of K-ras wild-type EPC cases (n = 24) (case-case analysis). Multivariate-adjusted odds ratios (OR) and their corresponding 95% confidence limits were estimated by unconditional logistic regression. Cases with K-ras mutations were significantly more likely than wild-type cases to have been exposed to dyes and organic pigments (OR 4.8; p<0.05). There was some indication of weaker associations between K-ras mutations and occupational exposure to lead, PAHs, benzo[a]pyrene, gasoline, nickel, inhalatory exposure to chromium and sedentary work. The association with chromium compounds was stronger for G to T transversions, a finding compatible with experimental studies on mutation spectra for chromium. Results lend moderate support to the hypothesis of indirect relationships between occupational exposure to dyes and organic pigments and the activation of the K-ras gene in the etiopathogenesis of human exocrine pancreatic cancer. © 2003 Wiley-Liss, Inc.
International Journal of Cancer
Case-case study
Genotoxicology
Ras genes
Dive into the research topics of 'Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer'. Together they form a unique fingerprint.
Occupational Exposure Medicine and Dentistry 100%
Ras Medicine and Dentistry 100%
Exocrine Pancreatic Cancer Medicine and Dentistry 100%
Mutation Chemistry 83%
Dye Medicine and Dentistry 66%
Polycyclic Aromatic Hydrocarbon Medicine and Dentistry 50%
Carcinogen Medicine and Dentistry 50%
Oncogene Ras Medicine and Dentistry 50%
Alguacil, J., Porta, M., Kauppinen, T., Malats, N., Kogevinas, M., & Carrato, A. (2003). Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer. International Journal of Cancer, 107, 635-641. https://doi.org/10.1002/ijc.11431
Alguacil, Juan ; Porta, Miquel ; Kauppinen, Timo et al. / Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer. In: International Journal of Cancer. 2003 ; Vol. 107. pp. 635-641.
@article{20bbd8a781a349f9a8427a201ef14e77,
title = "Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer",
abstract = "ras genes are known critical DNA targets for chemical carcinogens. Exocrine pancreatic cancer (EPC) is the human tumor with the highest prevalence of K-ras mutations at diagnosis. We analyzed the relationship between past occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons (PAHs) and other agents and mutations in codon 12 of the K-ras gene in 107 incident cases of EPC. Information on occupational and life-style factors was obtained from personal interviews conducted during hospital stay. Occupational exposures were examined using industrial hygienists (IH) assessment and the Finnish job-exposure matrix (Finjem). Specific occupational exposures among K-ras mutated EPC cases (n = 83) were compared to those of K-ras wild-type EPC cases (n = 24) (case-case analysis). Multivariate-adjusted odds ratios (OR) and their corresponding 95% confidence limits were estimated by unconditional logistic regression. Cases with K-ras mutations were significantly more likely than wild-type cases to have been exposed to dyes and organic pigments (OR 4.8; p<0.05). There was some indication of weaker associations between K-ras mutations and occupational exposure to lead, PAHs, benzo[a]pyrene, gasoline, nickel, inhalatory exposure to chromium and sedentary work. The association with chromium compounds was stronger for G to T transversions, a finding compatible with experimental studies on mutation spectra for chromium. Results lend moderate support to the hypothesis of indirect relationships between occupational exposure to dyes and organic pigments and the activation of the K-ras gene in the etiopathogenesis of human exocrine pancreatic cancer. {\textcopyright} 2003 Wiley-Liss, Inc.",
keywords = "Case-case study, Dyes, Genotoxicology, Metals, Occupation, Pancreas, Ras genes",
author = "Juan Alguacil and Miquel Porta and Timo Kauppinen and N{\'u}ria Malats and Manolis Kogevinas and Alfredo Carrato",
doi = "https://doi.org/10.1002/ijc.11431",
journal = "International Journal of Cancer",
Alguacil, J, Porta, M, Kauppinen, T, Malats, N, Kogevinas, M & Carrato, A 2003, 'Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer', International Journal of Cancer, vol. 107, pp. 635-641. https://doi.org/10.1002/ijc.11431
Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer. / Alguacil, Juan; Porta, Miquel; Kauppinen, Timo et al.
In: International Journal of Cancer, Vol. 107, 20.11.2003, p. 635-641.
T1 - Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer
AU - Alguacil, Juan
AU - Porta, Miquel
AU - Kauppinen, Timo
AU - Malats, Núria
AU - Kogevinas, Manolis
AU - Carrato, Alfredo
N2 - ras genes are known critical DNA targets for chemical carcinogens. Exocrine pancreatic cancer (EPC) is the human tumor with the highest prevalence of K-ras mutations at diagnosis. We analyzed the relationship between past occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons (PAHs) and other agents and mutations in codon 12 of the K-ras gene in 107 incident cases of EPC. Information on occupational and life-style factors was obtained from personal interviews conducted during hospital stay. Occupational exposures were examined using industrial hygienists (IH) assessment and the Finnish job-exposure matrix (Finjem). Specific occupational exposures among K-ras mutated EPC cases (n = 83) were compared to those of K-ras wild-type EPC cases (n = 24) (case-case analysis). Multivariate-adjusted odds ratios (OR) and their corresponding 95% confidence limits were estimated by unconditional logistic regression. Cases with K-ras mutations were significantly more likely than wild-type cases to have been exposed to dyes and organic pigments (OR 4.8; p<0.05). There was some indication of weaker associations between K-ras mutations and occupational exposure to lead, PAHs, benzo[a]pyrene, gasoline, nickel, inhalatory exposure to chromium and sedentary work. The association with chromium compounds was stronger for G to T transversions, a finding compatible with experimental studies on mutation spectra for chromium. Results lend moderate support to the hypothesis of indirect relationships between occupational exposure to dyes and organic pigments and the activation of the K-ras gene in the etiopathogenesis of human exocrine pancreatic cancer. © 2003 Wiley-Liss, Inc.
AB - ras genes are known critical DNA targets for chemical carcinogens. Exocrine pancreatic cancer (EPC) is the human tumor with the highest prevalence of K-ras mutations at diagnosis. We analyzed the relationship between past occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons (PAHs) and other agents and mutations in codon 12 of the K-ras gene in 107 incident cases of EPC. Information on occupational and life-style factors was obtained from personal interviews conducted during hospital stay. Occupational exposures were examined using industrial hygienists (IH) assessment and the Finnish job-exposure matrix (Finjem). Specific occupational exposures among K-ras mutated EPC cases (n = 83) were compared to those of K-ras wild-type EPC cases (n = 24) (case-case analysis). Multivariate-adjusted odds ratios (OR) and their corresponding 95% confidence limits were estimated by unconditional logistic regression. Cases with K-ras mutations were significantly more likely than wild-type cases to have been exposed to dyes and organic pigments (OR 4.8; p<0.05). There was some indication of weaker associations between K-ras mutations and occupational exposure to lead, PAHs, benzo[a]pyrene, gasoline, nickel, inhalatory exposure to chromium and sedentary work. The association with chromium compounds was stronger for G to T transversions, a finding compatible with experimental studies on mutation spectra for chromium. Results lend moderate support to the hypothesis of indirect relationships between occupational exposure to dyes and organic pigments and the activation of the K-ras gene in the etiopathogenesis of human exocrine pancreatic cancer. © 2003 Wiley-Liss, Inc.
KW - Case-case study
KW - Dyes
KW - Genotoxicology
KW - Metals
KW - Occupation
KW - Pancreas
KW - Ras genes
U2 - https://doi.org/10.1002/ijc.11431
DO - https://doi.org/10.1002/ijc.11431
JO - International Journal of Cancer
JF - International Journal of Cancer
Alguacil J, Porta M, Kauppinen T, Malats N, Kogevinas M, Carrato A. Occupational exposure to dyes, metals, polycyclic aromatic hydrocarbons and other agents and K-ras activation in human exocrine pancreatic cancer. International Journal of Cancer. 2003 Nov 20;107:635-641. doi: https://doi.org/10.1002/ijc.11431