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ABSTRACT: Results of studies for the association of BRCA1 genotypes and haplotypes with sporadic breast cancer have been inconsistent. Therefore, a candidate single nucleotide polymorphism (SNP) approach was used in a breast cancer case-control study to explore genotypes and haplotypes that have the potential to affect protein functions or levels. In a breast cancer case-control study, genotyping of BRCA1 polymorphisms Q356R, D693N, and E1038G was performed on 1,005 cases and 1,765 controls. Unconditional, polytomous logistic regression and χ(2) -tests were used to examine the associations of breast cancer with genotypes and haplotypes. In addition, interactions between genotype and smoking, benign breast disease, family history of breast cancer, body mass index (BMI), alcohol consumption, and hormonal risk factors, hormone receptor status, and breast cancer pathology were calculated also using logistic regression and χ(2) . Although sporadic breast cancer was not associated with BRCA1 genotypes or haplotypes overall or by menopausal status, there was evidence of an interaction between the E1038G BRCA1 genotype, smoking, and BMI among premenopausal women (P for interaction = 0.01 and 0.045, respectively) and between E1038G and D693N BRCA1 genotypes and hormone therapy use among postmenopausal women (P for interaction = 0.01 and 0.02, respectively). There were no other associations found between BRCA1 genotypes and stage, histological grade, or nuclear grade. However, the D693N SNP was associated with the risk of triple negative breast cancer (odds ratio = 2.31 95% confidence interval 1.08-4.93). The BRCA1 variants studied may play a role in the etiology of triple negative breast cancer and may interact with environmental factors such as hormone therapy or smoking and increase sporadic breast cancer risk.
Genetic Epidemiology 05/2013; · 3.44 Impact Factor
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ABSTRACT: Alcohol intake is a risk factor for breast cancer, but the association between alcohol and mortality among breast cancer survivors is poorly understood. We examined the association between alcohol intake from all sources, assessed by cognitive lifetime drinking history, and all-cause and breast cancer mortality among women with breast cancer (N = 1,097) who participated in a population-based case-control study. Vital status was ascertained through 2006 using the National Death Index. Using Cox proportional hazards models, we computed hazard ratios for all-cause and breast cancer mortality in association with alcohol intake. We examined lifetime volume and intensity (drinks per drinking day) of alcohol consumption as well as drinking status during various life periods. Analyses were stratified by menopausal status. After adjustment for total intake, postmenopausal women with consumption of four or more drinks per drinking day over their lifetimes were nearly three times more likely to die from any cause compared to abstainers (HR 2.94, 95 % CI 1.31, 6.62). There was a similar but non-significant association with breast cancer mortality (HR 2.68, 95 % CI 0.94, 7.67). Postmenopausal women who drank one drink or fewer per drinking day between menarche and first birth had a significantly decreased hazard of all-cause (HR 0.54, 95 % CI 0.31, 0.95) and breast cancer mortality (HR 0.27, 95 % CI 0.09, 0.77). Premenopausal breast cancer survival was not associated with drinking intensity. We observed no associations between drinking status or total volume of alcohol intake and breast cancer or all-cause mortality. High-intensity alcohol consumption may be associated with decreased survival in postmenopausal women with breast cancer. Low-intensity alcohol consumption between menarche and first birth may be inversely associated with all-cause and breast cancer mortality; this period may be critical for development of and survival from breast cancer. Intensity of alcohol intake may be a more important factor than absolute volume of intake on survival in women with breast cancer.
Breast Cancer Research and Treatment 04/2013; · 4.43 Impact Factor
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Adana A Llanos,
Theodore M Brasky,
Ramona G Dumitrescu,
Catalin Marian,
Kepher H Makambi,
Bhaskar V S Kallakury,
Scott L Spear,
David J Perry,
Rafael J Convit,
Mary E Platek,
Lucile L Adams-Campbell, Jo L Freudenheim,
Peter G Shields
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ABSTRACT: We investigated insulin-like growth factor (IGF)-1 and IGF binding protein (IGFBP)-3 concentrations in histologically normal breast tissues and assessed their association with plasma concentrations, and breast cancer risk factors. IGF-1 and IGFBP-3 were assessed in plasma and breast tissues of 90 women with no history of any cancer and undergoing reduction mammoplasty. Pearson correlations and ANOVAs were used to describe plasma-breast associations and biomarker differences by breast cancer risk factors, respectively. Multivariable regression models were used to determine associations between risk factors, and breast IGF-1 and IGFBP-3. The mean age of the study sample was 37.3 years, 58 % were white, and generally these women were obese (mean BMI = 30.8 kg/m2). We observed no plasma-breast correlation for IGF-1, IGFBP-3, or IGF-1/IGFBP-3 (r = -0.08, r = 0.14, and r = 0.03, respectively; p-values >0.05). Through age- and BMI-adjusted analysis, BMI and years of oral contraceptive (OC) use were inversely associated with breast IGF-1 (p-values = 0.02 and 0.003, respectively) and age was associated with breast IGFBP-3 (p = 0.01), while breast IGF-1/IGFBP-3 was higher in blacks than whites (1.08 vs. 0.68, p = 0.04) and associated with age and BMI (p-values = 0.03 and 0.002, respectively). In multivariable-adjusted models, some breast cancer risk factors studied herein explained 24, 10, and 15 % of the variation in breast IGF-1, IGFBP-3, and IGF-1/IGFBP-3, respectively. While reasons for the lack of plasma-breast hormone correlations in these cancer-free women are unknown, several factors were shown to be associated with breast concentrations. The lack of correlation between blood and tissue IGF-1 and IGFBP-3 suggests that studies of breast cancer risk assessing blood IGF-1 and IGFBP-3 may have important limitations in understanding their role in breast carcinogenesis.
Breast Cancer Research and Treatment 03/2013; · 4.43 Impact Factor
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American journal of epidemiology 12/2012; 176(12):1069-70. · 5.59 Impact Factor
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ABSTRACT: BACKGROUND: Oxidative stress has been implicated as a possible mechanism for adverse health effects associated with traffic emissions. We examined the association of an estimate of traffic emissions with blood biomarkers of antioxidant capacity (glutathione, glutathione peroxidase, trolox-equivalent antioxidant capacity) and oxidative damage (thiobarbituric acid-reactive substances (TBARS)) among 1810 healthy women, randomly selected from Erie and Niagara Counties in Western New York. METHODS: A geographic traffic emission and meteorological dispersion model was used to estimate annual polycyclic aromatic hydrocarbon (PAH) exposure from traffic emissions for each woman based on her residence at the time of study. Associations of traffic-related PAH exposure with measures of oxidative stress and antioxidant capacity were examined in multiple regression analyses with adjustment for potential confounders. RESULTS: Higher traffic-related PAH exposure was associated with decreased glutathione and increased glutathione peroxidase. Stronger associations between traffic-related PAH exposure and levels of glutathione and glutathione peroxidase were suggested among nonsmoking women without secondhand smoke exposure, especially among premenopausal nonsmoking women. Associations were also stronger for measurements made in warmer months. CONCLUSIONS: These findings suggest that PAHs or other components of traffic emissions may impact anti-oxidative capacity among healthy women, particularly premenopausal non-smokers without secondhand smoke exposure.
Environmental Research 11/2012; · 3.40 Impact Factor
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Adana A Llanos,
Ramona G Dumitrescu,
Catalin Marian,
Kepher H Makambi,
Scott L Spear,
Bhaskar V S Kallakury,
David J Perry,
Rafael J Convit,
Mary E Platek,
Amy E Millen,
Lucile L Adams-Campbell, Jo L Freudenheim,
Peter G Shields
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ABSTRACT: Blood adipokines are associated with breast cancer risk; however, blood-breast adipokine correlations and factors that explain variation in adipokines are unknown.
Plasma (n = 155) and breast (n = 85) leptin and adiponectin were assessed by immunoassays in women with no history of cancer. Multivariable-adjusted regression models were used to determine breast adipokine associations.
Through body mass index (BMI)-adjusted analyses, we initially observed positive plasma-breast correlations for leptin (r = 0.41, P = 0.0002) and adiponectin (r = 0.23, P = 0.05). The positive plasma-breast correlation for leptin was strongest among normal weight women (r = 0.62), whereas the correlation for adiponectin was strongest among obese women (r = 0.31). In multivariable models, adjusting for BMI, demographic, reproductive, and lifestyle factors, plasma leptin was not associated with breast leptin, and only the highest quartile of plasma adiponectin was associated with tissue levels. Of the risk factors investigated, those that contributed most to the variation in breast tissue adipokines were BMI and race for leptin, oral contraceptive use and smoking status for adiponectin.
Although we report positive plasma-breast adipokine correlations overall, plasma adipokine concentrations may not be good surrogates for breast concentrations among all women. Predictors of breast adipokines vary, depending on subject characteristics, possibly explaining inconsistent epidemiologic results and they implicate differing pathways toward carcinogenesis. Impact: A clearer understanding of the relationships between plasma adipokines and their levels within the target organ is necessary to better understand the impact of these hormones on breast cancer risk. Future studies are needed to identify additional factors associated with breast adipokines in target tissues. Cancer Epidemiol Biomarkers Prev; 21(10); 1745-55. ©2012 AACR.
Cancer Epidemiology Biomarkers & Prevention 08/2012; 21(10):1745-55. · 4.12 Impact Factor
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Anita Koushik,
Donna Spiegelman,
Demetrius Albanes,
Kristin E Anderson,
Leslie Bernstein,
Piet A van den Brandt,
Leif Bergkvist,
Dallas R English, Jo L Freudenheim,
Charles S Fuchs, [......],
Anthony B Miller,
Kim Robien,
Thomas E Rohan,
Arthur Schatzkin,
James M Shikany,
Rachael Z Stolzenberg-Solomon,
Walter C Willett,
Alicja Wolk,
Regina G Ziegler,
Stephanie A Smith-Warner
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ABSTRACT: Fruit and vegetable intake may protect against pancreatic cancer, since fruits and vegetables are rich in potentially cancer-preventive nutrients. Most case-control studies have found inverse associations between fruit and vegetable intake and pancreatic cancer risk, although bias due to reporting error cannot be ruled out. In most prospective studies, inverse associations have been weaker and imprecise because of small numbers of cases. The authors examined fruit and vegetable intake in relation to pancreatic cancer risk in a pooled analysis of 14 prospective studies from North America, Europe, and Australia (study periods between 1980 and 2005). Relative risks and 2-sided 95% confidence intervals were estimated separately for the 14 studies using the Cox proportional hazards model and were then pooled using a random-effects model. Of 862,584 men and women followed for 7-20 years, 2,212 developed pancreatic cancer. The pooled multivariate relative risks of pancreatic cancer per 100-g/day increase in intake were 1.01 (95% confidence interval (CI): 0.99, 1.03) for total fruits and vegetables, 1.01 (95% CI: 0.99, 1.03) for total fruits, and 1.02 (95% CI: 0.99, 1.06) for total vegetables. Associations were similar for men and women separately and across studies. These results suggest that fruit and vegetable intake during adulthood is not associated with a reduced pancreatic cancer risk.
American journal of epidemiology 08/2012; 176(5):373-86. · 5.59 Impact Factor
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Veronica Wendy Setiawan,
Malcolm C Pike,
Stalo Karageorgi,
Sandra L Deming,
Kristin Anderson,
Leslie Bernstein,
Louise A Brinton,
Hui Cai,
James R Cerhan,
Wendy Cozen, [......],
Pamela J Thompson,
Giske Ursin,
Penelope M Webb,
Noel S Weiss,
Nicolas Wentzensen,
Yong-Bing Xiang,
Hannah P Yang,
Herbert Yu,
Pamela L Horn-Ross,
Immaculata De Vivo
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ABSTRACT: Childbearing at an older age has been associated with a lower risk of endometrial cancer, but whether the association is independent of the number of births or other factors remains unclear. Individual-level data from 4 cohort and 13 case-control studies in the Epidemiology of Endometrial Cancer Consortium were pooled. A total of 8,671 cases of endometrial cancer and 16,562 controls were included in the analysis. After adjustment for known risk factors, endometrial cancer risk declined with increasing age at last birth (P(trend) < 0.0001). The pooled odds ratio per 5-year increase in age at last birth was 0.87 (95% confidence interval: 0.85, 0.90). Women who last gave birth at 40 years of age or older had a 44% decreased risk compared with women who had their last birth under the age of 25 years (95% confidence interval: 47, 66). The protective association was similar across the different age-at-diagnosis groups and for the 2 major tumor histologic subtypes (type I and type II). No effect modification was observed by body mass index, parity, or exogenous hormone use. In this large pooled analysis, late age at last birth was independently associated with a reduced risk of endometrial cancer, and the reduced risk persisted for many years.
American journal of epidemiology 07/2012; 176(4):269-78. · 5.59 Impact Factor
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ABSTRACT: PURPOSE: There is increasing evidence that exposures in early life affect breast cancer risk, and that breast cancer etiology differs by tumor subtype. If environmental exposures in early life contribute to risk, it is expected that there would be clustering of women with breast cancer by their place of birth, and that clustering might differ by subtype. We examined spatial associations between place of birth and breast cancer by subtype, using hormone receptor status and molecular profiles of breast tumors. METHODS: Data were drawn from the Western New York Exposures and Breast Cancer study, a population-based case-control study of incident, pathologically confirmed breast cancer (1996-2001) in Erie and Niagara Counties. Included were women born in the study area (579 cases and 931 controls). Clustering of breast cancer subgroups relative to controls was examined by the k-function method in groups stratified by estrogen receptor (ER), progesterone receptor (PR), and HER2 status, and by DNA methylation status and p53 mutation status, and the k-function difference was used to compare relative spatial aggregation and spatial range of the difference between case subgroups and controls. RESULTS: We found a tendency to cluster among ER positive, PR positive, and HER2 negative cases (i.e., luminal A subtype), especially among premenopausal women, but not among the other groups defined by hormonal receptor status, or by either methylation or p53 mutation status. CONCLUSIONS: While our findings cannot rule out clustering of cases by birth place because of shared behaviors related to residence location, they also suggest that early life environmental exposures may affect subsequent breast cancer risk, and that premenopausal breast tumors of the luminal A subtype may be more affected by these early life exposures than other subtypes.
Cancer Causes and Control 05/2012; · 2.88 Impact Factor
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Theodore M. Brasky,
Matthew R. Bonner,
Kirsten B. Moysich,
Christine B. Ambrosone,
Jing Nie,
Meng Hua Tao,
Stephen B. Edge,
Bhaskar V.S. Kallakury,
Catalin Marian,
Maurizio Trevisan,
Peter G. Shields, Jo L. Freudenheim
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ABSTRACT: ObjectiveChronic inflammation is suspected to have a role in breast carcinogenesis. Results of studies of non-steroidal anti-inflammatory
drugs (NSAIDs) and breast cancer have been inconsistent. Timing of exposure and analysis of individual NSAIDs should be considered.
MethodsWe conducted a population-based case–control study in western New York State between 1996 and 2001. Cases, 35–79years, had
incident, primary, histologically confirmed breast cancer (n=1,170). Controls (n=2,115) were randomly selected from NY Department of Motor Vehicles records (<65years) or Medicare rolls (≥65years). Participants
were queried on use of aspirin, ibuprofen, and acetaminophen in the year prior and on aspirin during adulthood. Unconditional
logistic regression was used to estimate adjusted odds ratios (OR) and 95% confidence intervals (95% CI).
ResultsRecent aspirin use was inversely associated with breast cancer risk (adjusted OR 0.80, 95% CI: 0.68–0.94); the strongest reduction
in risk was observed among those who took ≥2 pills/day on days that aspirin was taken (OR 0.74, 95% CI: 0.61–0. 90). Adult
lifetime use was also associated with breast cancer risk (>10days/month, adjusted OR 0.68, 95% CI: 0.46–1.00). Use of ibuprofen
or acetaminophen was not associated with breast cancer.
ConclusionsThis is the first study to investigate the association of adult lifetime aspirin intake with breast cancer risk. Our findings
provide evidence that aspirin use throughout a woman’s life may confer some benefit.
KeywordsAspirin-Breast cancer-Ibuprofen-Inflammation-Non-steroidal anti-inflammatory drugs
Cancer Causes and Control 04/2012; 21(9):1503-1512. · 2.88 Impact Factor
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Oscar H Franco,
Yim Lun Wong,
Ngianga-Bakwin Kandala,
Jane E Ferrie,
Joan M Dorn,
Mika Kivimäki,
Aileen Clarke,
Richard P Donahue,
Archana Singh Manoux, Jo L Freudenheim,
Maurizio Trevisan,
Saverio Stranges
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ABSTRACT: Measures of quality of life (QoL) have been found to be predictors of mortality and morbidity; however, there is still limited understanding of the multifaceted nature of these measures and of potential correlates. Using two large populations from the UK and US, we aimed to evaluate and compare measured levels of QoL and the key factors correlated with these levels. Participants were 6,472 white subjects (1,829 women) from the Whitehall II Study (mean age 55.8 years) and 3,684 white subjects (1,903 women) from the Western New York Health Study (mean age 58.7 years). QoL was assessed in both using the physical and mental health component summaries of the short form-36 questionnaire (SF-36). Analysis of covariance was used to compare gender-specific mean scores for the two populations across several potential correlates (including socio-demographic, lifestyle and co-morbidity factors). Levels of reported physical QoL tended to be higher in the UK population (51.2 vs. 48.6) while mental QoL was higher in the US group (53.1 vs. 51.1). Age, sleep duration and depressive symptoms were the main factors correlated with both physical and mental QoL in both samples. Increasing age was associated with poorer physical health but higher mental health scores in both populations (P<0.001). Sleep duration below 6 or above 8 h was associated with lower levels of QoL. Depressive symptoms were strongly associated with poorer mental health scores (P<0.001) while higher BMI, lower physical activity levels and presence of cardiovascular disease were associated with poorer physical health in both samples and gender (P<0.05). There were consistent findings for correlates of QoL in this cross-cultural comparison of two populations from the UK and US. Strongest associations were between lifestyle and co-morbidity factors and the physical health component of the SF-36 rather than the mental health component. This is a novel finding which warrants further consideration.
European Journal of Epidemiology 03/2012; 27(4):255-65. · 4.71 Impact Factor
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Jeanine M Genkinger,
Ruifeng Li,
Donna Spiegelman,
Kristin E Anderson,
Demetrius Albanes,
Leif Bergkvist,
Leslie Bernstein,
Amanda Black,
Piet A van den Brandt,
Dallas R English, [......],
James R Marshall,
Anthony B Miller,
Alpa V Patel,
Kim Robien,
Thomas E Rohan,
Catherine Schairer,
Rachael Stolzenberg-Solomon,
Alicja Wolk,
Regina G Ziegler,
Stephanie A Smith-Warner
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ABSTRACT: Coffee has been hypothesized to have pro- and anticarcinogenic properties, whereas tea may contain anticarcinogenic compounds. Studies assessing coffee intake and pancreatic cancer risk have yielded mixed results, whereas findings for tea intake have mostly been null. Sugar-sweetened carbonated soft drink (SSB) intake has been associated with higher circulating levels of insulin, which may promote carcinogenesis. Few prospective studies have examined SSB intake and pancreatic cancer risk; results have been heterogeneous.
In this pooled analysis from 14 prospective cohort studies, 2,185 incident pancreatic cancer cases were identified among 853,894 individuals during follow-up. Multivariate (MV) study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated using Cox proportional hazards models and then pooled using a random-effects model.
No statistically significant associations were observed between pancreatic cancer risk and intake of coffee (MVRR = 1.10; 95% CI, 0.81-1.48 comparing ≥900 to <0 g/d; 237g ≈ 8oz), tea (MVRR = 0.96; 95% CI, 0.78-1.16 comparing ≥400 to 0 g/d; 237g ≈ 8oz), or SSB (MVRR = 1.19; 95% CI, 0.98-1.46 comparing ≥250 to 0 g/d; 355g ≈ 12oz; P value, test for between-studies heterogeneity > 0.05). These associations were consistent across levels of sex, smoking status, and body mass index. When modeled as a continuous variable, a positive association was evident for SSB (MVRR = 1.06; 95% CI, 1.02-1.12). Conclusion and Impact: Overall, no associations were observed for intakes of coffee or tea during adulthood and pancreatic cancer risk. Although we were only able to examine modest intake of SSB, there was a suggestive, modest positive association for risk of pancreatic cancer for intakes of SSB.
Cancer Epidemiology Biomarkers & Prevention 12/2011; 21(2):305-18. · 4.12 Impact Factor
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Ying Bao,
Dominique S Michaud,
Donna Spiegelman,
Demetrius Albanes,
Kristin E Anderson,
Leslie Bernstein,
Piet A van den Brandt,
Dallas R English, Jo L Freudenheim,
Charles S Fuchs, [......],
Anthony B Miller,
Kim Robien,
Thomas E Rohan,
Arthur Schatzkin,
Victoria L Stevens,
Rachael Z Stolzenberg-Solomon,
Jarmo Virtamo,
Alicja Wolk,
Regina G Ziegler,
Stephanie A Smith-Warner
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ABSTRACT: Epidemiological studies evaluating the association between folate intake and risk of pancreatic cancer have produced inconsistent results. The statistical power to examine this association has been limited in previous studies partly because of small sample size and limited range of folate intake in some studies.
We analyzed primary data from 14 prospective cohort studies that included 319,716 men and 542,948 women to assess the association between folate intake and risk of pancreatic cancer. Folate intake was assessed through a validated food-frequency questionnaire at baseline in each study. Study-specific relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models and then pooled using a random effects model. All statistical tests were two-sided.
During 7-20 years of follow-up across studies, 2195 pancreatic cancers were identified. No association was observed between folate intake and risk of pancreatic cancer in men and women (highest vs lowest quintile: dietary folate intake, pooled multivariable RR = 1.06, 95% CI = 0.90 to 1.25, P(trend) = .47; total folate intake [dietary folate and supplemental folic acid], pooled multivariable RR = 0.96, 95% CI = 0.80 to 1.16, P(trend) = .90). No between-study heterogeneity was observed (for dietary folate, P(heterogeneity) = .15; for total folate, P(heterogeneity) = .22).
Folate intake was not associated with overall risk of pancreatic cancer in this large pooled analysis.
CancerSpectrum Knowledge Environment 12/2011; 103(24):1840-50. · 14.07 Impact Factor
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ABSTRACT: While there is accumulating evidence that use of nonsteroidal anti-inflammatory drugs (NSAID) decreases breast cancer risk, little is known about the impact of NSAIDs on survival after breast cancer diagnosis.
We assessed whether recent, prediagnostic NSAID use and lifetime cumulative aspirin use before diagnosis were associated with survival among 1,024 women with incident, primary, invasive breast cancer.
Recent prediagnostic use of aspirin, ibuprofen, and acetaminophen and lifetime use of aspirin up to diagnosis were not associated with either all-cause mortality or breast cancer-specific mortality. Neither dose nor frequency of use was associated with risk. Associations were not different for pre- and postmenopausal women.
In our data, prediagnostic NSAID use and lifetime cumulative aspirin use were not associated with breast cancer survival.
Our findings do not support a role of NSAIDs prior to diagnosis in breast cancer survival.
Cancer Epidemiology Biomarkers & Prevention 11/2011; 21(1):239-42. · 4.12 Impact Factor
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Meng-Hua Tao,
Joel B. Mason,
Catalin Marian,
Susan E. McCann,
Mary E. Platek,
Amy Millen,
Christine Ambrosone,
Stephen B. Edge,
Shiva S. Krishnan,
Maurizio Trevisan,
Peter G. Shields, Jo L. Freudenheim
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ABSTRACT: Aberrant DNA methylation plays a critical role in carcinogenesis, and the availability of dietary factors involved in 1-carbon metabolism may contribute to aberrant DNA methylation. We investigated the association of intake of folate, vitamins B2, B6, B12, and methionine with promoter methylation of E-cadherin, p16, and RAR-β2 genes in archived tumor tissues from incident, primary breast cancer cases in a population-based case-control study. Real-time methylation-specific PCR was performed on 803 paraffin-embedded samples; usual dietary intake was queried from a food frequency questionnaire. Unconditional logistic regression was used to derive adjusted odds ratios and 95% confidence intervals for likelihood of promoter methylation for high compared to low intake of those 1-carbon nutrients. Overall, in case-case comparisons, dietary intakes of folate, vitamins B2, B6, B12, and methionine were not associated with likelihood of promoter methylation of E- cadherin, p16, and RAR-β2 for all cases combined or within strata defined by menopausal status and estrogen receptor status in this study. This finding, however, does not exclude the possibility that intake of such nutrients might have the ability to modulate promoter methylation in normal or premalignant (dysplastic) breast tissue.
Nutrition and Cancer 10/2011; 63(7):1143-1150. · 2.78 Impact Factor
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Meng-Hua Tao,
Joel B Mason,
Catalin Marian,
Susan E McCann,
Mary E Platek,
Amy Millen,
Christine Ambrosone,
Stephen B Edge,
Shiva S Krishnan,
Maurizio Trevisan,
Peter G Shields, Jo L Freudenheim
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ABSTRACT: Aberrant DNA methylation plays a critical role in carcinogenesis, and the availability of dietary factors involved in 1-carbon metabolism may contribute to aberrant DNA methylation. We investigated the association of intake of folate, vitamins B(2), B(6), B(12), and methionine with promoter methylation of E-cadherin, p16, and RAR-β(2) genes in archived tumor tissues from incident, primary breast cancer cases in a population-based case-control study. Real-time methylation-specific PCR was performed on 803 paraffin-embedded samples; usual dietary intake was queried from a food frequency questionnaire. Unconditional logistic regression was used to derive adjusted odds ratios and 95% confidence intervals for likelihood of promoter methylation for high compared to low intake of those 1-carbon nutrients. Overall, in case-case comparisons, dietary intakes of folate, vitamins B(2), B(6), B(12), and methionine were not associated with likelihood of promoter methylation of E- cadherin, p16, and RAR-β(2) for all cases combined or within strata defined by menopausal status and estrogen receptor status in this study. This finding, however, does not exclude the possibility that intake of such nutrients might have the ability to modulate promoter methylation in normal or premalignant (dysplastic) breast tissue.
Nutrition and Cancer 09/2011; 63(7):1143-50. · 2.78 Impact Factor
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ABSTRACT: The mechanism of the observed association between body mass, particularly centralized body fat, and postmenopausal breast cancer risk is not well understood.
We hypothesized that body mass may affect DNA methylation through increased estrogen and chronic inflammation. The association between body mass and promoter methylation in breast tumors was investigated in a population-based, case-control study.
The promoter methylation of E-cadherin, p16, and RAR-β(2) genes was assessed in breast tumor blocks from 803 pre- and postmenopausal cases by using real-time methylation-specific polymerase chain reaction. Unconditional logistic regression was used to derive the adjusted OR and 95% CI for case-case comparisons of tumors with and without promoter methylation of the genes.
The frequency of promoter methylation was 20% for E-cadherin, 25.9% for p16, and 27.5% for RAR-β(2). There was no difference in the prevalence of the DNA methylation of individual genes by BMI, waist-to-hip ratio (WHR), or lifetime weight change between the age of 20 y and the present. However, in a case-case comparison of postmenopausal breast cancer, a greater WHR was associated with an increased likelihood of ≥1 of the 3 genes being methylated (OR: 1.85; 95% CI: 1.10, 3.11; P-trend < 0.02).
We showed that WHR was associated with DNA promoter methylation of ≥1 of 3 genes in postmenopausal breast tumors. It may be that the association of body fat composition and postmenopausal breast cancer is related to altered DNA methylation. However, future studies in other populations and with an examination of the methylation of more genes are needed.
American Journal of Clinical Nutrition 09/2011; 94(3):831-8. · 6.67 Impact Factor
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ABSTRACT: We conducted a study comparing the location of addresses recorded on birth certificates with self-reported birth addresses provided by adults who were participants in the Western New York Exposure and Breast Cancer (WEB) Study. We also evaluated whether birth certificate residence data may be used to reconstruct missing self-reported birth residence information.
Subjects were selected from WEB study participants born in Western New York State between 1920 and 1964 for whom we were able to obtain a New York State birth certificate. Addresses were geocoded and mean distance and SD between self-reported and certificate addresses were calculated.
Our findings indicate good agreement between self-reported and birth certificate addresses (77% are within 0.25 mile difference), and no difference in recall for cases compared with controls.
This study provides evidence that self-reported and birth certificate-based addresses may be used together to achieve increased accuracy of historical records in early life when place of birth is used as a proxy for early life environment in relation to the development of breast cancer or other chronic diseases.
Annals of epidemiology 09/2011; 21(9):710-3. · 2.95 Impact Factor
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ABSTRACT: Recent genome-wide association studies have revealed several new candidate genes for breast cancer, including fibroblast growth factor receptor 2 (FGFR2) gene. The associations were also replicated in several other independent studies. The next important step is to study whether these common variants interact with known breast cancer risk factors, exogenous exposures and tumor characteristics. In a population-based case-control study of 1,170 breast cancer cases and 2,115 controls, we examined genetic associations of four intronic FGFR2 single-nucleotide polymorphisms (SNPs) and breast tumor characteristics and assessed the potential interactions with smoking, alcohol consumption, adiposity and known breast cancer risk factors. FGFR2 variants were significantly associated with breast cancer risk regardless of estrogen and progesterone receptor status, metastasis, lymph node involvement and histologic and nuclear grade. The FGFR2-breast cancer association was modified by smoking status, with increased risk for former and current smokers compared to never smokers; former/current smokers carrying two copies of the rs1219648 minor allele were at highest risk with a crude OR (95% confidence interval) of 2.11 (1.52-2.92) compared to never smokers with no rs1219648 variant alleles. Our study found no evidence for either modification of FGFR2 and breast cancer by alcohol intake or adiposity, even when analyses were stratified by menopausal status. Although these results require further replication, they may provide new insight into the possible new exposures that may interact with FGFR2 susceptibility alleles.
International Journal of Cancer 08/2011; 129(3):702-12. · 5.44 Impact Factor
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Theodore M Brasky,
Matthew R Bonner,
Kirsten B Moysich,
Christine B Ambrosone,
Jing Nie,
Meng Hua Tao,
Stephen B Edge,
Bhaskar V S Kallakury,
Catalin Marian,
David S Goerlitz,
Maurizio Trevisan,
Peter G Shields, Jo L Freudenheim
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ABSTRACT: Use of non-steroidal anti-inflammatory drugs (NSAIDs) has been associated with reduced risk of breast cancer, though findings have been inconsistent. This inconsistency may result from differences in etiology for breast tumors of different subtypes. We examined the association between NSAID use and breast cancer characterized by molecular subtypes in a population-based case-control study in Western New York. Cases (n = 1,170) were women with incident, primary, histologically confirmed breast cancer. Controls (n = 2,115) were randomly selected from NY Department of Motor Vehicles records (<65 years) or Medicare rolls (≥ 65 years). Participants answered questions regarding their use of aspirin and ibuprofen in the year prior to interview and their use of aspirin throughout their adult life. Logistic regression models estimated odds ratios (OR) and 95% confidence intervals (95% CI). Recent and lifetime aspirin use was associated with reduced risk, with no differences by subtype. Recent use of ibuprofen was significantly associated with increased risk of ER+/PR+(OR 1.33, 95% CI: 1.09-1.62), HER2- (OR 1.27, 95% CI: 1.05-1.53), and p53- breast cancers (OR 1.28, 95% CI: 1.04-1.57), as well as luminal A or B breast cancers. These findings support the hypothesis of heterogeneous etiologies of breast cancer subtypes and that aspirin and ibuprofen vary in their effects.
Cancer Causes and Control 07/2011; 22(7):965-75. · 2.88 Impact Factor
