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Theodore M Brasky,
Yanli Li,
David J Jaworowicz,
Nancy Potischman,
Christine B Ambrosone,
Alan D Hutson, Jing Nie,
Peter G Shields,
Maurizio Trevisan,
Carole B Rudra,
Stephen B Edge,
Jo L Freudenheim
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ABSTRACT: Breast tissues undergo extensive physiologic changes during pregnancy, which may affect breast carcinogenesis. Gestational hypertension, preeclampsia/eclampsia, gestational diabetes, pregnancy weight gain, and nausea and vomiting (N&V) during pregnancy may be indicative of altered hormonal and metabolic profiles and could impact breast cancer risk. Here, we examined associations between these characteristics of a woman's pregnancy and her subsequent breast cancer risk. Participants were parous women that were recruited to a population-based case-control study (Western New York Exposures and Breast Cancer Study). Cases (n = 960), aged 35-79 years, had incident, primary, histologically confirmed breast cancer. Controls (n = 1,852) were randomly selected from motor vehicle records (<65 years) or Medicare rolls (≥65 years). Women were queried on their lifetime pregnancy experiences. Multivariable-adjusted logistic regression was used to estimate odds ratios (ORs) and 95 % confidence intervals (CIs). N&V during pregnancy was inversely associated with breast cancer risk. Relative to those who never experienced N&V, ever experiencing N&V was associated with decreased risk (OR 0.69, 95 % CI 0.56-0.84) as were increased N&V severity (p trend < 0.001), longer duration (p trend < 0.01), and larger proportion of affected pregnancies (p trend < 0.0001) among women with ≥3 pregnancies. Associations were stronger for more recent pregnancies (<5 years). Findings did not differ by menopausal status or breast cancer subtype including estrogen receptor and HER2 expression status. Other pregnancy characteristics examined were not associated with risk. We observed strong inverse associations between pregnancy N&V and breast cancer risk. Replication of these findings and exploration of underlying mechanisms could provide important insight into breast cancer etiology and prevention.
Cancer Causes and Control 06/2013; · 2.88 Impact Factor
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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: The use of geocoded historical residence as proxy for retrospective assessment of exposure in early life is increasing in epidemiological studies of chronic health outcomes. Dealing with historical residence poses challenges, primarily due to higher uncertainties associated with data collection and processing. A possible source of bias is connected with the exclusion of subjects, who cannot, for various reasons, be geocoded. We evaluated the potential bias that may arise due to incomplete geocoding, using birth residence data collected as part of a population-based case-control study of breast cancer in western New York state. We found that geocoded and non-geocoded populations did not differ in the distribution of most risk factors compared, and that the geocoding status did not modify the spatial patterns of the study populations. However, the results emphasize the need for epidemiological studies to consider the potential biases that may be introduced by geocoding of historical residence when investigating retrospectively chronic disease and early-life exposure.
Geospatial health 05/2013; 7(2):369-74. · 3.00 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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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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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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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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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: 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: 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
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Luisel J Ricks-Santi,
Lara E Sucheston,
Yang Yang,
Jo L Freudenheim,
Claudine J Isaacs,
Marc D Schwartz,
Ramona G Dumitrescu,
Catalin Marian, Jing Nie,
Dominica Vito,
Stephen B Edge,
Peter G Shields
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ABSTRACT: Inter-individual variation in DNA repair capacity is thought to modulate breast cancer risk. The phenotypic mutagen sensitivity assay (MSA) measures DNA strand breaks in lymphocytes; women with familial and sporadic breast cancers have a higher mean number of breaks per cell (MBPC) than women without breast cancer. Here, we explore the relationships between the MSA and the Rad51 gene, which encodes a DNA repair enzyme that interacts with BRCA1 and BRCA2, in BRCA1 mutation carriers and women with sporadic breast cancer.
Peripheral blood lymphoblasts from women with known BRCA1 mutations underwent the MSA (n = 138 among 20 families). BRCA1 and Rad51 genotyping and sequencing were performed to identify SNPs and haplotypes associated with the MSA. Positive associations from the study in high-risk families were subsequently examined in a population-based case-control study of breast cancer (n = 1170 cases and 2115 controls).
Breast cancer diagnosis was significantly associated with the MSA among women from BRCA1 families (OR = 3.2 95%CI: 1.5-6.7; p = 0.004). The Rad51 5'UTR 135 C>G genotype (OR = 3.64; 95% CI: 1.38, 9.54; p = 0.02), one BRCA1 haplotype (p = 0.03) and in a polygenic model, the E1038G and Q356R BRCA1 SNPs were significantly associated with MBPC (p = 0.009 and 0.002, respectively). The Rad51 5'UTR 135C genotype was not associated with breast cancer risk in the population-based study.
Mutagen sensitivity might be a useful biomarker of penetrance among women with BRCA1 mutations because the MSA phenotype is partially explained by genetic variants in BRCA1 and Rad51.
BMC Cancer 06/2011; 11:278. · 3.01 Impact Factor
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Michelle R Roberts,
Peter G Shields,
Christine B Ambrosone, Jing Nie,
Catalin Marian,
Shiva S Krishnan,
David S Goerlitz,
Ramakrishna Modali,
Michael Seddon,
Teresa Lehman,
Kandace L Amend,
Maurizio Trevisan,
Stephen B Edge,
Jo L Freudenheim
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ABSTRACT: Base excision repair (BER) and nucleotide excision repair (NER) pathways repair damaged DNA, and polymorphisms in these genes might affect breast cancer susceptibility. We evaluated associations between seven single-nucleotide polymorphisms in four DNA repair genes (ERCC4 rs1799801, XPC rs2227998, rs2228001, rs2228000, OGG1 rs1052133 and XRCC1 rs25487 and rs25486) and breast cancer risk, examining modification by smoking and alcohol consumption, using data from the Western New York Exposures and Breast Cancer Study. Women aged 35-79 years with incident breast cancer (n = 1170) and age- and race-matched controls (n = 2115) were enrolled. Genotyping was performed using matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Unconditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CIs). No significant associations were observed in premenopausal women. Among postmenopausal women, rs25487 and rs25486 (OR = 1.24; 95% CI 1.01-1.51 and OR = 1.23; 95% CI 1.01-1.49, respectively, for combined heterozygous and homozygous variant compared with reference) were associated with increased risk of breast cancer. Postmenopausal women carrying the variant allele of the synonymous XPC polymorphism (rs2227998) were also at borderline significantly increased risk (OR = 1.24; 95% CI 1.01-1.52, heterozygous variant compared with reference; OR = 1.22; 95% CI 1.01-1.48, for combined heterozygous and homozygous variant compared with reference). There was no evidence of genotype-smoking and genotype-alcohol consumption interactions for pre- and postmenopausal women. These results indicate that some of the variants in BER and NER genes may influence risk of postmenopausal breast cancer.
Carcinogenesis 05/2011; 32(8):1223-30. · 5.70 Impact Factor
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Theodore M Brasky,
Matthew R Bonner,
Kirsten B Moysich,
Heather M Ochs-Balcom,
Catalin Marian,
Christine B Ambrosone, Jing Nie,
Meng Hua Tao,
Stephen B Edge,
Maurizio Trevisan,
Peter G Shields,
Jo L Freudenheim
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ABSTRACT: Chronic inflammation has been consistently associated with cancers of several sites, including the breast, and inhibition of inflammation through the use of non-steroidal anti-inflammatory drugs (NSAIDs) has been inversely associated with risk. As NSAIDs bind with cyclooxygenase-2 (COX-2), genetic variation in COX-2 may influence breast cancer risk by affecting inflammatory response and response to NSAID use. We identified eight single nucleotide polymorphisms (SNPs) for COX-2 and examined their association with risk of breast cancer in a population-based case-control study in Western New York. Cases had incident, first primary, histologically confirmed breast cancer (n = 1077). Controls (n = 1910) were randomly selected from NY Department of Motor Vehicles records (< 65) or Medicare rolls (≥ 65). Participants were queried on adult lifetime use of aspirin and recent use of ibuprofen. Unconditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI). One SNP, rs2745559, was associated with an increased risk of breast cancer (OR 1.23, 95% CI 1.03-1.46). Associations with other variants were not evident. Significant interaction (P interaction = 0.04) between recent aspirin use and rs4648261 was also observed. Variation in COX-2 was modestly associated with breast cancer risk, indicating that COX-2 may play a role in breast carcinogenesis. Better understanding of the role of COX-2 genetic variation and interaction with NSAID use in breast carcinogenesis has potential to inform prevention strategies.
Breast Cancer Research and Treatment 02/2011; 126(1):157-65. · 4.43 Impact Factor
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Meng Hua Tao,
Catalin Marian,
Peter G Shields, Jing Nie,
Susan E McCann,
Amy Millen,
Christine Ambrosone,
Alan Hutson,
Stephen B Edge,
Shiva S Krishnan,
Bin Xie,
Janet Winston,
Dominica Vito,
Marcia Russell,
Thomas H Nochajski,
Maurizio Trevisan,
Jo L Freudenheim
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ABSTRACT: The mechanism for the observed association of alcohol consumption breast cancer risk is not known; understanding that mechanism could improve understanding of breast carcinogenesis and optimize prevention strategies. Alcohol may impact breast malignancies or tumor progression by altering DNA methylation. We examined promoter methylation of three genes, the E-cadherin, p16, and retinoic acid-binding receptor-β2 (RAR-β2) genes in archived breast tumor tissues from participants in a population-based case-control study. Real time methylation-specific PCR was performed on 803 paraffin-embedded samples, and lifetime alcohol consumption was queried. Unordered polytomous and unconditional logistic regression were used to derive adjusted odds ratios (ORs) and 95% confidence intervals (CIs). RAR-β2 methylation was not associated with drinking. Among premenopausal women, alcohol consumption was also not associated with promoter methylation for E-cadherin and p16 genes. In case-case comparisons of postmenopausal breast cancer, compared with lifetime never drinkers, promoter methylation likelihood was increased for higher alcohol intake for E-cadherin (OR=2.39; 95% CI, 1.15-4.96), in particular for those with estrogen receptor-negative tumors (OR=4.13; 95% CI, 1.16-14.72), and decreased for p16 (OR=0.52; 95% CI, 0.29-0.92). There were indications that the association with p16 was stronger for drinking at younger ages. Methylation was also associated with drinking intensity independent of total consumption for both genes. We found alcohol consumption was associated with DNA methylation in postmenopausal breast tumors, suggesting that the association of alcohol and breast cancer may be related, at least in part, to altered methylation, and may differ by drinking pattern.
Alcohol (Fayetteville, N.Y.) 12/2010; 45(7):689-99. · 2.41 Impact Factor
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Susan E McCann,
Lilian U Thompson, Jing Nie,
Joan Dorn,
Maurizio Trevisan,
Peter G Shields,
Christine B Ambrosone,
Stephen B Edge,
Hsin-Fang Li,
Christina Kasprzak,
Jo L Freudenheim
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ABSTRACT: Dietary lignan intakes have been associated with reduced breast cancer risks; however, no previous studies have investigated whether lignan intake might be associated with breast cancer survival. We examined the association of dietary lignan intakes with survival in 1122 women with primary, incident, histologically confirmed breast cancer identified between 1996 and 2001, and with vital status determined through December 31, 2006. Diet in the 12-24 months before diagnosis was assessed with an extensive food frequency questionnaire, and potential confounders assessed from an extensive epidemiologic interview and abstracted clinical data. Lignan intake was calculated using published food composition data. Hazard ratios (HR), and 95% confidence intervals (CIs) for dietary lignan intakes with all cause, and breast cancer mortality were estimated using Cox proportional hazards adjusting for age, education, race, total energy intake, tumor stage, and body mass index. Of the 1122 women with complete dietary data, 160 had died by the end of follow-up. Among postmenopausal women only, those in the highest versus lowest quartile of lignan intakes had a statistically significant reduction in the risk of all cause mortality (HR 0.49, 95% CI 0.26-0.91) and a significantly reduced risk of breast cancer mortality (HR 0.29, 95% CI 0.11-0.76). Higher intakes of dried beans (HR 0.61, 95% CI 0.36-1.03), but not fruits, vegetables, or grains, were also weakly associated with overall mortality. In summary, our results suggest that higher lignan intakes may be associated with improved survival among postmenopausal women with breast cancer.
Breast Cancer Research and Treatment 07/2010; 122(1):229-35. · 4.43 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
[show abstract]
[hide abstract]
ABSTRACT: Chronic 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.
We conducted a population-based case-control study in western New York State between 1996 and 2001. Cases, 35-79 years, had incident, primary, histologically confirmed breast cancer (n = 1,170). Controls (n = 2,115) were randomly selected from NY Department of Motor Vehicles records (<65 years) or Medicare rolls (>or=65 years). 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).
Recent 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 >or=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 (>10 days/month, adjusted OR 0.68, 95% CI: 0.46-1.00). Use of ibuprofen or acetaminophen was not associated with breast cancer.
This 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.
Cancer Causes and Control 05/2010; 21(9):1503-12. · 2.88 Impact Factor
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Mary E Platek,
Peter G Shields,
Duanjun Tan,
Catalin Marian,
Matthew R Bonner,
Susan E McCann, Jing Nie,
Gregory E Wilding,
Christine Ambrosone,
Amy E Millen,
Maurizio Trevisan,
Marcia Russell,
Thomas H Nochajski,
Stephen B Edge,
Janet Winston,
Jo L Freudenheim
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ABSTRACT: Mitochondrial DNA (mtDNA) mutations are frequent in breast tumors, but the etiology of these mutations is unknown. We hypothesized that these mutations are associated with exposures that affect oxidative stress such as alcohol metabolism. Using archived tumor blocks from incident breast cancer cases in a case control study, the Western New York Exposures and Breast Cancer (WEB) study, analysis of mtDNA mutations was conducted on 128 breast cancer cases selected based on extremes of alcohol intake. Temporal temperature gradient gel electrophoresis (TTGE) was used to screen the entire mtDNA genome and sequencing was completed for all TTGE positive samples. Case-case comparisons were completed using unconditional logistic regression to determine the relative prevalence of the mutations by exposures including alcohol consumption, manganese superoxide dismutase (MnSOD) genotype, nutrient intake related to oxidative stress and established breast cancer risk factors. Somatic mtDNA mutations were found in 60 of the 128 tumors examined. There were no differences in the prevalence of mtDNA mutations by alcohol consumption, MnSOD genotype or dietary intake. The likelihood of mtDNA mutations was reduced among those with a positive family history for breast cancer (OR = 0.33, CI = 0.12-0.92), among postmenopausal women who used hormone replacement therapy (OR = 0.46, CI = 0.19-1.08, P = 0.08) and was increased for ER negative tumors (OR = 2.05, CI = 0.95-4.43, P = 0.07). Consistent with previous studies, we found that mtDNA mutations are a frequent occurrence in breast tumors. An understanding of the etiology of mtDNA mutations may provide insight into breast carcinogenesis.
Breast Cancer Research and Treatment 10/2009; 121(2):453-60. · 4.43 Impact Factor
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Mary E Platek,
Peter G Shields,
Catalin Marian,
Susan E McCann,
Matthew R Bonner, Jing Nie,
Christine B Ambrosone,
Amy E Millen,
Heather M Ochs-Balcom,
Sylvia K Quick,
Maurizio Trevisan,
Marcia Russell,
Thomas H Nochajski,
Stephen B Edge,
Jo L Freudenheim
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ABSTRACT: It has been hypothesized that effects of alcohol consumption on one-carbon metabolism may explain, in part, the association of alcohol consumption with breast cancer risk. The methylenetetrahydrofolate reductase (MTHFR) and 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR) genes express key enzymes in this pathway. We investigated the association of polymorphisms in MTHFR (rs1801133 and rs1801131) and MTR (rs1805087) with breast cancer risk and their interaction with alcohol consumption in a case-control study--the Western New York Exposures and Breast Cancer study. Cases (n = 1,063) were women with primary, incident breast cancer and controls (n = 1,890) were frequency matched to cases on age and race. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by unconditional logistic regression. We found no association of MTHFR or MTR genotype with risk of breast cancer. In the original case-control study, there was a nonsignificant increased odds of breast cancer among women with higher lifetime drinking. In the current study, there was no evidence of an interaction of genotype and alcohol in premenopausal women. However, among postmenopausal women, there was an increase in breast cancer risk for women who were homozygote TT for MTHFR C677T and had high lifetime alcohol intake (>or=1,161.84 oz; OR, 1.92; 95% CI, 1.13-3.28) and for those who had a high number of drinks per drinking day (>1.91 drinks/day; OR, 1.80; 95% CI, 1.03-3.28) compared with nondrinkers who were homozygote CC. Our findings indicate that among postmenopausal women, increased breast cancer risk with alcohol consumption may be as a result of effects on one-carbon metabolism.
Cancer Epidemiology Biomarkers & Prevention 09/2009; 18(9):2453-9. · 4.12 Impact Factor
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Meng Hua Tao,
Peter G Shields, Jing Nie,
Catalin Marian,
Christine B Ambrosone,
Susan E McCann,
Mary Platek,
Shiva S Krishnan,
Bin Xie,
Stephen B Edge,
Janet Winston,
Dominica Vito,
Maurizio Trevisan,
Jo L Freudenheim
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ABSTRACT: Aberrant promoter methylation is recognized as an important feature of breast carcinogenesis. We hypothesized that genetic variation of genes for methylenetetrahydrofolate reductase (MTHFR) and methionine synthase (MTR), two critical enzymes in the one-carbon metabolism, may alter DNA methylation levels and thus influence DNA methylation in breast cancer. We evaluated case-control association of MTHFR C677T, A1298C, and MTR A2756G polymorphisms for cases strata-defined by promoter methylation status for each of three genes, E-cadherin, p16, and RAR-beta2 in breast cancer; in addition, we evaluated case-case comparisons of the likelihood of promoter methylation in relation to genotypes using a population-based case-control study conducted in Western New York State. Methylation was evaluated with real-time methylation-specific PCRs for 803 paraffin-embedded breast tumor tissues from women with primary, incident breast cancer. We applied unordered polytomous regression and unconditional logistic regression to derive adjusted odds ratios and 95% confidence intervals. We did not find any association of MTHFR and MTR polymorphisms with breast cancer risk stratified by methylation status nor between polymorphisms and likelihood of promoter methylation of any of the genes. There was no evidence of difference within strata defined by menopausal status, estrogen receptor status, folate intake, and lifetime alcohol consumption. Overall, we found no evidence that these common polymorphisms of the MTHFR and MTR genes are associated with promoter methylation of E-cadherin, p16, and RAR-beta2 genes in breast cancer.
Cancer Epidemiology Biomarkers & Prevention 03/2009; 18(3):998-1002. · 4.12 Impact Factor
