| 1. |
- Hedelin, Maria, 1964, et al.
(author)
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Dietary phytoestrogens are not associated with risk of overall breast cancer but diets rich in coumestrol are inversely associated with risk of estrogen receptor and progesterone receptor negative breast tumors in Swedish women.
- 2008
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In: The Journal of nutrition. - : Elsevier BV. - 1541-6100 .- 0022-3166. ; 138:5, s. 938-945
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Journal article (peer-reviewed)abstract
- Results from epidemiological and experimental studies indicate that phytoestrogens may protect against breast cancer. Because one of the biological effects of phytoestrogens is probably estrogenic, it's possible that the preventive effect on breast cancer differs by estrogen receptor (ER) or progesterone receptor (PR) status of the tumor. We evaluated the associations between dietary phytoestrogen (isoflavonoids, lignans, and coumestrol) intake and risk of breast cancer and whether the ER/PR statuses of the tumor influence this relationship. In 1991-2 a prospective population-based cohort study among Swedish pre- and postmenopausal women was performed, making questionnaire data available for 45,448 women. A total of 1014 invasive breast cancers were diagnosed until December 2004. Cox proportional hazards models were performed to estimate multivariate risk ratios, 95% CI for associations with risk of breast cancer. Intakes of lignan, isoflavonoid, or coumestrol were not associated with breast cancer risk overall or before or after 50 y of age. The effects of lignans or isoflavonoids were independent of receptor status. However, intake of coumestrol was associated with decreased risk of receptor negative tumors (ER-PR-) but not positive tumors. The risk of ER-PR- tumors was significantly lower (50%) in women with intermediate coumestrol intake compared with those who did not consume any. In conclusion, we found no association between intake of isoflavonoids or lignans and breast cancer risk. Our results of a decreased risk of ER-PR- tumors in women with intermediate intake of coumestrol could be due to chance because of the low intake. The results should be confirmed in other studies.
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| 2. |
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| 3. |
- Kuper, Hannah, et al.
(author)
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Prospective Study of Solar Exposure, Dietary Vitamin D Intake, and Risk of Breast Cancer among Middle-aged Women
- 2009
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In: Cancer Epidemiology, Biomarkers and Prevention. - Philadelphia, Pennsylvania : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 18:9, s. 2558-2561
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Journal article (other academic/artistic)abstract
- The relationship between solar exposure or dietary vitamin D intake and breast cancer risk has not been fully elucidated. These associations were studied within the Womens Lifestyle and Health Cohort Study, a cohort of 49,259 Swedish women ages 30 to 50 years at baseline (1991-1992). Women were asked about solar exposure and completed a food frequency questionnaire and were followed-up through linkages to national registries until December 2004. In the current analyses, 41,889 women were included, 840 of whom were diagnosed with breast cancer during follow-up. Breast cancer risk was not related to solar exposure variables, including sun sensitivity, annual number of sunburns, time spent on sunbathing vacations, or solarium use at any age period of exposure. There was also no association with dietary vitamin D intake or supplementary multivitamin use. These relationships were not modified after stratifying by estrogen or progesterone receptor status.
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| 4. |
- Löf, Marie, et al.
(author)
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Dietary fat intake and gestational weight gain in relation to estradiol and progesterone plasma levels during pregnancy : a longitudinal study in Swedish women.
- 2009
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In: BMC Women's Health. - : Springer Science and Business Media LLC. - 1472-6874. ; 9:10
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Journal article (peer-reviewed)abstract
- BACKGROUND: Elevated pregnancy hormone levels, such as oestrogen and progesterone, may increase the risk of developing breast cancer both in mothers and offspring. However, the reasons for large inter-individual variations in estrogen and progesterone levels during pregnancy remain unknown. The objectives of this study were to investigate whether a) intakes of total dietary fat, types of fat (monounsaturated: MUFA, polyunsaturated: n-3 and n-6 PUFA, and saturated) and b) gestational weight gain are associated with estradiol and progesterone levels in plasma during pregnancy. METHODS: We measured body weight as well as estradiol and progesterone in plasma among 226 healthy pregnant Swedish women on gestation weeks 12, 25 and 33. At the same time points, dietary intake of total fat and types of fat (MUFA, PUFA, SFA, n-3 and n-6 PUFA) were estimated using 3-day food diaries. RESULTS: A large variation in estradiol and progesterone levels was evident.Nulliparous women had 37%, 12% and 30% higher mean estradiol levels on gestation weeks 12, 25 and 33 compared to parous women (P = 0.008). No associations were found between dietary intake of total fat or fat subtypes (including n-3 PUFA and n-6 PUFA) and plasma estradiol or progesterone levels. Gestational weight gain was associated with progesterone levels (P = 0.03) but the effect was very small (20% increase in progesterone levels between gestational weeks 12 and 33 per kg body weight/week). CONCLUSION: No associations among gestational weight gain, maternal dietary fat intake (total or subtypes including n-3 PUFA and n-6 PUFA) and plasma estradiol levels were found. However, pregnancy progesterone levels correlated with weight gain during pregnancy. Identification of other possible determinants of pregnancy estradiol and progesterone levels, important for the development of breast cancer in both mothers and offspring, are needed.
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| 5. |
- Löf, Marie, et al.
(author)
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Effects of pre-pregnancy physical activity and maternal BMI on gestational weight gain and birth weight.
- 2008
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In: Acta obstetricia et gynecologica Scandinavica. - : Wiley. - 1600-0412 .- 0001-6349. ; 87:5, s. 524-530
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Journal article (peer-reviewed)abstract
- BACKGROUND: Western women frequently exhibit excessive gestational weight gain (GWG). The effects of maternal physical activity level (PAL) and body mass index (BMI) on the timing of GWG are insufficiently known. PURPOSE: To assess the impact of pre-pregnancy PAL and BMI on GWG during the second and third trimester and on birth weight. METHODS: Body weight was measured in 223 healthy Swedish women in gestational weeks 12, 25 and 33, and GWG during the second (weeks 12-25) and third trimesters (weeks 25-33) was determined (kg/week). PAL was assessed using a questionnaire. Birth weights were obtained from birth records. The results were evaluated by the fitting of linear statistical models. RESULTS: Some 50 and 80% of the women exhibited excessive GWG during the second and third trimesters, respectively. Women with a high pre-pregnancy PAL gained 0.10 kg/week (p=0.04) less weight during the third trimester than women with a medium PAL. A 5 kg/m(2) higher BMI was associated with a 0.06 kg/week lower GWG in the second trimester (p=0.005), but with a 0.05 higher GWG in the third trimester (p=0.03). Maternal BMI (p=0.014) and total GWG (p=0.05) correlated with birth weight. CONCLUSIONS: High BMI and low pre-pregnancy PAL were associated with excessive GWG. BMI and GWG, but not pre-pregnancy PAL, were linked to birth weight. However, together with smoking, parity, education and age, pre-pregnancy PAL and BMI explained only 4% of the variation in GWG. Thus, identification of other factors that could explain excessive GWG is an important area of future research.
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| 6. |
- Löf, Marie, 1971-, et al.
(author)
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Epidemiologic evidence suggests that dietary phytoestrogen intake is associated with reduced risk of breast, endometrial, and prostate cancers
- 2006
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In: Nutrition Research. - : Elsevier BV. - 0271-5317 .- 1879-0739. ; 26:12, s. 609-619
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Journal article (peer-reviewed)abstract
- Phytoestrogens are natural estrogen-like plant substances. The possible protective effect of phytoestrogens on cancer risk, particularly on hormone-related cancers, has been the focus of many epidemiologic studies during the last 2 decades. We performed a qualitative review of the epidemiologic literature published in the English language and identified on MEDLINE from 1966 until 24 September 2006 on (1) dietary intake of soy, isoflavones, or lignans; (2) urinary excretion of isoflavones or lignans; (3) blood measurements of isoflavones or lignans in relation to breast, prostate, and endometrial cancer risk. Epidemiologic data do seem to support a small protective effect of isoflavones on breast cancer risk, although timing of exposure and the mechanisms of isoflavones at physiologic levels need to be further explored. The epidemiologic evidence to date is conflicting regarding lignans and breast cancer, but recent studies suggest that the effect may be restricted to premenopausal women, differ by estrogen receptor status, and be modified by diet-gene interactions. The 3 case-control studies on dietary intake of phytoestrogens and endometrial cancer risk have provided some evidence for a protective effect, but more prospective data are needed. There is some epidemiologic evidence for a protective effect of soy or isoflavones on prostate cancer, but corresponding data for lignans are inconclusive. Recent data indicate that diet-gene interactions may modify the effect of phytoestrogens on prostate cancer risk. Prospective studies on dietary lignans in relation to prostate cancer risk are lacking.
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| 7. |
- Monge, Patricia, et al.
(author)
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Parental occupational exposure to pesticides and the risk of childhood leukemia in Costa Rica
- 2007
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In: Scandinavian Journal of Work, Environment and Health. - : Scandinavian Journal of Work, Environment and Health. - 0355-3140 .- 1795-990X. ; 33:4, s. 293-303
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Journal article (peer-reviewed)abstract
- OBJECTIVES: Parental exposure to pesticides and the risk of leukemia in offspring were examined in a population-based case-control study in Costa Rica. METHODS: All cases of childhood leukemia (N=334), in 1995-2000, were identified at the Cancer Registry and the Children's Hospital. Population controls (N=579) were drawn from the National Birth Registry. Interviews of parents were conducted using conventional and icon-based calendar forms. An exposure model was constructed for 25 pesticides in five time periods. RESULTS: Mothers' exposures to any pesticides during the year before conception and during the first and second trimesters were associated with the risk [odds ratio (OR) 2.4, 95% confidence interval (95% CI) 1.0-5.9; OR 22, 95% CI 2.8-171.5; OR 4.5, 95% CI 1.4-14.7, respectively] and during anytime (OR 2.2, 95% CI 1.0-4.8). An association was found for fathers' exposures to any pesticides during the second trimester (OR 1.5, 95% CI 1.0-2.3). An increased risk with respect to organophosphates was found for mothers during the first trimester (OR 3.5, 95% CI 1.0-12.2) and for fathers during the year before conception and the first trimester (OR 1.5, 95% CI 1.0-2.2 and OR 1.6, 95% CI 1.0-2.6, respectively), and benzimidazoles during the first, second, and third trimesters of pregnancy (OR 2.2, 95% CI 1.0-4.4; OR 2.2, 95% CI 1.0-5.0; OR 2.2, 95% CI 1.0-5.2, respectively). There was a suggestion of an exposure-response gradient for fathers as regards picloram, benomyl, and paraquat. Age at diagnosis was positively associated with fathers' exposures and inversely associated with mothers' exposures. CONCLUSIONS: The results suggest that parental exposure to certain pesticides may increase the risk of leukemia in offspring.
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| 8. |
- Wedrén, Sara, et al.
(author)
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Associations between androgen and Vitamin D receptor microsatellites and postmenopausal breast cancer
- 2007
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In: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 16:9, s. 1775-1783
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Journal article (peer-reviewed)abstract
- We investigated the association between polymorphism in the androgen receptor (AR) and vitamin D receptor (VDR) genes and breast cancer risk in a large population-based case-control study of genetically homogenous Swedish women. We successfully determined both AR CAG(n) and VDR A(n) genotype in 1,502 women with invasive breast cancer and in 1,510 control women. We did not find any associations between AR or VDR microsatellite lengths and breast cancer when we used a priori determined cutoffs (/=22 repeats for AR and /=19 for VDR) to define long and short alleles. There was statistically significant interaction between VDR genotype and parity, such that women with two short alleles had a halved risk for breast cancer, irrespective of parity, compared with nulliparous women with two long alleles. Homozygosity for the long VDR allele was associated with a more advanced clinical stage at diagnosis. In exploratory analyses, we determined cutoffs based on visual inspection of distributions of allele lengths among cases and controls and found that women carrying two alleles with <20 AR CAG(n) repeats had an increased risk for breast cancer, odds ratio of 1.67 (95% confidence interval, 1.17-2.38), compared with those with two alleles with >/=20 repeats. Women carrying two VDR alleles with <21 A(n) were also at an increased risk, odds ratio of 1.26 (95% confidence interval, 1.04-1.51). Our data do not support major roles for AR or VDR polymorphism as breast cancer risk factors. However, we did find an interaction between VDR genotype and parity that remains to be corroborated.
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| 9. |
- Wedrén, Sara, et al.
(author)
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Estrogen receptor alpha gene polymorphism and endometrial cancer risk : a case-control study
- 2008
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In: BMC Cancer. - : Springer Science and Business Media LLC. - 1471-2407 .- 1471-2407. ; 8, s. 322-
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Journal article (peer-reviewed)abstract
- BACKGROUND: Estrogen is an established endometrial carcinogen. One of the most important mediators of estrogenic action is the estrogen receptor alpha. We have investigated whether polymorphic variation in the estrogen receptor alpha gene (ESR1) is associated with endometrial cancer risk. METHODS: In 702 cases with invasive endometrial cancer and 1563 controls, we genotyped five markers in ESR1 and used logistic regression models to estimate odds ratios (OR) and 95 percent confidence intervals (CI). RESULTS: We found an association between rs2234670, rs2234693, as well as rs9340799, markers in strong linkage disequilibrium (LD), and endometrial cancer risk. The association with rs9340799 was the strongest, OR 0.75 (CI 0.60-0.93) for heterozygous and OR 0.53 (CI 0.37-0.77) for homozygous rare compared to those homozygous for the most common allele. Haplotype models did not fit better to the data than single marker models. CONCLUSION: We found that intronic variation in ESR1 was associated with endometrial cancer risk.
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| 10. |
- Yang, Ling, et al.
(author)
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Predictors of ovarian cancer survival: A population-based prospective study in Sweden
- 2008
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In: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 123:3, s. 672-679
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Journal article (peer-reviewed)abstract
- Ovarian cancer is the leading cause of death from gynecologic malignancies among women worldwide. Little is known about reproductive factors or lifestyle determinants and ovarian cancer prognosis. The objective of this study was to examine whether ovarian cancer survival is influenced by reproductive history, anthropometric characteristics, prediagnostic life-style factors and family history or breast or ovarian cancer. The study population consisted of 635 epithelial Ovarian, cancer (EOC) cases derived from a nationwide population-based case-control study conducted in Sweden between 1993 and 1995. Exposure data on prediagnostic factors of interest were collected through questionnaires at the beginning of the parent study. Clinical data were abstracted from medical records. Cases were followed-up by means of record linkage to nationwide registers until December 31, 2002. Cox proportional hazard regression model was used to estimate the prognostic effect of each factor in terms of hazard ratios (HR) and 95% confidence intervals (CI), following adjustment for age at diagnosis, FIGO tumor stage and WHO grade of tumor differentiation. Tumor characteristics significantly influenced the risk of death from EOC. After adjustment for these, no clear associations were detected between reproductive history (parity, age at first or last birth, oral contraceptive use, age at menarche or menopause), anthropometric characteristics (body size and shape in different periods of life), lifestyle factors before diagnosis (alcohol consumption, smoking and physical activity over lifetime), nor family history of breast cancer or ovarian cancer and EOC survival. Our findings indicate that these prediagnostic factors do not influence the EOC survival. Nevertheless, among women with early stage disease (FIGO stage I and II), there was some indication that overweight in young adulthood or recent years increased the risk of death, while physical activity in young adult life appeared to reduce the risk of death due to EOC.
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