| 1. |
- Goodman, Anna, et al.
(författare)
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Maternal pelvic size not predictive of daughter's breast cancer or ovarian cancer in a large Swedish cohort
- 2009
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 18:8, s. 2333-2335
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Tidskriftsartikel (refereegranskat)abstract
- Recent studies from Finland reported that maternal pelvic size predicted daughters' breast and ovarian cancer, possibly because maternal pelvic size is a marker for in utero hormone exposure. We sought to replicate this association in 3,845 women born between 1915 and 1929 in Uppsala, Sweden, and followed from 1960 to 2002. Archived obstetric records provided the standard measures of maternal pelvic size (intercristal distance, interspinous distance, the intercristal-interspinous difference, and the external conjugate distance). The Swedish Cancer Registry ascertained cancer incidence, with 273 cohort members developing primary breast cancer, and 52 developing primary ovarian cancer during the follow-up period. There was no evidence (P > 0.1) of an association between any measure of maternal pelvic size and incidence of either breast or ovarian cancer. This was true both before and after adjustment for various characteristics of the women and their mothers, and in analyses stratified by age at diagnosis (<50 versus ≥50 years of age, as a proxy for premenopausal and postmenopausal ages). There was also no evidence of an association in subgroup analyses restricted specifically to those groups in which the Finnish data found the greatest effect. Our study is of comparable size to the Finnish studies and was highly powered (>99%) to detect effects of the magnitude they reported. Our nonreplication therefore casts doubt on the link between maternal pelvic size and risk of breast and ovarian cancer in the offspring. (Cancer Epidemiol Biomarkers
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| 2. |
- Hochstenbach, Kevin, et al.
(författare)
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Global gene expression analysis in cord blood reveals gender specific differences in response to carcinogenic exposure in utero
- 2012
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 21:10, s. 1756-1767
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Tidskriftsartikel (refereegranskat)abstract
- Background: It has been suggested that fetal carcinogenic exposure might lead to predisposition to develop cancer during childhood or in later life possibly through modulation of the fetal transcriptome. Because gender effects in the incidence of childhood cancers have been described, we hypothesized differences at the transcriptomic level in cord blood between male and female newborns as a consequence of fetal carcinogenic exposure. The objective was to investigate whether transcriptomic responses to dietary genotoxic and nongenotoxic carcinogens show gender-specific mechanisms-of-action relevant for chemical carcinogenesis. Methods: Global gene expression was applied in umbilical cord blood samples, the CALUX-assay was used for measuring dioxin(-like), androgen(-like), and estrogen(-like) internal exposure, and acrylamide-hemoglobin adduct levels were determined by mass spectrometry adduct-FIRE-procedure (TM). To link gene expression to an established phenotypic biomarker of cancer risk, micronuclei frequencies were investigated. Results: While exposure levels did not differ between sexes at birth, important gender-specific differences were observed in gene expressions associated with these exposures linked with cell cycle, the immune system and more general cellular processes such as posttranslation. Moreover, oppositely correlating leukemia/lymphoma genes between male and female newborns were identified in relation to the different biomarkers of exposure that might be relevant to male-specific predisposition to develop these cancers in childhood. Conclusions/Impact: This study reveals different transcriptomic responses to environmental carcinogens between the sexes. In particular, male-specific TNF-alpha-NF-kB signaling upon dioxin exposure and activation of the Wnt-pathway in boys upon acrylamide exposure might represent possible mechanistic explanations for gender specificity in the incidence of childhood leukemia.
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| 3. |
- Kotova, Natalia, 1975-, et al.
(författare)
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Urinary Thymidine Dimer as a Marker of Total BodyBurden of UV-Inflicted DNA Damage in Humans
- 2005
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 14:12, s. 2868-2872
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Tidskriftsartikel (refereegranskat)abstract
- High levels of DNA damage are induced in human skin following exposure to UV radiation. Cyclobutane thymidine dimer (T = T) is the most common of these lesions, which are enzymatically removed as oligonucleotides from DNA and further degraded before excretion in urine. Analysis of such repair products in the urine could serve as a biomarker of total body burden of UV exposure. The aim of this study was to examine the kinetics of T = T excretion following a single tanning session in a commercial solarium and to validate the method by delivering different doses. Ten individuals used the solarium for a total of 35 sessions of body tanning. Urine was collected before UV exposure and daily thereafter (up to 5 or 11 days) and T = T was analyzed using a very sensitive and quantitative P-32-postlabeling technique combined with high-performance liquid chromatography. Following exposure, T = T levels increased dramatically and reached a peak 3 days later; afterwards, the T = T levels gradually decreased. The total amount of T = T excreted differed about 5-fold among subjects given an equal dose. A 50% excretion time was calculated using the excretion data for the first 5 days and it was found to be between 55 and 76 hours for different individuals. There was a good correlation between the amount of T = T excreted during days 1 to 5 and the delivered UV dose. Reducing exposure time to 50% lowered the amount of T = T to 47%; if half of the lamps were covered, T = T decreased to 44%. Our data show that urinary T = T could be a suitable noninvasive biomarker for UV exposure; a finding which could also be applicable to studies in children.
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