Peter G Shields

James A. Haley Veterans Hospital, Tampa, Florida, United States

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Publications (259)1493.66 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Mutations in the p53 gene are among the most frequent genetic events in human cancer and may be triggered by environmental and occupational exposures. We examined the association of clinical and pathological characteristics of breast tumors and breast cancer risk factors according to the prevalence and type of p53 mutations. Using tumor blocks from incident cases from a case-control study in western New York, we screened for p53 mutations in exons 2-11 using the Affymetrix p53 Gene Chip array and analyzed case-case comparisons using logistic regression. The p53 mutation frequency among cases was 28.1 %; 95 % were point mutations (13 % of which were silent) and the remainder were single base pair deletions. Sixty seven percent of all point mutations were transitions; 24 % of them are G:C>A:T at CpG sites. Positive p53 mutation status was associated with poorer differentiation (OR, 95 % CI 2.29, 1.21-4.32), higher nuclear grade (OR, 95 % CI 1.99, 1.22-3.25), and increased Ki-67 status (OR, 95 % CI 1.81, 1.10-2.98). Cases with P53 mutations were more likely to have a combined ER-positive and PR-negative status (OR, 95 % CI 1.65, 1.01-2.71), and a combined ER-negative and PR-negative status (OR, 95 % CI 2.18, 1.47-3.23). Body mass index >30 kg/m(2), waist circumference >79 cm, and waist-to-hip ratio >0.86 were also associated with p53 status; obese breast cancer cases are more likely to have p53 mutations (OR, 95 % CI 1.78, 1.19-2.68). We confirmed that p53 mutations are associated with less favorable tumor characteristics and identified an association of p53 mutation status and adiposity.
    Breast Cancer Research and Treatment 09/2015; DOI:10.1007/s10549-015-3570-5 · 3.94 Impact Factor
  • Cancer Research 08/2015; 75(15 Supplement):884-884. DOI:10.1158/1538-7445.AM2015-884 · 9.33 Impact Factor
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    ABSTRACT: The number of validated biomarkers of tobacco smoke exposure is limited, and none exist for tobacco-related cancer. Additional biomarkers for smoke, effects on cellular systems in vivo are needed to improve early detection of lung cancer, and to assist the Food and Drug Administration in regulating exposures to tobacco products. We assessed the effects of smoking on the gene expression using human cell cultures and blood from a cross-sectional study. We profiled global transcriptional changes in cultured smokers' peripheral blood mononuclear cells (PBMCs) treated with cigarette smoke condensate (CSC) in vitro (n = 7) and from well-characterized smokers' blood (n = 36). ANOVA with adjustment for covariates and Pearson correlation were used for statistical analysis in this study. CSC in vitro altered the expression of 1 178 genes (177 genes with > 1.5-fold-change) at P < 0.05. In vivo, PBMCs of heavy and light smokers differed for 614 genes (29 with > 1.5-fold-change) at P < 0.05 (309 remaining significant after adjustment for age, race, and gender). Forty-one genes were persistently altered both in vitro and in vivo, 22 having the same expression pattern reported for non-small cell lung cancer. Our data provides evidence that persistent alterations of gene expression in vitro and in vivo may relate to carcinogenic effects of cigarette smoke, and the identified genes may serve as potential biomarkers for cancer. The use of an in vitro model to corroborate results from human studies provides a novel way to understand human exposure and effect. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Cancer Research 08/2015; 75(15 Supplement):833-833. DOI:10.1158/1538-7445.AM2015-833 · 9.33 Impact Factor
  • Cancer Research 08/2015; 75(15 Supplement):1066-1066. DOI:10.1158/1538-7445.AM2015-1066 · 9.33 Impact Factor
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    ABSTRACT: There is increasing evidence that chronic inflammation is associated with increased breast cancer risk. Long-chain omega-3 polyunsaturated fatty acids (LCω-3PUFA) may reduce circulating biomarkers of inflammation; however associations of blood LCω-3PUFA with breast tissue LCω-3PUFA and breast tissue biomarkers of inflammation are not well understood. We conducted a cross-sectional analysis of breast tissue and blood samples from n=85 women with no history of breast cancer, who underwent breast reduction surgery. Fatty acids of erythrocytes and undissected breast tissues were analyzed by gas chromatography; C-reactive protein (CRP), interleukin (IL)-6 and IL-8 in plasma and tissue were measured by ELISA. Multivariable-adjusted regression models were used to estimate associations between erythrocyte LCω-3PUFA and breast tissue biomarkers. Women in the highest erythrocyte LCω-3PUFA tertile had LCω-3PUFA concentrations in the breast 73% (95% CI: 31%-128%; P trend<0.0001) higher than women in the lowest tertile. Associations for each individual LCω-3PUFA were similar in magnitude. No significant association was found for the shorter ω-3 PUFA, α-linolenic acid. Although compatible with no association, women in the highest tertile of erythrocyte eicosapentaenoic acid had a non-significant 32% (95% CI: -23% to 62%) reduced breast tissue CRP. No correlation was observed between erythrocyte ω-3 PUFA and tissue IL-6 or IL-8 concentrations. Our findings provide evidence that erythrocyte ω-3 fatty acids are valid measures of breast tissue concentrations, and limited evidence that inverse associations from prospective epidemiologic studies of blood LCω-3PUFA and breast cancer risk may be partly explained by reductions in breast tissue inflammation; however these findings require replication. This article is protected by copyright. All rights reserved. © 2014 Wiley Periodicals, Inc. © 2015 UICC.
    International Journal of Cancer 07/2015; DOI:10.1002/ijc.29675 · 5.09 Impact Factor
  • Cancer Epidemiology Biomarkers & Prevention 07/2015; 24(7):1144-8. DOI:10.1158/1055-9965.EPI-15-0476 · 4.13 Impact Factor
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    ABSTRACT: Genome-wide DNA hypomethylation is an early event in the carcinogenic process. Percent methylation of long interspersed nucleotide element-1 (LINE-1) is a biomarker of genome-wide methylation and is a potential biomarker for breast cancer. Understanding factors associated with percent LINE-1 DNA methylation in histologically normal tissues could provide insight into early stages of carcinogenesis. In a cross-sectional study of 121 healthy women with no prior history of cancer who underwent reduction mammoplasty, we examined associations between plasma and breast folate, genetic variation in one-carbon metabolism, and percent LINE-1 methylation using multivariable regression models (adjusting for race, oral contraceptive use, and alcohol use). Results are expressed as the ratio of LINE-1 methylation relative to that of the referent group, with the corresponding 95% confidence intervals (CI). We found no significant associations between plasma or breast folate and percent LINE-1 methylation. Variation in MTHFR, MTR, and MTRR were significantly associated with percent LINE-1 methylation. Variant allele carriers of MTHFR A1289C had 4% lower LINE-1 methylation (Ratio 0.96, 95% CI 0.93-0.98), while variant allele carriers of MTR A2756G (Ratio 1.03, 95% CI 1.01-1.06) and MTRR A66G (Ratio 1.03, 95% CI 1.01-1.06) had 3% higher LINE-1 methylation, compared to those carrying the more common genotypes of these SNPs. DNA methylation of LINE-1 elements in histologically normal breast tissues is influenced by polymorphisms in genes in the one-carbon metabolism pathway. Future studies are needed to investigate the sociodemographic, environmental and additional genetic determinants of DNA methylation in breast tissues and the impact on breast cancer susceptibility.
    Epigenetics: official journal of the DNA Methylation Society 06/2015; 10(8). DOI:10.1080/15592294.2015.1062205 · 4.78 Impact Factor
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    ABSTRACT: In this report the associations between telomere length variation (TLV), mean telomere length in blood lymphocytes and lung cancer risk were examined. The study design is case-control. Cases (N=191) were patients newly diagnosed with histologically confirmed non-small cell lung cancer. Controls (N=207) were healthy individuals recruited from the same counties as cases and matched to cases on age and gender. Telomere fluorescent in situ hybridization was used to measure telomere features using short-term cultured blood lymphocytes. Logistic regression was used to estimate the strength of association between telomere features and lung cancer risk. Telomere length variation across all chromosomal ends was significantly associated with lung cancer risk; adjusted odds ratios 4.67 [95% confidence interval (CI): 1.46-14.9] and 0.46 (95% CI: 0.25-0.84) for younger (age≤60) and older (age>60) individuals, respectively. TLV and mean telomere length jointly affected lung cancer risk: when comparing individuals with short telomere length and high TLV to those with long telomere length and low TLV, adjusted odd ratios were 8.21 (95% CI: 1.71-39.5) and 0.33 (95% CI: 0.15-0.72) for younger and older individuals, respectively. TLV in blood lymphocytes is significantly associated with lung cancer risk and the associations were modulated by age. TLV in combination with mean telomere length might be useful in identifying high risk population for lung cancer computerized tomography screening. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Lung cancer (Amsterdam, Netherlands) 03/2015; 88(3). DOI:10.1016/j.lungcan.2015.03.011 · 3.96 Impact Factor
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    ABSTRACT: Combustible tobacco use remains the number one preventable cause of disease, disability, and death in the United States. Electronic nicotine delivery systems (ENDS), which include e-cigarettes, are devices capable of delivering nicotine in an aerosolized form. ENDS use by both adults and youth has increased rapidly, and some have advocated these products could serve as harm-reduction devices and smoking cessation aids. ENDS may be beneficial if they reduce smoking rates or prevent or reduce the known adverse health effects of smoking. However, ENDS may also be harmful, particularly to youth, if they increase the likelihood that nonsmokers or formers smokers will use combustible tobacco products or if they discourage smokers from quitting. The American Association for Cancer Research (AACR) and the American Society of Clinical Oncology (ASCO) recognize the potential ENDS have to alter patterns of tobacco use and affect the public's health; however, definitive data are lacking. AACR and ASCO recommend additional research on these devices, including assessing the health impacts of ENDS, understanding patterns of ENDS use, and determining what role ENDS have in cessation. Key policy recommendations include supporting federal, state, and local regulation of ENDS; requiring manufacturers to register with the FDA and report all product ingredients, requiring childproof caps on ENDS liquids, and including warning labels on products and their advertisements; prohibiting youth-oriented marketing and sales; prohibiting child-friendly ENDS flavors; and prohibiting ENDS use in places where cigarette smoking is prohibited. Clin Cancer Res; 21(3); 1-12. ©2015 AACR. American Association for Cancer Research and American Society of Clinical Oncology. ©2015 American Association for Cancer Research and American Society of Clinical Oncology.
    Clinical Cancer Research 01/2015; 21(3). DOI:10.1158/1078-0432.CCR-14-2544 · 8.72 Impact Factor
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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; 36(1). DOI:10.1093/carcin/bgu219 · 5.33 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):4157-4157. DOI:10.1158/1538-7445.AM2014-4157 · 9.33 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):265-265. DOI:10.1158/1538-7445.AM2014-265 · 9.33 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; 23(8). DOI:10.1158/1055-9965.EPI-14-0173 · 4.13 Impact Factor
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    ABSTRACT: Polychlorinated biphenyls (PCBs) are ubiquitous in the environment. Concerns have been raised about cancer and other disease risks. This follow-up mortality study of PCB workers addresses some of these concerns. Mortality among 7,061 PCB capacitor workers was updated through 2008 (287,712 person-years; mean follow-up 41 years). Adjusted standardized mortality ratios (SMRs) and 95 % confidence intervals (CIs) were calculated for USA and New York State referent rates. Standardized rate ratios (SRRs) were calculated based on employment duration and latency. Standardized mortality ratios for all causes of death were statistically significantly lower in the total cohort (SMR 92; 95 % CI 89-96) and in males (SMR 88; 95 % CI 83-92), but not in females (SMR 100; 95 % CI 94-106). For all cancers combined, SMRs for the total cohort (SMR 103; 95 % CI 96-111) and for males (SMR 96; 95 % CI 87-105) did not differ from the expected rates, in contrast to females (SMR 114; 95 % CI 103-126). Buccal cavity and pharyngeal cancers were statistically increased in the combined cohort (SMR 169; 95 % CI 108-251) and in females (SMR 273; 95 % CI 131-502). Respiratory system malignancies were statistically lower in males (SMR 83; 95 % CI 70-97), while they were increased in females (SMR 143; 95 % CI 118-172). Melanomas were statistically significantly increased in male salaried workers only. No positive trends (SRRs) with increasing length of employment and increasing latency were found. The positive results lacking exposure-response relationships are subject to confounding and probably do not represent causal associations.
    International Archives of Occupational and Environmental Health 04/2014; 88(1). DOI:10.1007/s00420-014-0940-y · 2.20 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; 74(12). DOI:10.1158/0008-5472.CAN-14-0109 · 9.33 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; 23(4). DOI:10.1158/1055-9965.EPI-13-1209 · 4.13 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; 5(1). DOI:10.18632/oncotarget.1599 · 6.36 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; 24(12). DOI:10.1007/s10552-013-0294-x · 2.74 Impact Factor
  • Cancer Research 08/2013; 73(8 Supplement):3223-3223. DOI:10.1158/1538-7445.AM2013-3223 · 9.33 Impact Factor

Publication Stats

11k Citations
1,493.66 Total Impact Points


  • 2015
    • James A. Haley Veterans Hospital
      Tampa, Florida, United States
  • 2011–2015
    • The Ohio State University
      • • The James Comprehensive Cancer Center
      • • College of Medicine
      Columbus, Ohio, United States
  • 2001–2013
    • Georgetown University
      • • Lombardi Cancer Center
      • • Department of Oncology
      Washington, Washington, D.C., United States
  • 2008–2010
    • University of Texas MD Anderson Cancer Center
      Houston, Texas, United States
  • 2007–2010
    • District of Columbia Department of Health
      Washington, Washington, D.C., United States
    • Virginia State University
      Петербург, Virginia, United States
    • University of Toronto
      • Department of Pharmacology and Toxicology
      Toronto, Ontario, Canada
  • 2004–2010
    • Roswell Park Cancer Institute
      • Division of Cancer Prevention and Population Sciences
      Buffalo, New York, United States
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, United States
  • 1991–2007
    • National Institutes of Health
      • Laboratory of Human Carcinogenesis
      Bethesda, MD, United States
  • 2006
    • University of Bristol
      • School of Experimental Psychology
      Bristol, ENG, United Kingdom
  • 2005
    • Uniformed Services University of the Health Sciences
      Maryland, United States
    • University of Alabama at Birmingham
      • Department of Biostatistics
      Birmingham, AL, United States
  • 1990–2005
    • National Cancer Institute (USA)
      • • Laboratory of Human Carcinogenesis
      • • Division of Cancer Epidemiology and Genetics
      • • Occupational and Environmental Epidemiology
      • • Cancer Etiology Branch (CEB)
      Maryland, United States
  • 1996–2004
    • University at Buffalo, The State University of New York
      • • School of Medicine and Biomedical Sciences (1)
      • • Department of Social and Preventive Medicine
      Buffalo, NY, United States
  • 2000
    • Washington DC VA Medical Center
      Washington, Washington, D.C., United States
    • Harvard Medical School
      Boston, Massachusetts, United States
  • 1998–1999
    • Fox Chase Cancer Center
      Filadelfia, Pennsylvania, United States
    • U.S. Food and Drug Administration
      • Division of Epidemiology
      Washington, D. C., DC, United States
  • 1995–1996
    • Nippon Medical School
      • Nippon Medical School Hospital
      Tokyo, Tokyo-to, Japan
  • 1993–1995
    • NCI-Frederick
      Фредерик, Maryland, United States
    • Lawrence Livermore National Laboratory
      Livermore, California, United States