Peter G Shields

Columbus State University, Columbus, Georgia, United States

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Publications (229)1286.19 Total impact

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    ABSTRACT: p16(INK4a) is a tumor suppressor gene, frequently hypermethylated in breast cancer; this epigenetic silencing of p16(INK4a) occurs early in carcinogenesis. The risk factors and functional consequences of p16(INK4a) methylation are unknown. Alcohol consumption, a breast cancer risk factor, impedes folate metabolism and may thereby alter gene methylation since folate plays a pivotal role in DNA methylation. In a cross-sectional study of 138 women with no history of breast cancer who underwent reduction mammoplasty, we studied breast cancer risk factors, plasma and breast folate concentrations, variation in one-carbon metabolism genes, p16(INK4a) promoter methylation, and P16 protein expression. Logistic regression was used to estimate multivariable-adjusted odds ratios (OR) and 95% confidence intervals (CI). p16(INK4a) methylation was negatively correlated with P16 expression (r=-0.28; P=0.002). Alcohol consumption was associated with lower breast folate (P=0.03), higher p16(INK4a) promoter methylation (P=0.007), and less P16 expression (P=0.002). Higher breast folate concentrations were associated with lower p16(INK4a) promoter methylation (P=0.06). Genetic variation in MTRR (rs1801394) and MTHFD1 (rs1950902) was associated with higher p16(INK4a) promoter methylation (OR=2.66, 95% CI: 1.11-6.42 and OR=2.72, 95% CI: 1.12-6.66, respectively), while variation in TYMS (rs502396) was associated with less P16 protein expression (OR=0.22, 95% CI: 0.05-0.99). Given that this is the first study to indicate that alcohol consumption, breast folate, and variation in one-carbon metabolism genes are associated with p16(INK4a) promoter methylation and P16 protein expression in healthy tissues, these findings require replication.
    Carcinogenesis 10/2014; · 5.27 Impact Factor
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    ABSTRACT: Background: Circulating adipokines may be associated with breast cancer risk. Genetic variants governing adipokines and adipokine receptors may also predict risk, but their effect on breast adipokine concentrations is unknown. Methods: We conducted a cross-sectional analysis of functional single nucleotide polymorphisms (SNPs) in 5 adipokine genes (adiponectin, leptin (LEP), and their receptors) among 85 cancer-free women who were undergoing reduction mammoplasty. Results: In multivariable-adjusted regression models, compared to the common GG genotype, the AA genotype of the LEP A19G SNP was associated with 27% lower plasma adiponectin (Ratio 0.73, 95% CI [confidence interval]: 0.54-0.98) and leptin (Ratio 0.73, 95% CI: 0.55-0.96). Women with the AG genotype of LEP A19G had 39% lower breast leptin (Ratio 0.61, 95% CI: 0.39-0.97) compared to those with the GG genotype. No associations were observed for SNPs in the remaining genes. Conclusions: Genetic variation in LEP may alter endogenous adipokine concentrations in circulation and in breast tissues. Impact: These preliminary findings may support the hypothesis that genetic variation in adipokine genes modifies circulating adipokine concentrations and possibly leptin concentrations in local breast tissues, which may be associated with breast cancer risk.
    Cancer Epidemiology Biomarkers & Prevention 05/2014; · 4.56 Impact Factor
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    ABSTRACT: Lung cancer remains the most common cause of cancer deaths worldwide, yet there is currently a lack of diagnostic noninvasive biomarkers that could guide treatment decisions. Small molecules (<1500 Da) were measured in urine collected from 469 lung cancer patients and 536 population controls using unbiased liquid chromatography-mass spectrometry. Clinical putative diagnostic and prognostic biomarkers were validated by quantitation and normalized to creatinine levels at two different time points and further validated in an independent sample set, which comprises 80 cases and 78 population controls, with similar demographic and clinical characteristics when compared to the training set. Creatine riboside (IUPAC name: 2-{2-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)-oxolan-2-yl]-1-methylcarbamimidamido}acetic acid), a novel molecule identified in this study, and N-acetylneuraminic acid (NANA), were each significantly (P <0.00001) elevated in non-small cell lung cancer (NSCLC) and associated with worse prognosis (hazard ratio (HR) =1.81 [P =0.0002], and 1.54 [P =0.025], respectively). Creatine riboside was the strongest classifier of lung cancer status in all and stage I-II cases, important for early detection, and also associated with worse prognosis in stage I-II lung cancer (HR =1.71, P =0.048). All measurements were highly reproducible with intraclass correlation coefficients ranging from 0.82 - 0.99. Both metabolites were significantly (P <0.03) enriched in tumor tissue compared to adjacent non-tumor tissue (N =48), thus revealing their direct association with tumor metabolism. Creatine riboside and NANA may be robust urinary clinical metabolomic markers that are elevated in tumor tissue and associated with early lung cancer diagnosis and worse prognosis.
    Cancer Research 04/2014; · 9.28 Impact Factor
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    ABSTRACT: Cancer prevention postdoctoral fellowships have existed since the 1970s. The National Cancer Institute facilitated a meeting by a panel of experts in April 2013 to consider four important topics for future directions for cancer prevention postdoctoral training programs: (i) future research needs; (ii) underrepresented disciplines; (iii) curriculum; and (iv) career preparation. Panelists proffered several areas needing more research or emphasis, ranging from computational science to culture. Health care providers, along with persons from nontraditional disciplines in scientific training programs such as engineers and lawyers, were among those recognized as being underrepresented in training programs. Curriculum suggestions were that fellows receive training in topics such as leadership and human relations, in addition to learning the principles of epidemiology, cancer biologic mechanisms, and behavioral science. For career preparation, there was a clear recognition of the diversity of employment options available besides academic positions, and that program leaders should do more to help fellows identify and prepare for different career paths. The major topics and strategies covered at this meeting can help form the basis for cancer prevention training program leaders to consider modifications or new directions, and keep them updated with the changing scientific and employment climate for doctoral degree recipients and postdoctoral fellows. Cancer Epidemiol Biomarkers Prev; 1-5. ©2014 AACR.
    Cancer Epidemiology Biomarkers & Prevention 03/2014; · 4.56 Impact Factor
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    ABSTRACT: American women of African ancestry (AA) are more likely than European-Americans (EA) to be diagnosed with aggressive, estrogen receptor (ER) negative breast tumors; mechanisms underlying these disparities are poorly understood. We conducted a genome wide (450K loci) methylation analysis to determine if there were differences in DNA methylation patterns between tumors from AA and EA women and if these differences were similar for both ER positive and ER negative breast cancer. Methylation levels at CpG loci within CpG islands (CGI)s and CGI-shores were significantly higher in tumors (n=138) than in reduction mammoplasty samples (n=124). In hierarchical cluster analysis, there was separation between tumor and normal samples, and in tumors, there was delineation by ER status, but not by ancestry. However, differential methylation analysis identified 157 CpG loci with a mean β value difference of at least 0.17 between races, with almost twice as many differences in ER-negative tumors compared to ER-positive cancers. This first genome-wide methylation study to address disparities indicates that there are likely differing etiologic pathways for the development of ER negative breast cancer between AA and EA women. Further investigation of the genes most differentially methylated by race in ER negative tumors can guide new approaches for cancer prevention and targeted therapies, and elucidate the biologic basis of breast cancer disparities.
    Oncotarget 11/2013; · 6.63 Impact Factor
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    ABSTRACT: Physical activity both before and after breast cancer diagnosis has been associated with improved survival. However, it is not clear whether this association differs by molecular features of the tumor or by recency of the physical activity to the time of diagnosis. We examined the association of prediagnostic physical activity with survival in a cohort of 1,170 women with primary, incident, and histologically confirmed breast cancer, examining tumor molecular subtypes. Cox regression models were used to estimate hazard ratios (HR) and 95 % confidence intervals (95 % CI). Mean follow-up time was 87.4 months after breast cancer diagnosis; there were 170 deaths identified. Compared with inactive patients (<3 h/week), women with higher average lifetime physical activity (>6 h/week) had reduced risk of all-cause mortality (adjusted HR = 0.61, 95 % CI 0.40-0.95; p trend =0.04). There were no clear differences in the associations for lifetime and more recent physical activity. Lifetime physical activity was also weakly associated with decreased risk of breast cancer-specific mortality. Higher lifetime physical activity was associated with reduced risk of all-cause mortality among women with ER-positive tumors (HR = 0.52, 95 % CI 0.29-0.93) and mutant TP53 tumors (HR = 0.22, 95 % CI 0.06-0.72); however, no statistically significant interactions were observed for ER or TP53 status. Our study further supports that prediagnostic physical activity improves overall survival following breast cancer and suggests that the associations of prediagnostic physical activity with survival following breast cancer may vary by molecular features of the tumor, particularly ER and TP53 status.
    Cancer Causes and Control 09/2013; · 3.20 Impact Factor
  • Cancer Research 08/2013; 73(8 Supplement):116-116. · 9.28 Impact Factor
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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; · 3.20 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; · 2.95 Impact Factor
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    ABSTRACT: We conducted a translational genomics pilot study to evaluate the impact of genomic information related to colorectal cancer (CRC) risk on psychosocial, behavioral and communication outcomes. In 47 primary care participants, 96% opted for testing of three single nucleotide polymorphisms (SNPs) related to CRC risk. Participants averaged 2.5 of 6 possible SNP risk alleles (10% lifetime risk). At 3-months, participants did not report significant increases in cancer worry/distress; over half reported physical activity and dietary changes. SNP risk scores were unrelated to behavior change at 3-months. Many participants (64%) shared their SNP results, including 28% who shared results with a physician. In this pilot, genomic risk education, including discussion of other risk factors, appeared to impact patients' health behaviors, regardless of the level of SNP risk. Future work can compare risk education with and without SNP results to evaluate if SNP information adds value to existing approaches.
    Genomics 04/2013; · 2.79 Impact Factor
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    ABSTRACT: There is evidence that epigenetic changes occur early in breast carcinogenesis. We hypothesized that early-life exposures associated with breast cancer would be associated with epigenetic alterations in breast tumors. In particular, we examined DNA methylation patterns in breast tumors in association with several early-life exposures in a population-based case–control study. Promoter methylation of E-cadherin, p16 and RAR-β2 genes was assessed in archived tumor blocks from 803 cases with real-time methylation-specific PCR. Unconditional logistic regression was used for case–case comparisons of those with and without promoter methylation. We found no differences in the prevalence of DNA methylation of the individual genes by age at menarche, age at first live birth and weight at age 20. In case–case comparisons of premenopausal breast cancer, lower birth weight was associated with increased likelihood of E-cadherin promoter methylation (OR = 2.79, 95% CI, 1.15–6.82, for ≤2.5 v. 2.6–2.9 kg); higher adult height with RAR-β2 methylation (OR = 3.34, 95% CI, 1.19–9.39, for ≥1.65 v. <1.60 m); and not having been breastfed with p16 methylation (OR = 2.75, 95% CI, 1.14–6.62). Among postmenopausal breast cancers, birth order was associated with increased likelihood of p16 promoter methylation. Being other than first in the birth order was inversely associated with likelihood of ≥1 of the three genes being methylated for premenopausal breast cancers, but positively associated with methylation in postmenopausal women. These results suggest that there may be alterations in methylation associated with early-life exposures that persist into adulthood and affect breast cancer risk.
    Journal of Developmental Origins of Health and Disease 04/2013; 4(2):182-9. · 0.77 Impact Factor
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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; · 4.47 Impact Factor
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    ABSTRACT: Although single nucleotide polymorphism (SNP) testing for disease susceptibility is commercially available, translational studies are necessary to understand how to communicate genomic information and potential implications for public health. We explored attitudes about and initial responses to genomic testing for colon cancer risk. Following development of the educational materials, we offered testing for three colon cancer SNPs in a pilot study with primary care patients. Participants completed pre- and post-test sessions and interviews. We analyzed interview transcripts with qualitative software using thematic analysis. All 20 participants opted for SNP testing. Qualitative analysis identified several themes: Motivations for SNP Testing, Before/After: Meaning of Results, Emotional Responses to SNP Results and Genomic Literacy/ Information Delivery. Results demonstrate that individuals will pursue SNP testing in the context of pre and post-test education. SNP results may influence health behaviors like healthy eating and exercise yet did not appear to impact colon cancer screening intentions.
    Translational behavioral medicine. 03/2013; 3(1):17-29.
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    ABSTRACT: Background: Recent research suggests that the Bayesian paradigm may be useful for modeling biases in epidemiological studies, such as those due to misclassification and missing data. We used Bayesian methods to perform sensitivity analyses for assessing the robustness of study findings to the potential effect of these two important sources of bias. Methods: We used data from a study of the joint associations of radiotherapy and smoking with primary lung cancer among breast cancer survivors. We used Bayesian methods to provide an operational way to combine both validation data and expert opinion to account for misclassification of the two risk factors and missing data. For comparative purposes we considered a "full model" that allowed for both misclassification and missing data, along with alternative models that considered only misclassification or missing data, and the naïve model that ignored both sources of bias. Results: We identified noticeable differences between the four models with respect to the posterior distributions of the odds ratios that described the joint associations of radiotherapy and smoking with primary lung cancer. Despite those differences we found that the general conclusions regarding the pattern of associations were the same regardless of the model used. Overall our results indicate a nonsignificantly decreased lung cancer risk due to radiotherapy among nonsmokers, and a mildly increased risk among smokers. Conclusions: We described easy to implement Bayesian methods to perform sensitivity analyses for assessing the robustness of study findings to misclassification and missing data.
    Cancer epidemiology. 01/2013;
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    ABSTRACT: Metabolomics is likely an ideal tool to assess tobacco smoke exposure and the impact of cigarette smoke on human exposure and health. In order to assess reproducibility and feasibility of this by UPLC-QTOF-MS, three experiments were designed for the assessment of smokers' blood. Experiment I was an analysis of 8 smokers with 8 replicates. Experiment II was an analysis of 62 pooled quality control (QC) samples from 7 non-smokers' plasma placed as every tenth sample among a study of 613 samples from 160 smokers. Finally, in order to examine the feasibility of metabolomic study in assessing smoke exposure, Experiment III consisted of nine smokers and ten non-smokers' serum to evaluate differences of their global metabolome. There was minimal measurement and sample preparation variation in all experiments, although some caution is needed when analyzing specific parts of chromatogram. When assessing QC samples in the large scale study, QC clustering indicated high stability, reproducibility and consistency. Finally, in addition to the identification of nicotine metabololites as expected, there was a characteristic profile distinguishing smokers from non-smokers. Metabolites selected from putative identifications were verified by MSMS, showing the potential to identify metabolic phenotypes and new metabolites relating to cigarette smoke exposure and toxicity.
    Journal of Proteome Research 12/2012; · 5.06 Impact Factor
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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. · 4.56 Impact Factor
  • The Breast Journal 06/2012; 18(4):394-5. · 1.43 Impact Factor
  • Cancer Research 06/2012; 72(8 Supplement):4483-4483. · 9.28 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; · 3.20 Impact Factor
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    ABSTRACT: Lipid levels, including high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides, have been reported to be associated with breast cancer risk. We studied African American women (97 breast cancer cases and 102 controls) accrued through a population-based, case-control study in the Washington, DC metropolitan area during 1997 and 1998. Plasma lipid levels were measured using enzymatic methods. Logistic regressions (adjusted for age, age at menarche, parity, previous alcohol consumption, and education) were used to explore the associations between lipid levels and breast cancer. Through multivariable-adjusted regression, we observed a significant inverse association between breast cancer risk and increasing levels of total cholesterol (OR=.46, 95% Cl = .25-.85) and LDL (OR = .41, 95% CI = .21-.81), whereas lower levels of HDL were associated with a significant increase in risk (OR = 1.99, 95% CI = 1.06-3.74). Our data demonstrate significant reductions in breast cancer risk with high levels of total cholesterol and significant increase in risk when HDL levels are low. These data are in support of a protective effect of cholesterol which has been reported in other populations; further, these findings add to the literature in an understudied population, African American women.
    Ethnicity & disease 01/2012; 22(3):281-7. · 0.92 Impact Factor

Publication Stats

9k Citations
1,286.19 Total Impact Points


  • 2013
    • Columbus State University
      Columbus, Georgia, United States
    • Howard University Hospital
      Washington, Washington, D.C., United States
  • 2011–2013
    • The Ohio State University
      • The James Comprehensive Cancer Center
      Columbus, OH, United States
    • Mount Sinai School of Medicine
      • • Institute for Translational Epidemiology
      • • Department of Preventive Medicine
      Manhattan, NY, United States
    • Howard University
      Washington, West Virginia, United States
  • 2012
    • Morgan State University
      Baltimore, Maryland, United States
    • Texas A&M University System Health Science Center
      • Department of Epidemiology and Biostatistics
      Bryan, TX, United States
  • 1998–2012
    • Georgetown University
      • • Department of Oncology
      • • Lombardi Cancer Center
      Washington, D. C., DC, United States
    • U.S. Food and Drug Administration
      • Division of Epidemiology
      Washington, D. C., DC, United States
  • 1995–2011
    • University at Buffalo, The State University of New York
      • • Department of Social and Preventive Medicine
      • • School of Medicine and Biomedical Sciences (1)
      Buffalo, NY, United States
  • 2010
    • American Legacy Foundation
      Washington, Washington, D.C., United States
  • 2000–2010
    • Roswell Park Cancer Institute
      • • Division of Cancer Prevention and Population Sciences
      • • Department of Epidemiology
      • • Department of Cancer Prevention, Epidemiology and Biostatistics
      Buffalo, New York, United States
    • Harvard Medical School
      Boston, Massachusetts, United States
  • 2009
    • University of Minnesota Twin Cities
      Minneapolis, Minnesota, United States
  • 2008
    • University of Maryland, Baltimore
      Baltimore, Maryland, United States
  • 2003–2007
    • University of Toronto
      • Department of Pharmacology and Toxicology
      Toronto, Ontario, Canada
    • Università degli Studi di Torino
      Torino, Piedmont, Italy
  • 2001–2007
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, United States
  • 1990–2007
    • National Cancer Institute (USA)
      • • Laboratory of Human Carcinogenesis
      • • Division of Cancer Epidemiology and Genetics
      • • Genetic Epidemiology
      • • Occupational and Environmental Epidemiology
      • • Cancer Etiology Branch (CEB)
      Maryland, United States
    • National Institutes of Health
      • Laboratory of Human Carcinogenesis
      Bethesda, MD, United States
  • 2006
    • University of Bristol
      • School of Experimental Psychology
      Bristol, ENG, United Kingdom
    • The Catholic University of America
      • Department of Electrical Engineering and Computer Science
      Washington, D. C., DC, United States
  • 2005
    • University of Alabama at Birmingham
      • Department of Biostatistics
      Birmingham, AL, United States
    • Uniformed Services University of the Health Sciences
      Maryland, United States
  • 2004
    • Maastricht University
      Maestricht, Limburg, Netherlands
  • 2002
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 1999
    • City of Hope National Medical Center
      Duarte, California, United States
  • 1995–1997
    • Nippon Medical School
      • Nippon Medical School Hospital
      Tokyo, Tokyo-to, Japan
  • 1993
    • NCI-Frederick
      Maryland, United States
    • Institute of Cancer Research
      Londinium, England, United Kingdom
    • University of Colorado
      • Department of Pathology
      Denver, CO, United States