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Gene-exposure interaction in occupational and environmental epidemiology: Results from an ongoing study

By Elin H. Kure, Marit Thorsen and Inger-Lise Hansteen

Abstract

<strong><span style="font-family: TimesNewRomanPS-BoldMT;"><span style="font-family: TimesNewRomanPS-BoldMT;"><p align="left"> </p></span></span><p align="left"><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;">ABSTRACT</span></span></p></strong><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left">A tissue bank is established in our department on a total of 659 persons whereof 341 are included in the</p><p align="left">Nordic data base on somatic chromosome damage in humans. Genotyping of susceptibility genes relevant</p><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left">to the exposures of the cohort is an ongoing undertaking in our laboratory.</p></span></span></span><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left"> </p></span></span><p align="left"><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;">GST</span></span></em><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;">'s and </span></span><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;">mEH </span></span></em><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;">have been<span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left">genotyped for 80 persons so far,</p></span></span></span><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left"> </p></span></span></p><p align="left"><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;">CYP</span></span></em><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;">'s for 20 persons. When the mean number of chromatide breaks and of<p align="left">cells with aberrations were related to genotypes no statistical difference could be observed between the</p><p align="left">genotypes for either parameter. No difference in cytogenetic damage between exposed and referents or</p><p align="left">between smokers and non-smokers were identified for the two separate occupational studies these 80</p><p align="left">persons represent. The results of the various cytogenetic endpoints were trichotomized and compared to the</p><p align="left">genotype distribution. Although not statistically significant, the observed trend with higher percentage of</p><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left">persons with polymorphic</p></span></span></span><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left"> </p></span></span></p><p align="left"><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;">GST</span></span></em><span style="font-size: x-small; font-family: Symbol;"><span style="font-size: x-small; font-family: Symbol;">p</span></span><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;">1 </span></span></em><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;">in particular, but also for </span></span><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;">GST</span></span></em><span style="font-size: x-small; font-family: Symbol;"><span style="font-size: x-small; font-family: Symbol;">q</span></span><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;">1 </span></span></em><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;">and </span></span><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;">mEH </span></span></em><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;">(exon 4) in the group with<p align="left">high frequency of chromosome aberrations will be interesting to follow. For further follow-up studies, a</p><p align="left">nested case-control study within the cohort would give a more rapid and less expensive approach than</p><p align="left">analysing each study separately as a traditional case-control study. As high frequency of chromosomal</p><p align="left">damage is associated with cancer development, the hypothesis to be tested would be whether genetic polymorphisms</p><p>for the most appropriate susceptibility genes could be an explanatory factor for this association.</p></span></span></p

Topics: Public aspects of medicine, RA1-1270, Medicine, R
Publisher: Norsk Forening for Epidemiologi
Year: 2009
OAI identifier: oai:doaj.org/article:def6ad7e593e48279755c5704c04351a
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