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4 results on '"Gundy, S"'

1. Chromosomal aberrations and cancer risk: Results of a cohort study from Central Europe

Author

Boffetta, P., van der Hel, O., Norppa, H., Fabianova, E., Fučić, Aleksandra, Gundy, S., Lazutka, J., Cebulska-Wasilewska, A., Puskailerova, D., Znaor, A., Kelecsenyi, Z., Rachtan, J., Forni, A., Vermeulen, R., and Bonassi, S.

Subjects
chromosomal aberrations, cancer, cytogenetics, epidemiology
Abstract

High level of chromosomal aberrations (CA) in peripheral blood lymphocytes may be an early marker of cancer risk, but data on risk of specific cancers and types of CA (chromosome-type [CSA] and chromatid-type [CTA] aberration) are limited. A total of 6430 healthy individuals from nine laboratories in Croatia, Hungary, Lithuania, Poland and Slovakia, included in CA surveys performed during 1978-2002, were followed-up for cancer incidence or mortality for an average of 8.5 years. 200 cancer cases were observed. Compared with the low tertile of CA level, the relative risk (RR) of cancer was 1.78 (95% confidence interval [CI] 1.19, 2.67) for medium tertile and 1.81 (95% CI 1.20, 2.73) for high tertile. The RR for CSA above vs. below the median was 1.50 (95% CI 1.12, 2.01), while that for CTA was 0.97 (95% CI 0.72, 1.31). The analyses of risk of specific cancers were limited by small numbers, but the association was stronger for stomach cancer. This study confirms the previously reported association between CA level and cancer risk and provides novel information on the type of aberrations more strongly predictive of cancer risk, on the types of cancer more strongly predicted by CA.

Published
2007

2. Chromosomal aberrations and SCEs as biomarkers of cancer risk

Author

Norppa, H., Bonassi, S., Hansteen, I.-L., Hagmar, L., Strömberg, U., Rössner, P., Boffetta, P., Lindholm, C., Gundy, S., Lazutka, J., Cebulska-Wasilewska, A., Fabiánová, E., Šrám, R.J., Knudsen, L.E., Barale, R., and Fucic, A.

Subjects
*CANCER, *GENETIC polymorphisms, *CHROMOSOME replication, *CHROMOSOME abnormalities
Abstract

Abstract: Previous studies have suggested that the frequency of chromosomal aberrations (CAs), but not of sister chromatid exchanges (SCEs), predicts cancer risk. We have further examined this relationship in European cohorts comprising altogether almost 22,000 subjects, in the framework of a European collaborative project (CancerRiskBiomarkers). The present paper gives an overview of some of the results of the project, especially as regards CAs and SCEs. The results confirm that a high level of CAs is associated with an increased risk of cancer and indicate that this association does not depend on the time between CA analysis and cancer detection, i.e., is obviously not explained by undetected cancer. The present evidence indicates that both chromatid-type and chromosome-type CAs predict cancer, even though some data suggest that chromosome-type CAs may have a more pronounced predictive value than chromatid-type CAs. CA frequency appears to predict cancers at various sites, although there seems to be a particular association with gastrointestinal cancers. SCE frequency does not appear to have cancer predictive value, at least partly due to uncontrollable technical variation. A number of genetic polymorphisms of xenobiotic metabolism, DNA repair, and folate metabolism affect the level of CAs and might collectively contribute to the cancer predictivity of CAs. Other factors that may influence the association between CAs and cancer include, e.g., exposure to genotoxic carcinogens and internal generation of genotoxic species. Although the association between CA level and cancer is seen at the group level, an association probably also exists for the individual, although it is not known if an individual approach could be feasible. However, group level evidence should be enough to support the use of CA analysis as a tool in screening programs and prevention policies in occupational and environmental health. [Copyright &y& Elsevier]

Published
2006
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3. Chromosomal aberration frequency in lymphocytes predicts the risk of cancer: results from a pooled cohort study of 22 358 subjects in 11 countries

Author

Ulf Strömberg, Stefano Bonassi, Alexandra Fucic, Juozas R. Lazutka, Radim J. Sram, Pavel Rossner, Inger Lise Hansteen, Sarolta Gundy, Roel Vermeulen, Hannu Norppa, Antonina Cebulska-Wasilewska, Marcello Ceppi, Lisbeth E. Knudsen, Ariana Znaor, Paolo Boffetta, Eleonora Fabianova, Bonassi, S., Norppa, H., Ceppi, M., Strömberg, U., Vermeulen, R., Znaor, A., Cebulska-Wasilewska, A., Fabianova, E., Fucic, A., Gundy, S., Hansteen, I.-L., Knudsen, L.E., Lazutka, J., Rossner, P., Sram, R.J., and Boffetta, P.

Subjects
Oncology, Adult, Male, Cancer Research, medicine.medical_specialty, Pathology, Chromosome aberration, Risk Assessment, RR, relative risk, Cohort Studies, Risk Factors, Internal medicine, Neoplasms, medicine, Humans, Genetic Predisposition to Disease, Lymphocytes, Risk factor, Stomach cancer, Aged, Aged, 80 and over, Chromosome Aberrations, Molecular Epidemiology, business.industry, Incidence (epidemiology), Incidence, Cancer, chromosome aberration, cancer, General Medicine, Middle Aged, medicine.disease, Confidence interval, CI, confidence interval, Relative risk, IR, ionizing radiation, Female, CA, chromosomal aberration, business, Cohort study
Abstract

Mechanistic evidence linking chromosomal aberration (CA) to early stages of cancer has been recently supported by the results of epidemiological studies that associated CA frequency in peripheral lymphocytes of healthy individuals to future cancer incidence. To overcome the limitations of single studies and to evaluate the strength of this association, a pooled analysis was carried out. The pooled database included 11 national cohorts and a total of 22 358 cancer-free individuals who underwent genetic screening with CA for biomonitoring purposes during 1965-2002 and were followed up for cancer incidence and/ or mortality for an average of 10.1 years; 368 cancer deaths and 675 incident cancer cases were observed. Subjects were classified within each laboratory according to tertiles of CA frequency. The relative risk (RR) of cancer was increased for subjects in the medium [RR = 1.31, 95% confidence interval (CI) = 1.07-1.60] and in the high (RR = 1.41; 95% CI = 1.16-1.72) tertiles when compared with the low tertile. This increase was mostly driven by chromosome-type aberrations. The presence of ring chromosomes increased the RR to 2.22 (95% CI = 1.34-3.68). The strongest association was found for stomach cancer [RRmedium = 1.17 (95% CI = 0.37-3.70), RRhigh = 3.13 (95% CI = 1.17-8.39)]. Exposure to carcinogens did not modify the effect of CA levels on overall cancer risk. These results reinforce the evidence of a link between CA frequency and cancer risk and provide novel information on the role of aberration subclass and cancer type. © The Author 2008. Published by Oxford University Press. All rights reserved.

Published
2008

4. N-2-Ethyldeoxyguanosine as a Potential Biomarker for Assessing Effects of Alcohol Consumption on DNA

Author

Renato Talamini, Ivana Holcatova, Lorenzo Richiardi, Sarolta Gundy, Ariana Znaor, Silvia Balbo, Paolo Boffetta, Stephen S. Hecht, Vladimir Bencko, Franco Merletti, Paul Brennan, Antonio Agudo, Myngiayo Wang, Cristina Canova, Mia Hashibe, Xavier Castellsagué, Lorenzo Simonato, Balbo, S., Hashibe, M., Gundy, S., Brennan, P., Canova, C., Simonato, L., Merletti, F., Richiardi, L., Agudo, A., Castellsagué, X., Znaor, A., Talamini, R., Bencko, V., Holcátová, I., Wang, M., Hecht, S.S., and Boffetta, P.

Subjects
Adult, Male, medicine.medical_specialty, Spectrometry, Mass, Electrospray Ionization, QUANTITATION, BLOOD, Alcohol Drinking, Epidemiology, Alcohol, medicine.disease_cause, Adduct, ACETALDEHYDE ADDUCT, chemistry.chemical_compound, DNA Adducts, Internal medicine, DNA adduct, ETHANOL, medicine, Humans, Carcinogen, Chromatography, High Pressure Liquid, Ethanol, Molecular Structure, IDENTIFICATION, Smoking, Case-control study, Acetaldehyde, Deoxyguanosine, Middle Aged, N2-ethyldeoxyguanosine potential biomarker assessing effects alcohol consumption DNA, head and neck cancer, alcohol consumption, biomarkers, ACETALDEHYDE ADDUCT, ETHANOL, IDENTIFICATION, QUANTITATION, CANCER, BLOOD, CANCER, Endocrinology, Oncology, chemistry, Biochemistry, Case-Control Studies, Female, Carcinogenesis, Biomarkers
Abstract

Head and neck cancers are causally related to alcohol consumption, but the underlying mechanisms are unclear. Ethanol is metabolized to acetaldehyde, an experimental carcinogen. Quantitation of the major DNA adduct of acetaldehyde, N2-ethylidenedeoxyguanosine, in human tissues could help to elucidate the mechanism of alcohol carcinogenicity. We applied a quantitative method for the analysis of this adduct, measured as the NaBH3CN reduction product N2-ethyldeoxyguanosine (N2-ethyl-dGuo) by liquid chromatography-electrospray ionization-tandem mass spectrometry-selected reaction monitoring, on DNA (0.04 ± 0.03 mg) isolated from blood collected from control subjects recruited from two studies conducted in different areas of Europe between 1999 and 2005. The group selected from the first study (n = 127) included alcohol drinkers and abstainers while the group from the second study (n = 50) included only heavy drinkers. N2-ethyl-dGuo was detected in all DNA samples. After adjusting for potential confounders, in the first study, drinkers showed a higher level of N2-ethyl-dGuo (5,270 ± 8,770 fmol/μmol dGuo) compared with nondrinkers (2,690 ± 3040 fmol/μmol dGuo; P = 0.04). A significant trend according to dose was observed in both studies (P = 0.02 and 0.04, respectively). Taking into account the amount of alcohol consumption, adduct levels were higher in younger compared with older subjects (P = 0.01), whereas no differences were observed comparing men with women. These results show the feasibility of quantifying N2-ethyl-dGuo in small-volume blood samples and are consistent with the hypothesis that ethanol contributes to carcinogenesis through DNA adducts formation. (Cancer Epidemiol Biomarkers Prev 2008;17(11):3026–32)

Published
2008

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