Guidelines for the Statistical Evaluation of SCE

Hc, Wulf; Husum, B.; Engberg-Pedersen, H.; Niebuhr, Erik

doi:10.1007/978-1-4684-4889-4_34

Sister Chromatid Exchanges 1984

DOI: 10.1007/978-1-4684-4889-4_34

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Guidelines for the Statistical Evaluation of SCE

Wulf Hc¹,

B. Husum²,

H. Engberg-Pedersen³

et al.

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1986

1992

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Cited by 11 publications

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Genetic and environmental influences on baseline SCE

Hirsch

Sentz²

1992

Environ and Mol Mutagen

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Previous population-based studies have identified subject characteristics that, when combined, can account for approximately 20% of the observed interindividual variation in baseline SCE rates. In the present investigation, a classic twin study design was used to address the issue of the relevance of genetic factors to baseline SCE rates and to identify other demographic, hematologic, and exposure variables predictive of SCE rate. Questionnaire data and peripheral blood samples from 136 monozygotic and 88 dizygotic twins (age range: 25-81 years) were obtained. Among the large number of variables examined, univariate analyses (including ANOVA tests for the categorical variables and Pearson-product moment correlations for the quantitative variables) revealed smoking status, coffee drinking status, sex, white blood cell count, and absolute numbers of lymphocytes and neutrophils to have significant effects on SCE rates. A stepwise multiple regression analysis showed that together, smoking and coffee drinking status entered at the first step accounted for 21% of the observed variance in SCE, with a further 6% being contributed by the demographic and hematologic variables added in subsequent steps. Finally, the twin analyses showed that after adjustment of the data set for smoking and other significant predictors, genetic factors accounted for approximately 30% of the variation in SCE rates. Thus these data support the hypothesis of a significant genetic influence on baseline SCE.

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Genetic and environmental influences on baseline SCE

Hirsch

Sentz²

1992

Environ and Mol Mutagen

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Normal sister chromatid exchange in lymphocytes from patients with multiple epidermal cancer?

Frentz¹,

Hc²,

Munch‐Petersen

et al. 1987

Arch Dermatol Res

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Exposure to toxins in the environment and due to personal habits, e.g., tobacco smoking, may increase the rate of spontaneous sister chromatid exchange (SCE). The SCE in lymphocytes from a group of 31 patients with multiple epidermal cancer, who in the past had been exposed to various skin carcinogens, as a whole exceeded that of a control group--matched by sex, age, and smoking habits--but the difference was not statistically significant (p = 0.08). The individual SCE in these patients was also statistically independent of the nature of the carcinogenic exposure. We were unable to detect correlations between the SCE and UVC-radiation induced DNA synthesis, UVC-radiation tolerance, or rate of X-ray damage repair. This suggests that the molecular mechanisms involved in SCE induction and in repair of radiation damage are basically independent.

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The effect of agent dose and treatment time on the intercellular distribution of sister-chromatid exchanges induced by genotoxic agents in mouse bone marrow cells in vivo

Tice

Ormiston

McFee

1989

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Guidelines for the Statistical Evaluation of SCE

Cited by 11 publications

References 4 publications

Genetic and environmental influences on baseline SCE

Genetic and environmental influences on baseline SCE

Normal sister chromatid exchange in lymphocytes from patients with multiple epidermal cancer?

The effect of agent dose and treatment time on the intercellular distribution of sister-chromatid exchanges induced by genotoxic agents in mouse bone marrow cells in vivo

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