Jennifer L Beebe-Dimmer

Wayne State University, Detroit, Michigan, United States

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Publications (57)384.96 Total impact

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    ABSTRACT: A rare non-conservative substitution (G84E) in the HOXB13 gene has been shown to be associated with risk of prostate cancer. DNA samples from male patients included in the Mayo Clinic Biobank (MCB) were genotyped to determine the frequency of the G84E mutation and its association with various cancers. Subjects were genotyped using a custom TaqMan (Applied Biosystems) assay for G84E (rs138213197). In addition to donating a blood specimen, all MCB participants completed a baseline questionnaire to collect information on medical history and family history of cancer. Forty-nine of 9,012 male patients were carriers of G84E (0.5%). Thirty-one percent (n=2,595) of participants had been diagnosed with cancer, including 51.1% of G84E carriers compared to just 30.6% of non-carriers (p=0.004). G84E was most frequently observed among men with prostate cancer compared to men without cancer (p<0.0001). However, the mutation was also more commonly observed in men with bladder cancer (p=0.06) and leukemia (p=0.01). G84E carriers were more likely to have a positive family history of prostate cancer in a first degree relative compared to non-carriers (36.2% v. 16.0%, p=0.0003). Our study confirms the association between the HOXB13 G84E variant and prostate cancer and suggests a novel association between G84E and leukemia and a suggestive association with bladder cancer. Future investigation is warranted to confirm these associations in order to improve our understanding of the role of germline HOXB13 mutations in human cancer. The associations between HOXB13 and prostate, leukemia and bladder suggest that this gene is important in carcinogenesis. Copyright © 2015, American Association for Cancer Research.
    Cancer Epidemiology Biomarkers & Prevention 06/2015; DOI:10.1158/1055-9965.EPI-15-0247 · 4.32 Impact Factor
  • Cancer Research 05/2015; 75(9 Supplement):P6-10-04-P6-10-04. DOI:10.1158/1538-7445.SABCS14-P6-10-04 · 9.28 Impact Factor
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    The Journal of Urology 04/2015; 193(4):e496. DOI:10.1016/j.juro.2015.03.083 · 3.75 Impact Factor
  • The Journal of Urology 04/2015; 193(4):e156. DOI:10.1016/j.juro.2015.02.877 · 3.75 Impact Factor
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    ABSTRACT: Evidence suggests that the risk of breast and prostate cancer is increased among those with a family history of the same disease and particularly among first-degree relatives. However, less is known about the relationship between breast and prostate cancer within families and particularly among minority populations. Analyses of participants in the Women's Health Initiative observational cohort who were free of breast cancer at the time of their baseline examination were conducted. Subjects were followed for breast cancer through August 31, 2009. A Cox proportional hazards regression modeling approach was used to estimate the risk of breast cancer associated with a family history of prostate cancer, breast cancer, and both among first-degree relatives. There were 78,171 eligible participants, and 3506 breast cancer cases were diagnosed during the study period. A family history of prostate cancer was associated with a modest increase in breast cancer risk after adjustments for confounders (adjusted hazard ratio [aHR], 1.14; 95% confidence interval [CI], 1.02-1.26). In a separate analysis examining the joint impact of both cancers, a family history of both breast and prostate cancer was associated with a 78% increase in breast cancer risk (aHR, 1.78; 95% CI, 1.45-2.19). Risk estimates associated with a family history of both breast and prostate cancer were higher among African American women (aHR, 2.34; 95% CI, 1.09-5.02) versus white women (aHR, 1.66; 95% CI, 1.33-2.08). These findings suggest that prostate cancer diagnosed among first-degree family members increases a woman's risk of developing breast cancer. Future studies are needed to determine the relative contributions of genes and a shared environment to the risk for both cancers. Cancer 2015. © 2015 American Cancer Society. © 2015 American Cancer Society.
    Cancer 03/2015; 121(8). DOI:10.1002/cncr.29075 · 4.90 Impact Factor
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    ABSTRACT: To evaluate the association between statins and breast cancer stage and mortality in the Women's Health Initiative. The study population included 128,675 postmenopausal women aged 50-79 years, out of which there were 7,883 newly diagnosed cases of in situ (19 %), local (61 %)-, regional (19 %)- and distant (1 %)-stage breast cancer and 401 deaths due to breast cancer after an average of 11.5 (SD = 3.7) years of follow-up. Stage was coded using SEER criteria and was stratified into early (in situ and local)- versus late (regional and distant)-stage disease. Information on statins and other risk factors were collected by self- and interviewer-administered questionnaires. Cause of death was based on medical record review. Multivariable-adjusted hazards ratios (HR) and 95 % confidence intervals (CIs) evaluating the relationship between statin use (at baseline only and in a time-dependent manner) and diagnosis of late-stage breast cancer and breast cancer-specific mortality were computed from Cox proportional hazards analyses after adjusting for appropriate confounders. Statins were used by 10,474 women (8 %) at baseline. In the multivariable-adjusted time-dependent model, use of lipophilic statins was associated with a reduction in diagnosis of late-stage breast cancer (HR 0.80, 95 % CI 0.64-0.98, p = 0.035) which was also significant among women with estrogen receptor-positive disease (HR 0.72, 95 % CI 0.56-0.93, p = 0.012). Breast cancer mortality was marginally lower in statin users compared with nonusers (HR 0.59, 95 % CI 0.32-1.06, p = 0.075). Prior statin use is associated with lower breast cancer stage at diagnosis.
    Cancer Causes and Control 03/2015; 26(4). DOI:10.1007/s10552-015-0530-7 · 2.96 Impact Factor
  • David Schottenfeld · Jennifer Beebe-Dimmer
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    ABSTRACT: A review of cohort and case-control studies that attempt to quantify the proportion of cancer cases diagnosed in the United States and throughout the world that may be attributed to biologic or infectious agents.Methods Epidemiologic studies published primarily since the year 2000 are summarized that estimate population attributable fractions (PAFs) based on consensus estimates of relative risk and of the exposure prevalence to putative oncogenic infectious agents in representative populations.ResultsThe proportion of incident cancers attributable to infectious agents diagnosed in low-and middle-income countries, comprising more than 80% of the world`s population, has been estimated to vary from 20% to 30%, in contrast to a range of ≤ 5% to 10 % in the USA and other highly industrialized populations. More than 90% of the global cancer cases attributed to infectious agents have been caused by hepatitis B virus (HBV), hepatitis C virus (HCV), human papillomaviruses (HPVs), and the gram-negative bacterium, Helicobacter pylori.Conclusions Epidemiologic and pathologic studies that utilize molecular diagnostic probes and immunologic and biochemical assays have described the substantial impact of infectious agents on global cancer incidence. These compelling observations have stimulated the development of effective HBV and HPV vaccines, and the rationale for eradication of Helicobacter pylori.
    Annals of Epidemiology 11/2014; 25(3). DOI:10.1016/j.annepidem.2014.11.016 · 2.15 Impact Factor
  • Elizabeth J Davis · Jennifer L Beebe-Dimmer · Cecilia L Yee · Kathleen A Cooney
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    ABSTRACT: BACKGROUND: The survival of men diagnosed with prostate cancer has improved over time, and the current 10-year relative survival rate is 99.7%. The long survival of patients with this common cancer raises questions about the risk of a second primary cancer and the need for continued surveillance. METHODS: A population-based cohort of 441,504 men who were diagnosed with prostate cancer between 1992 and 2010 was identified from Surveillance, Epidemiology and End Results Program (SEER) data (SEER13). The standardized incidence ratio (SIR) was calculated as an estimate of the risk of a second primary malignancy based on the incidence in the general population. RESULTS: Prostate cancer survivors had a lower risk of being diagnosed with another cancer overall compared with the US population (SIR = 0.60; 95% confidence interval, 0.60-0.61). The risks of leukemia and cancers of the oral cavity and pharynx, esophagus, stomach, colon and rectum, liver, gallbladder, pancreas, lung and bronchus, and larynx were significantly lower. Conversely, these patients had a greater risk of bladder, kidney, and endocrine and soft tissue cancers. Men who received treatment with radiation therapy (external-beam radiation therapy) had long-term increases in their risk of bladder cancer (SIR = 1.42) and rectal cancer (SIR = 1.70) risk compared with who did not receive radiation (SIRbladder = 0.76; SIRrectal = 0.74). There were significant racial differences in the risk of being diagnosed with a second primary cancer, and the magnitude and direction of these risks depended on tumor type. CONCLUSIONS: Prostate cancer survivors remain at risk of subsequent malignancies, and race and treatment choice important determinants of long-term risk. (C) 2014 American Cancer Society.
    Cancer 09/2014; 120(17). DOI:10.1002/cncr.28769 · 4.90 Impact Factor
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    ABSTRACT: Background: Multiple primary cancers account for ~16% of all incident cancers in the U.S.. While genome-wide association studies (GWAS) have identified many common genetic variants associated with various cancer sites, no study has examined the association of these genetic variants with risk of multiple primary cancers (MPC). Methods: As part of the NHGRI Population Architecture using Genomics and Epidemiology (PAGE) study, we used data from the Multiethnic Cohort and Women's Health Initiative. Incident MPC (IMPC) cases (n=1,385) were defined as participants diagnosed with >1 incident cancers after cohort entry. Participants diagnosed with only one incident cancer after cohort entry with follow-up equal to or longer than IMPC cases served as controls (single-index cancer controls; n= 9,626). Fixed-effects meta-analyses of unconditional logistic regression analyses were used to evaluate the association between cancer risk variants and IMPC risk. To account for multiple comparisons, we used the false positive report probability (FPRP) to determine statistical significance. Results: A nicotine dependence-associated and lung cancer variant, CHRNA3 rs578776 (OR=1.16, 95% CI=1.05-1.26; p=0.004) and two breast cancer variants, EMBP1 rs11249433 and TOX3 rs3803662 (OR=1.16, 95% CI=1.04-1.28; p=0.005 and OR=1.13, 95% CI=1.03-1.23; p=0.006) were significantly associated with risk of IMPC. The associations for rs578776 and rs11249433 remained (p<0.05) after removing subjects who had lung or breast cancers, respectively (p-values≤0.046). These associations did not show significant heterogeneity by smoking status (p-heterogeneity≥0.53). Conclusions: Our study has identified rs578776 and rs11249433 as risk variants for IMPC. Impact: These findings may help to identify genetic regions associated with IMPC risk.
    Cancer Epidemiology Biomarkers & Prevention 08/2014; 23(11). DOI:10.1158/1055-9965.EPI-14-0129 · 4.32 Impact Factor
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    ABSTRACT: A single nucleotide polymorphism, rs10486567, in JAZF1 has consistently been associated with increased risk of prostate cancer. The physical interaction of zinc finger proteins, such as JAZF1, with heavy metals may play a role in carcinogenesis. This study assessed potential gene-environment statistical interactions (G×E) between rs10486567 and heavy metals in prostate cancer. In a case-only study of 228 African American prostate cancer cases, G×E between rs10486567 and sources of cadmium and lead (Pb) were assessed. Unconditional logistic regression was used to estimate interaction odds ratios (IORs), and generalized estimating equations were used for models containing nested data. Case-control validation of IORs was performed, using 82 controls frequency matched to cases on age-race. Among cases, a potential G×E interaction was observed between rs10486567 CC genotype and living in a Census tract with a high proportion of housing built before 1950, a proxy for household Pb exposure, when compared to CT or TT carriers (OR 1.81; 95 % CI 1.04-3.16; p = 0.036). A stronger G×E interaction was observed when both housing and occupational Pb exposure were taken into account (OR 2.62; 95 % CI 1.03-6.68; p = 0.04). Case-control stratified analyses showed the odds of being a CC carrier were higher in cases compared to controls among men living in areas with older housing (OR 2.03; CI 0.99-4.19; p = 0.05) or having high occupational Pb exposure (OR 2.50; CI 1.01-6.18; p = 0.05). In African American men, the association between JAZF1 rs10486567 and prostate cancer may be modified by exposure to heavy metals such as Pb.
    Cancer Causes and Control 05/2014; 25(7). DOI:10.1007/s10552-014-0387-1 · 2.96 Impact Factor
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    ABSTRACT: Black men have historically had higher blood lead levels than white men in the U.S. and have the highest incidence of prostate cancer in the world. Inorganic lead has been classified as a probable human carcinogen. Lead (Pb) inhibits delta-aminolevulinic acid dehydratase (ALAD), a gene recently implicated in other genitourinary cancers. The ALAD enzyme is involved in the second step of heme biosynthesis and is an endogenous inhibitor of the 26S proteasome, a master system for protein degradation and a current target of cancer therapy. Using a case-only study design, we assessed potential gene-environment (G × E) interactions between lifetime occupational Pb exposure and 11 tagSNPs within ALAD in black (N = 260) and white (N = 343) prostate cancer cases. Two ALAD tagSNPs in high linkage disequilibrium showed significant interaction with high Pb exposure among black cases (rs818684 interaction odds ratio or IOR = 2.73, 95% CI 1.43-5.22, P = 0.002; rs818689 IOR = 2.20, 95% CI 1.15-4.21, P = 0.017) and an additional tagSNP, rs2761016, showed G × E interaction with low Pb exposure (IOR = 2.08, 95% CI 1.13-3.84, P = 0.019). Further, the variant allele of rs818684 was associated with a higher Gleason grade in those with high Pb exposure among both blacks (OR 3.96, 95% CI 1.01-15.46, P = 0.048) and whites (OR 2.95, 95% CI 1.18-7.39, P = 0.020). Genetic variation in ALAD may modify associations between Pb and prostate cancer. Additional studies of ALAD, Pb, and prostate cancer are warranted and should include black men. Prostate. © 2014 Wiley Periodicals, Inc.
    The Prostate 05/2014; 74(6). DOI:10.1002/pros.22781 · 3.57 Impact Factor
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    ABSTRACT: To determine the prevalence and clinical correlates of the G84E mutation in the homeobox transcription factor (or HOXB13) gene using DNA samples from 9,559 men with prostate cancer undergoing radical prostatectomy. DNA samples from men treated with radical prostatectomy at the University of Michigan and John Hopkins University were genotyped for G84E and confirmed by Sanger sequencing. The frequency and distribution of this allele was determined according to specific patient characteristics (family history, age at diagnosis, pathologic Gleason grade and stage). 128 of 9,559 patients were heterozygous carriers of G84E (1.3%). Patients who possessed the variant were more likely to have a family history of prostate cancer (46.0% vs. 35.4% p=0.006). G84E carriers were also more likely diagnosed at a younger age compared to non-carriers (55.2 years vs. 58.1 years; p<0.0001). No difference in the proportion of patients diagnosed with high-grade or advanced stage tumors by carrier status was observed. In our study, carriers of the rare G84E variant in HOXB13 were both younger at the time of diagnosis and more likely to have a family history of prostate cancer compared to homozygotes for the wild-type allele. No significant differences in allele frequency were detected according to select clinical characteristics of prostate cancer. Further investigation is required to evaluate the role of HOXB13 in prostate carcinogenesis.
    BJU International 10/2013; 113(5). DOI:10.1111/bju.12522 · 3.13 Impact Factor
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    ABSTRACT: To investigate whether renal cell carcinoma (RCC) histologic subtypes possess different etiologies, we conducted analyses of established RCC risk factors by subtype (clear cell, papillary, chromophobe) in two case-control studies conducted in the United States (1,217 cases, 1,235 controls) and Europe (1,097 cases, 1,476 controls). Histology was ascertained for 706 U.S. cases (58% of total) and 917 European cases (84%) through a central slide review conducted by a single pathologist. For the remaining cases, histology was abstracted from the original diagnostic pathology report. Case-only analyses were performed to compute odds ratios (ORs) and 95% confidence intervals (CI) summarizing subtype differences by age, sex, and race. Case-control analyses were performed to compute subtype-specific ORs for other risk factors using polytomous regression. In case-only analyses, papillary cases (N=237) were older (OR=1.2, 95% CI=1.1-1.4 per 10-year increase), less likely to be female (OR=0.5, 95 % CI=0.4- 0.8) and more likely to be black (OR=2.6, 95% CI=1.8-3.9) compared to clear cell cases (N=1,524). In case-control analyses, BMI was associated with clear cell (OR=1.2, 95% CI=1.1-1.3 per 5kg/m(2) increase) and chromophobe RCC (N=80; OR=1.2, 95% CI=1.1- 1.4), but not papillary RCC (OR=1.1, 95% CI=1.0-1.2; test vs. clear cell, P=0.006). No subtype differences were observed for associations with smoking, hypertension or family history of kidney cancer. Our findings support the existence of distinct age, sex and racial distributions for RCC subtypes, and suggest that the obesity-RCC association differs by histology. © 2012 Wiley Periodicals, Inc.
    International Journal of Cancer 06/2013; 132(11). DOI:10.1002/ijc.27934 · 5.01 Impact Factor
  • David Schottenfeld · Jennifer L Beebe-Dimmer · Patricia A Buffler · Gilbert S Omenn
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    ABSTRACT: Our objective is to provide a current perspective on the avoidable causes of global and US cancer incidence and mortality. Cancer registry-based incidence patterns, population behavioral risk-factor survey data, and systematic reviews of epidemiologic studies are the basis for estimates of relative risk, the prevalence of exposures to various lifestyle and environmental risk factors, and their impact expressed as population attributable fractions (PAFs). Of the total 59 million global deaths in 2008, 12-13% were attributed to cancer. The increasing burden of cancers in low- and middle-income countries (LMICs) is attributable in part to increasing urbanization, expansion of the adult population at risk, and increasing or persistent exposures to infectious agents, tobacco, and dietary deficiencies. Attributable fractions for lifestyle and environmental risk factors are summarized for the United States, the United Kingdom, and France. Assuming minimal overlap in the distribution of risk factors in the population and discounting the potential for interaction in their combined effects, we estimate that a maximum of 60% of cancer deaths in the United States may be attributed to eight risk factors: tobacco, alcohol, ionizing and solar radiations, occupations, infectious agents, obesity, and physical inactivity.
    Annual Review of Public Health 03/2013; 34(1):97-117. DOI:10.1146/annurev-publhealth-031912-114350 · 6.63 Impact Factor
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    Jennifer L Beebe-Dimmer · Stephen J Freedland
    BJU International 02/2013; 111(5). DOI:10.1111/j.1464-410X.2013.11797.x · 3.13 Impact Factor
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    ABSTRACT: Background: Obesity is a risk factor for renal cell (or renal) cancer. The increasing prevalence of obesity may be contributing to the rising incidence of this cancer over the past several decades. The effects of early-age obesity and change in body mass index (BMI) on renal cancer have been studied less thoroughly, and the influence of race has never been formally investigated. Methods: Using data gathered as part of a large case-control study of renal cancer (1214 cases and 1234 controls), we investigated associations with BMI at several time points, as well as with height. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were computed using logistic regression modeling. Race-and sex-stratified analyses were conducted to evaluate subgroup differences. Results: Obesity (BMI ≥ 30kg/m²) early in adulthood (OR = 1.6 [95% CI = 1.1 to 2.4]) and 5 years before diagnosis (1.6 [1.1 to 2.2]) was associated with renal cancer. The association with early-adult obesity was stronger among whites than blacks (test for interaction, P = 0.006), whereas the association with obesity near diagnosis was marginally stronger in women than men (test for interaction, P = 0.08). The strongest association with renal cancer was observed for obese whites both in early adulthood and before interview (2.6 [1.5 to 4.4]); this association was not present among blacks. Estimates of the annual excess rate of renal cancer (per 100,000 persons) attributed to both overweight and obesity (BMI > 25 kg/m²) ranged from 9.9 among black men to 5.6 among white women. Conclusion: Obesity, both early and later in life, is associated with an increased risk of renal cancer. The association with early obesity seems to be stronger among whites than blacks.
    Epidemiology 11/2012; 23(6):821-828. DOI:10.2307/41739679 · 6.18 Impact Factor
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    R Asmar · J L Beebe-Dimmer · K Korgavkar · G R Keele · K A Cooney
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    ABSTRACT: Background:The metabolic syndrome (MetS) comprises a constellation of risk factors associated with an increased risk for cardiovascular disease. Components of MetS have emerged as putative risk factors for prostate carcinoma. In this study, we examine the association between three features of the MetS (obesity, hypertension and diabetes) and the risk of biochemical recurrence (BCR) after radical prostatectomy (RP).Methods:We examined data from 1428 men in the University of Michigan Prostate Cancer Data Bank who elected to have RP as their primary treatment. We calculated body mass index from patients' weight and height measured at the time of prostate cancer diagnosis. We used the University of Michigan's Electronic Medical Record Search Engine to identify subjects with hypertension and/or diabetes before their prostate cancer diagnosis.Results:Of 1428 men who underwent RP, 107 (8%) subsequently developed BCR with a median length of follow-up post-surgery of 3.6 years. Obesity and hypertension were each associated with an increased risk of BCR (adjusted hazard ratio (aHR)=1.37; 95% CI 0.92-2.09 and aHR=1.51, 95% CI 1.01-2.26), whereas no association was observed between diabetes and BCR (aHR=0.73; 95% CI 0.40-1.33).Conclusions:Obesity and hypertension were each associated with an increased risk for BCR of prostate cancer after RP, independent of age at diagnosis and tumor pathological features. Given the increasing rates of obesity, hypertension and prostate cancer, a better understanding of the relationship between these entities is of significant public health importance. Elucidation of the involved pathogenic mechanisms will be needed to establish causality.Prostate Cancer and Prostatic Disease advance online publication, 21 August 2012; doi:10.1038/pcan.2012.32.
    Prostate cancer and prostatic diseases 08/2012; 16(1). DOI:10.1038/pcan.2012.32 · 2.83 Impact Factor
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    ABSTRACT: Ingestion of groundwater with high concentrations of inorganic arsenic has been linked to adverse health outcomes, including bladder cancer, however studies have not consistently observed any elevation in risk at lower concentrations. Genetic variability in the metabolism and clearance of arsenic is an important consideration in any investigation of its potential health risks. Therefore, we examined the association between genes thought to play a role in the metabolism of arsenic and bladder cancer. Single nucleotide polymorphisms (SNPs) in GSTO-1, As3MT and MTHFR were genotyped using DNA from 219 bladder cancer cases and 273 controls participating in a case-control study in Southeastern Michigan and exposed to low to moderate (<50 μg/L) levels of arsenic in their drinking water. A time-weighted measure of arsenic exposure was constructed using measures from household water samples combined with past residential history, geocoded and merged with archived arsenic data predicted from multiple resources. While no single SNP in As3MT was significantly associated with bladder cancer overall, several SNPs were associated with bladder cancer among those exposed to higher arsenic levels. Individuals with one or more copies of the C allele in rs11191439 (the Met287Thr polymorphism) had an elevated risk of bladder cancer (OR = 1.17; 95% CI = 1.04-1.32 per 1 μg/L increase in average exposure). However, no association was observed between average arsenic exposure and bladder cancer among TT homozygotes in the same SNP. Bladder cancer cases were also 60% less likely to be homozygotes for the A allele in rs1476413 in MTHFR compared to controls (OR = 0.40; 95% CI = 0.18-0.88). Variation in As3MT and MTHFR is associated with bladder cancer among those exposed to relatively low concentrations of inorganic arsenic. Further investigation is warranted to confirm these findings.
    Environmental Health 06/2012; 11(1):43. DOI:10.1186/1476-069X-11-43 · 2.71 Impact Factor
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    ABSTRACT: Fractures are a recognized consequence of androgen deprivation therapy (ADT); however, less is known about the incidence of fracture in relation to the timing of ADT use or the impact of fracture on mortality in men with prostate cancer. Using data from the Surveillance, Epidemiology, and End Results-Medicare linked database, we estimated adjusted hazard ratios (aHRs) using time-dependent Cox regression for fracture incidence related to the recency of exposure and dose among prostate cancer patients on gonadotropin-releasing hormone (GnRH) agonists, as well as mortality associated with fractures. In our cohort of 80 844 patients, ADT was associated with an increased rate of fracture in both non-metastatic patients (aHR = 1.34; 95% confidence interval [CI] = 1.29-1.39) and metastatic patients (aHR = 1.51; 95%CI = 1.36-1.67). Fracture rates increased with increasing cumulative GnRH dose but decreased with increasing number of months since last use in each dose category. The mortality rate doubled for men experiencing a fracture after their diagnosis compared with that for men who did not experience a fracture (aHR = 2.05; 95%CI = 1.98-2.12). ADT in elderly men with prostate cancer increased the incidence of fractures, and the effect appears to diminish with increasing time since the last dose of a GnRH agonist. Experiencing a fracture after the diagnosis of prostate cancer was associated with decreased survival.
    Pharmacoepidemiology and Drug Safety 03/2012; 21(1):70-8. DOI:10.1002/pds.2258 · 3.17 Impact Factor
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    ABSTRACT: Metabolic syndrome refers to a set of conditions that increases the risk of cardiovascular disease and has been associated with an increased risk of prostate cancer, particularly among African American men. This study aimed to estimate the association of metabolic syndrome with biochemical recurrence (BCR) in a racially diverse population. Among 383 radical prostatectomy patients, 67 patients had documented biochemical recurrence. Hypertension was significantly, positively associated with the rate of BCR (hazard ratio (HR) = 2.1; 95%  CI = 1.1, 3.8). There were distinct racial differences in the prevalence of individual metabolic syndrome components; however, the observed associations with BCR did not differ appreciably by race. We conclude that hypertension may contribute to a poorer prognosis in surgically treated prostate cancer patients. Our findings suggest that targeting components of the metabolic syndrome which are potentially modifiable through lifestyle interventions may be a viable strategy to reduce risk of BCR in prostate cancer.
    09/2011; 2011(2090-3111):245642. DOI:10.1155/2011/245642

Publication Stats

2k Citations
384.96 Total Impact Points

Institutions

  • 2009–2015
    • Wayne State University
      • • Division of Hematology and Oncology
      • • Department of Internal Medicine
      Detroit, Michigan, United States
  • 2008–2015
    • Karmanos Cancer Institute
      Detroit, Michigan, United States
  • 2014
    • Henry Ford Health System
      • Department of Public Health Sciences
      Detroit, Michigan, United States
  • 2004–2006
    • University of Michigan
      • • Department of Epidemiology
      • • Department of Internal Medicine
      Ann Arbor, MI, United States
    • Fred Hutchinson Cancer Research Center
      Seattle, Washington, United States
  • 2003–2006
    • Concordia University–Ann Arbor
      Ann Arbor, Michigan, United States