Howard D Strickler

Albert Einstein College of Medicine, New York, New York, United States

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Publications (183)1099.77 Total impact

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    ABSTRACT: This study investigated the association of cervical human papillomavirus (HPV) infection with cumulative psychosocial risk reflecting family disadvantage, psychological distress, and unhealthy lifestyle. The sample (N = 745) comprised sexually active female adolescent patients (12-19 yr), primarily ethnic minorities, enrolled in a free HPV vaccination program. Subjects completed questionnaires and provided cervical swabs for HPV DNA testing. Unweighted and weighted principal component analyses for categorical data were used to derive multisystemic psychosocial risk indices using 9 indicators: low socioeconomic status, lack of adult involvement, not attending high school/college, history of treatment for depression/anxiety, antisocial/delinquent behavior, number of recent sexual partners, use of alcohol, use of drugs, and dependency risk for alcohol/drugs. The association between cervical HPV (any type, high-risk types, vaccine types) assayed by polymerase chain reaction and self-reported number of psychosocial risk indicators was estimated using multivariable logistic regression. Subjects had a median of 3 psychosocial risk indicators. Multiple logistic regression analyses showed associations with unweighted and weighted number of psychosocial indicators for HPV any type (adjusted odds ratio [aOR] = 1.1; 95% confidence interval [CI], 1.0-1.2), with the strongest associations between weighted drug/alcohol use, drug/alcohol dependency risk, and antisocial/delinquent behavior and detection of HPV vaccine types (aOR = 1.5; 95% CI, 1.1-2.0) independent of number of recent sexual partners and vaccine dose (0-3). Increased HPV infections including HPV vaccine types were associated with greater number of psychosocial risk indicators even after controlling for demographics, sexual behavior, history of chlamydia, and vaccine dose.
    Journal of developmental and behavioral pediatrics: JDBP 05/2015; DOI:10.1097/DBP.0000000000000178 · 2.12 Impact Factor
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    ABSTRACT: The association between oral HPV16 DNA viral load and infection clearance was evaluated among 88 individuals with oral HPV16 infection identified within a prospective cohort of 1,470 HIV-infected and uninfected individuals. Oral rinses were collected semi-annually for up to five years. Oral HPV16 viral load at the first positive test was significantly associated with time to clearance of infection (continuous p-trends<0.01). Notably, clearance rates by 24-month were 41% and 94% in the highest and lowest HPV16 viral load tertiles (p=0.03), respectively. High oral HPV16 viral load warrants consideration as a biomarker for infection persistence, the presumed precursor of HPV16-associated oropharyngeal cancer. © The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
    The Journal of Infectious Diseases 05/2015; DOI:10.1093/infdis/jiv273 · 5.78 Impact Factor
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    ABSTRACT: Objectives To determine whether changes in insulin-like growth factor (IGF) protein levels are greater in participants with type 2 diabetes mellitus or worsening glycemia than in normoglycemic individuals over a 9-year follow-up period.DesignRetrospective analysis of a cohort study.SettingParticipants were recruited from North Carolina, California, Maryland, and Pennsylvania.ParticipantsCardiovascular Health Study All Stars participants, a cohort study of community-dwelling adults aged 65 and older (N = 897).MeasurementsPlasma IGF-I, IGF binding protein (IGFBP)-1, and IGFBP-3 levels were assessed and American Diabetes Association cut-points for impaired glucose tolerance (IGT), impaired fasting glucose (IFG), and diabetes mellitus were used to classify participants at baseline (1996–97) and follow-up (2005–06).ResultsAt baseline, mean age was 76.3 ± 3.6, and 18.5% had diabetes mellitus. Participants with IFG alone and IGT plus IFG had higher IGF-I levels and lower IGFBP-1 levels than those with normoglycemia or diabetes mellitus. The greatest percentage change in IGF levels occurred in those who had diabetes mellitus at baseline (9-year changes: −9.3% for IGF-I, 59.7% for IGFBP-1, −13.4% for IGFBP-3), the smallest in individuals who remained normoglycemic at follow-up (9-year changes: −3.7% for IGF-I, 25.6% for IGFBP-1, −6.4% for IGFBP-3), and intermediate in those who were normoglycemic but developed IFG at follow-up.Conclusion Degrees of glycemic impairment are associated with varying degrees of change in IGF protein levels. The changes observed in the diabetes mellitus group have been previously shown to be associated with heart failure, cancer, and noncancer mortality.
    Journal of the American Geriatrics Society 05/2015; 63(5). DOI:10.1111/jgs.13390 · 4.22 Impact Factor
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    ABSTRACT: To describe changes in knowledge of cervical cancer prevention, human papillomavirus (HPV), and HPV vaccination among women at high risk for cervical cancer in the first five years after introduction of HPV vaccination. In 2007, 2008-9, and 2011, women in a multicenter U.S. cohort study completed 44-item self-report questionnaires assessing knowledge of cervical cancer prevention, HPV, and HPV vaccination. Results across time were assessed for individuals, and three study enrollment cohorts were compared. Knowledge scores were correlated with demographic variables, measures of education and attention, and medical factors. Associations were assessed in multivariable models. In all, 974 women completed three serial questionnaires; most were minority, low income, and current or former smokers. The group included 652 (67%) HIV infected and 322 (33%) uninfected. Summary knowledge scores (possible range 0-24) increased from 2007 (12.8, S.D. 5.8) to 2008-9 (13.9, S.D. 5.3, P < 0.001) and to 2011 (14.3, S.D 5.2, P < 0.0001 vs 2007 and <0.04 vs 2008-9). Higher knowledge scores at first and follow-up administration of questionnaires, higher income, and higher education level were associated with improved knowledge score at third administration. Women not previously surveyed had scores similar to those of the longitudinal group at baseline. Substantial gaps in understanding of HPV and cervical cancer prevention exist despite years of health education. While more effective educational interventions may help, optimal cancer prevention may require opt-out vaccination programs that do not require nuanced understanding.
    04/2015; 12. DOI:10.1016/j.gore.2015.02.007
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    ABSTRACT: Longitudinal studies of rare events such as cervical high-grade lesions or colorectal polyps that can recur often involve correlated binary data. Risk factor for these events cannot be reliably examined using conventional statistical methods. For example, logistic regression models that incorporate generalized estimating equations often fail to converge or provide inaccurate results when analyzing data of this type. Although exact methods have been reported, they are complex and computationally difficult. The current paper proposes a mathematically straightforward and easy-to-use two-step approach involving (i) an additive model to measure associations between a rare or uncommon correlated binary event and potential risk factors and (ii) a permutation test to estimate the statistical significance of these associations. Simulation studies showed that the proposed method reliably tests and accurately estimates the associations of exposure with correlated binary rare events. This method was then applied to a longitudinal study of human leukocyte antigen (HLA) genotype and risk of cervical high grade squamous intraepithelial lesions (HSIL) among HIV-infected and HIV-uninfected women. Results showed statistically significant associations of two HLA alleles among HIV-negative but not HIV-positive women, suggesting that immune status may modify the HLA and cervical HSIL association. Overall, the proposed method avoids model nonconvergence problems and provides a computationally simple, accurate, and powerful approach for the analysis of risk factor associations with rare/uncommon correlated binary events. © The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.
    Statistical Methods in Medical Research 04/2015; DOI:10.1177/0962280215581112 · 2.96 Impact Factor
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    ABSTRACT: OBJECTIVE: To evaluate the association of 3 hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor (statin) use and concordant polypharmacy with disease-specific survival from endometrial cancer. METHODS: A retrospective cohort study was conducted of 985 endometrial cancer cases treated from January 1999 through December 2009 at a single institution. Disease-specific survival was estimated by Kaplan-Meier analyses. A Cox proportional hazards model was used to study factors associated with survival. All statistical tests were two-sided and performed using Stata. RESULTS: At the time of analysis, 230 patients (22% of evaluable patients) died of disease and median follow-up was 3.28 years. Disease-specific survival was greater (179/220 [81%]) for women with endometrial cancer taking statin therapy at the time of diagnosis and staging compared with women not using statins (423/570 [74%]) (log rank test, P=.03). This association persisted for the subgroup of patients with nonendometrioid endometrial tumors who were statin users (59/87 [68%]) compared with nonusers (93/193 [43%]) (log rank test, P=.02). The relationship remained significant (hazard ratio 0.63, 95% confidence interval [CI] 0.40-0.99) after adjusting for age, clinical stage, radiation, and other factors. Further evaluation of polypharmacy showed an association between concurrent statin and aspirin use with an especially low disease-specific mortality (hazard ratio 0.25, 95% CI 0.09-0.70) relative to those who used neither. CONCLUSION: Statin and aspirin use was associated with improved survival from nonendometrioid endometrial cancer.
    Gynecologic Oncology 04/2015; 137. DOI:10.1016/j.ygyno.2015.01.074 · 3.69 Impact Factor
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    ABSTRACT: Although overall there is a positive association between obesity and risk of prostate cancer (PrCa) recurrence, results of individual studies are somewhat inconsistent. We investigated whether the failure to exclude diabetics in prior studies could have increased the likelihood of conflicting results. A total of 610 PrCa patients who underwent radical prostatectomy between 2005 and 2012 were followed for recurrence, defined as a rise in serum PSA ≥ 0.2 ng/ml following surgery. Body mass index (BMI) and history of type 2 diabetes were documented prior to PrCa surgery. The analysis was conducted using Cox proportional hazard models. Obesity (25.6 %) and diabetes (18.7 %) were common in this cohort. There were 87 (14.3 %) recurrence events during a median follow-up of 30.8 months after surgery among the 610 patients. When analyzed among all PrCa patients, no association was observed between BMI/obesity and PrCa recurrence. However, when analysis was limited to non-diabetics, obese men had a 2.27-fold increased risk (95 % CI 1.17-4.41) of PrCa recurrence relative to normal weight men, after adjusting for age and clinical/pathological tumor characteristics. This study found a greater than twofold association between obesity/BMI and PrCa recurrence in non-diabetics. We anticipated these results because the relationship between BMI/obesity and the biologic factors that may underlie the PrCa recurrence-BMI/obesity association, such as insulin, may be altered by the use of anti-diabetes medication or diminished beta-cell insulin production in advanced diabetes. Studies to further assess the molecular factors that explain the BMI/obesity-PrCa recurrence relationship are warranted.
    Cancer Causes and Control 03/2015; 26(6). DOI:10.1007/s10552-015-0554-z · 2.96 Impact Factor
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    ABSTRACT: We evaluated the risk factors associated with oral human papillomavirus (HPV) infection and oral lesions in 161 HIV-positive and 128 HIV-negative patients presenting for oral examination at two urban health-care centers. Patients were interviewed on risk factors and provided oral-rinse samples for HPV-DNA typing by PCR. Statistical associations were assessed by logistic regression. Oral HPV was prevalent in 32% and 16% of HIV-positive and negative patients, including high-risk type 16 (8% and 2%, respectively, p=0.049) and uncommon types 32/42 (6% and 5%, p=0.715). Among HIV-negative patients, significant risk factors for oral HPV included multiple sexual partners (≥21 vs. ≤5; odds ratio [OR]=9.1, 95% confidence interval [CI]:1.7-49.3), heavy tobacco smoking (>20 pack-years vs. none; OR=9.2, 95%CI:1.4-59.4), and marijuana use (OR=4.0, 95%CI:1.3-12.4). Among HIV-positive patients, lower CD4 count only was associated with oral HPV detection (≤200 vs. ≥500 T-cells/mm(3); OR=4.5, 95%CI:1.3-15.5). Detection of high-risk HPV was also associated with concurrent detection of potentially cancerous oral lesions in HIV-negative patients but not among HIV-positive patients. The observed risk factor associations with oral HPV in HIV-negative patients are consistent with sexual transmission and local immunity, whereas in HIV-positive patients, oral HPV detection is strongly associated with low CD4 count. © The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
    The Journal of Infectious Diseases 02/2015; DOI:10.1093/infdis/jiv080 · 5.78 Impact Factor
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    ABSTRACT: Individuals with human papillomavirus (HPV) infections can develop IgG antibodies to HPV proteins including the L1 capsid and E6 and E7 oncoproteins. Evidence on whether L1 antibodies reduce the risk of cervical HPV infection is mixed, but this has not been explored for oral HPV infections. Antibodies to HPV16's E6 oncoprotein have been detected in some oropharyngeal cancer cases years before cancer diagnosis, but it is unknown if these antibodies are associated with oral HPV16 DNA. Enzyme-linked immunosorbent assays tested for serum antibodies to HPV16's L1 capsid in 463 HIV-infected and 293 HIV-uninfected adults, and for antibodies to recombinantly expressed E6 and E7 oncoproteins to HPV16 in 195 HIV-infected and 69 HIV-uninfected cancer-free participants at baseline. Oral rinse samples were collected semiannually for up to 3 years and tested for HPV DNA using PGMY 09/11 primers. Adjusted Poisson, logistic, and Wei-Lin-Weissfeld regression models were used. Human papillomavirus 16 L1 seroreactivity did not reduce the subsequent risk of incident oral HPV16 infection in unadjusted (hazard ratio, 1.4; 95% confidence interval, 0.59-3.3) or adjusted (adjusted hazard ratio = 1.1; 95% confidence interval, 0.41-3.0) analysis. Antibodies to HPV16 E6 and E7 oncoproteins were detected in 7.6% and 3.4% of participants, respectively, but they were not associated with baseline oral HPV16 DNA prevalence or oral HPV16 persistence (each P > 0.40). Naturally acquired HPV16 L1 antibodies did not reduce the risk of subsequent oral HPV16 infection. Human papillomavirus 16 E6 and E7 seropositivity was not a marker for oral HPV16 infection in this population without HPV-related cancer.
    Sex Transm Dis 02/2015; 42(2):93-7. DOI:10.1097/OLQ.0000000000000236 · 2.75 Impact Factor
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    ABSTRACT: Adiposity is an established risk factor for postmenopausal breast cancer. Recent data suggest that high insulin levels in overweight women may play a major role in this relationship, due to insulin's mitogenic/antiapoptotic activity. However, whether overweight women who are metabolically healthy (i.e., normal insulin sensitivity) have elevated risk of breast cancer is unknown. We investigated whether overweight women with normal insulin sensitivity [i.e., homeostasis model assessment of insulin resistance (HOMA-IR) index, or fasting insulin level, within the lowest quartile (q1)] have increased breast cancer risk. Subjects were incident breast cancer cases (N = 497) and a subcohort (N = 2,830) of Women's Health Initiative (WHI) participants with available fasting insulin and glucose levels. In multivariate Cox models, metabolically healthy overweight women, defined using HOMA-IR, were not at elevated risk of breast cancer compared with metabolically healthy normal weight women [HRHOMA-IR, 0.96; 95% confidence interval (CI), 0.64-1.42]. In contrast, the risk among women with high (q3-4) HOMA-IRs was elevated whether they were overweight (HRHOMA-IR, 1.76; 95% CI, 1.19-2.60) or normal weight (HRHOMA-IR, 1.80; 95% CI, 0.88-3.70). Similarly, using fasting insulin to define metabolic health, metabolically unhealthy women (insulin q3-4) were at higher risk of breast cancer regardless of whether they were normal weight (HRinsulin, 2.06; 95% CI, 1.01-4.22) or overweight (HRinsulin, 2.01; 95% CI, 1.35-2.99), whereas metabolically healthy overweight women did not have significantly increased risk of breast cancer (HRinsulin, 0.96; 95% CI, 0.64-1.42) relative to metabolically healthy normal weight women. Metabolic health (e.g., HOMA-IR or fasting insulin) may be more biologically relevant and more useful for breast cancer risk stratification than adiposity per se. Cancer Res; 75(2); 270-4. ©2014 AACR. ©2014 American Association for Cancer Research.
    Cancer Research 01/2015; 75(2):270-4. DOI:10.1158/0008-5472.CAN-14-2317 · 9.28 Impact Factor
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    ABSTRACT: Background: Obesity is a risk factor for several cancers in postmenopausal women. We attempted to determine cutoffs of adiposity measures in relation to risk of obesity-related cancers among postmenopausal women and to examine the effects of hormone therapy (HT) use on the cutoffs, neither of which has been broadly studied. Methods: We used data from the Women's Health Initiative cohort (n=144,701) and applied Cox-proportional hazards regressions to each combination of 17 cancer types and 6 anthropometric measures (weight, body mass index [BMI], weight to height ratio, waist circumference, waist to hip ratio [WHR], and waist to height ratio). Interactions between the anthropometric measures and HT use were also examined. Cutoffs were determined by applying a grid search followed by a two-fold cross validation method. Survival ROC analysis of 5- and 10-year incidence followed. Results: Breast, colorectal, colon, endometrium, kidney, and all cancers combined were significantly positively associated with all six anthropometric measures, whereas lung cancer among ever smokers was significantly inversely associated with all measures except WHR. The derived cutoffs of each obesity measure varied across cancers (e.g., BMI cutoffs for breast and endometrium cancers were 30 kg/m(2) and 34 kg/m(2), respectively), and also depended on HT use. The Youden indices of the cutoffs for predicting 5- and 10-year cancer incidence were higher among HT never users. Conclusion: Using a panel of different anthropometric measures, we derived optimal cut-offs categorizing populations into high- and low-risk groups, which differed by cancer type and HT use. Although the discrimination abilities of these risk categories were generally poor, the results of this study could serve as a starting point from which to determine adiposity cutoffs for inclusion in risk prediction models for specific cancer types.
    Journal of Women's Health 01/2015; 24(3). DOI:10.1089/jwh.2014.4977 · 1.90 Impact Factor
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    ABSTRACT: Atypical hyperplasia of the breast (AH) is associated with increased risk of subsequent invasive breast cancer, yet little is known about the etiology of AH. Insulin-like growth factor binding protein 2 (IGFBP-2) may contribute to the development of AH due to its proliferative effects on mammary tissue. We conducted a nested case-control study of postmenopausal women enrolled in Women’s Health Initiative-Clinical Trial. Cases were 275 women who developed incident AH during follow-up, individually (1 : 1) matched to controls. Levels of IGFBP-2 were determined from fasting serum collected at baseline. Multivariable conditional logistic regression models were used to estimate odds ratios for the association of IGFBP-2 with risk of AH. Serum IGFBP-2 was associated with a nonsignificant decrease in risk for AH, when comparing the highest quartile to lowest quartile (OR = 0.65; 95% CI = 0.32-1.31). This decrease in risk was most evident when analyses were restricted to nondiabetic, nonusers of hormone therapy (OR = 0.33, 95% CI = 0.13-0.86, ptrend = 0.06) and nondiabetic women who were overweight or obese (OR = 0.43, 95% CI = 0.18-1.03, ptrend = 0.05). Results from this study provide some support for an inverse association between serum IGFBP2 levels and risk of AH, particularly in nondiabetic women who are overweight or obese. Further studies are required to confirm these results.
    Journal of Cancer Epidemiology 01/2015; 2015:1-7. DOI:10.1155/2015/203284
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    ABSTRACT: To estimate the impact of HIV infection on the incidence of high grade cervical intraepithelial neoplasia (CIN). HIV seropositive and comparison seronegative women enrolled in a prospective U.S. cohort study were followed with semiannual Pap testing, with colposcopy for any abnormality. Histology results were retrieved to identify CIN3+ (CIN3, adenocarcinoma in situ, and cancer and CIN2+ (CIN2 and CIN3+). Annual detection rates were calculated and risks compared using Cox analysis. Median follow-up (IQR) was 11.0 (5.4-17.2) years for HIV seronegative and 9.9 (2.5-16.0) for HIV seropositive women. CIN3+ was diagnosed in 139 (5%) HIV seropositive and 19 (2%) seronegative women (P < 0.0001), with CIN2+ in 316 (12%) and 34 (4%) (P < 0.0001). The annual CIN3+ detection rate was 0.6/100 person-years in HIV seropositive women and 0.2/100 person years in seronegative women (P < 0.0001). The CIN3+ detection rate fell after the first two years of study, from 0.9/100 person-years among HIV seropositive women to 0.4/100 person-years during subsequent follow-up (P < 0.0001). CIN2+ incidence among these women fell similarly with time, from 2.5/100 person-years during the first two years after enrollment to 0.9/100 person-years subsequently (p < 0.0001). In Cox analyses controlling for age, the hazard ratio for HIV seropositive women with CD4 counts <200/cmm compared to HIV seronegative women was 8.1 (95% C.I. 4.8, 13.8) for CIN3+ and 9.3 (95% C.I. 6.3, 13.7) for CIN2+ (P < 0.0001). Although HIV seropositive women have more CIN3+ than seronegative women, CIN3+ is uncommon and becomes even less frequent after initiation of regular cervical screening. Copyright © 2014 Elsevier Inc. All rights reserved.
    American Journal of Obstetrics and Gynecology 12/2014; 212(5). DOI:10.1016/j.ajog.2014.12.003 · 3.97 Impact Factor
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    ABSTRACT: New World Health Organization guidelines recommend high-risk human papillomavirus (hrHPV) screen-and-treat strategies for cervical cancer prevention. We describe risk of, and risk factors for, testing hrHPV positive in a pilot study of hrHPV screen-and-treat conducted in Rwanda. A total of 2,964 women, 1,289 HIV-infected (HIV [+]) and 1,675 HIV-uninfected (HIV [-]), aged 30-60 years and living in Rwanda were enrolled in 2010. Cervical specimens were collected and tested by careHPV, a DNA test for a pool of 14 hrHPV types. Prevalence with binomial 95% confidence intervals (95% CI) and determinants of testing hrHPV positive were calculated. hrHPV prevalence was higher in HIV [+] (31.8%, 95% CI = 29.2-34.4%) than HIV [-] women (8.2%, 95% CI = 6.7-9.8%; P < 0.0001). Among HIV [+] women, there was a significant trend (ptrend <0.001) of higher hrHPV prevalence with lower CD4 cell count, with the highest hrHPV prevalence among those with <200 CD4 cell counts (45.5%, 95% CI = 34.8-56.4%). In multivariate analysis of HIV [+] women, testing hrHPV positive was positively associated CD4 count of <200 cells/μL, history of 3 or more sexual partners, and history of using hormonal contraception, and negatively associated with older age. In HIV [-] women, testing hrHPV positive was negatively associated only with older age groups of 45-49 and 50-60 years and surprisingly was not associated with lifetime number of sexual partners. hrHPV prevalence is high in HIV [+], especially in women with the lowest CD4 cell counts, which may have implications for utilizing hrHPV-based screening strategies such as screen-and-treat in these high-risk subgroups.
    Infectious Agents and Cancer 12/2014; 9:40. DOI:10.1186/1750-9378-9-40 · 2.07 Impact Factor
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    ABSTRACT: Human papillomavirus (HPV) causes the majority of oropharyngeal cancers in the United States, yet the risk factors for and natural history of oral HPV infection are largely unknown. In 2010-2011, a US-based longitudinal cohort study of 761 human immunodeficiency virus (HIV)-infected and 469 at-risk HIV-uninfected participants from the Multicenter AIDS Cohort Study and the Women's Interagency HIV Study was initiated. Semiannually collected oral rinses were evaluated for 37 HPV genotypes using the Roche LINEAR ARRAY HPV Genotyping Test (Roche Molecular Systems, Pleasanton, California), and factors associated with oral HPV incidence and clearance were explored using adjusted Wei-Lin-Weissfeld modeling. Through 2013, the 2-year cumulative incidence of any type of oral HPV infection was 34% in HIV-infected persons and 19% in HIV-uninfected persons. However, many of these infections cleared. Seven percent of incident infections and 35% of prevalent infections persisted for at least 2 years. After adjustment for other risk factors, HIV infection (adjusted hazard ratio = 2.3, 95% confidence interval: 1.7, 3.2), reduced current CD4 cell count, and increased numbers of oral sex and "rimming" partners increased the risk of incident oral HPV infection, whereas male sex, older age, and current smoking increased the risk of oral HPV persistence (each P < 0.05). This helps explain the consistent associations observed between these factors and prevalent oral HPV infection in previous cross-sectional studies. © The Author 2014. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
    American Journal of Epidemiology 12/2014; DOI:10.1093/aje/kwu247 · 4.98 Impact Factor
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    ABSTRACT: Background:Hepatitis C virus (HCV) viremia is thought to have broad systemic effects on the cellular immune system that go beyond its impact on just those T cells that are HCV specific. However, previous studies of chronic HCV and circulating T-cell subsets (activation and differentiation phenotypes) in HIV negatives used general population controls, rather than a risk-appropriate comparison group. Studies in HIV positives did not address overall immune status (total CD4(+) count).Methods:We used fresh blood from HIV-positive and at-risk HIV-negative women, with and without chronic HCV, to measure percentages of activated CD4(+) and CD8(+) T cells, Tregs, and T-cell differentiation phenotypes (naive, central memory, effector memory (EM), and terminally differentiated effector). This included 158 HIV negatives and 464 HIV positives, of whom 18 and 63, respectively, were HCV viremic.Results:In multivariate models of HIV negatives, HCV viremia was associated with 25% fewer naive CD4(+) (P = 0.03), 33% more EM CD4(+) (P = 0.0002), and 37% fewer central memory CD8(+) (P = 0.02) T cells. Among HIV positives, we observed only 1 of these 3 relationships: higher percentage of EM CD4(+) among HCV viremic women. Furthermore, the association with EM CD4(+) among HIV positives was limited to individuals with diminished immune status (total CD4(+) count 500 cells/L), as were associations of HCV viremia with higher percentages of activated CD4(+) and Tregs. Among HIV positives with high CD4(+) count, no significant associations were observed.Conclusions:These data suggest that HCV viremia in HIV negatives is associated with accelerated T-cell differentiation, but among HIV positives, the impact of HCV viremia is less straightforward and varies by total CD4(+) count.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 11/2014; 67(3):295-303. DOI:10.1097/QAI.0000000000000310 · 4.39 Impact Factor
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    ABSTRACT: Objective: To estimate the effects of infection by HIV on the type-specific cumulative detection of cervicovaginal infection by human papillomavirus (HPV). Design: Retrospective assessment of prospectively collected data in a multicenter US cohort. Methods: HIV-seropositive and at-risk seronegative participants in the Women's Interagency HIV Study were followed semiannually for up to 11 years. HPV typing was determined from cervicovaginal lavage specimens by PCR; types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68 were considered carcinogenic. Results: Among the 3438 women enrolled (2543 HIV-seropositive, 895 seronegative), the cumulative detection of any HPV infection rose among HIV-seropositive women from 53% at baseline to 92% at 8 years, and among seronegative women from 22 to 66% (P< 0.0001 for HIV-seropositive vs. seronegative women). The 8-year cumulative detection of carcinogenic and noncarcinogenic HPV was 67 and 89% among HIV-seropositive, and 36 and 56% among seronegative women (P = 0.001 for both carcinogenic and noncarcinogenic HPV). The 8-year cumulative detection of HPV16 and HPV18 was 15.2 and 15.0% in HIV-seropositive, and 6.7 and 6.1% in HIV-seronegative women (P< 0.0001 for both). In multivariable regression analyses, lower CD4(+) cell count, age under 30 years, and smoking, but not number of lifetime sexual partners, were significant correlates of cumulative HPV detection. Conclusion: More than 90% of the HIV-seropositive women have HPV detected during a long follow-up. The rates are lower among at-risk HIV-seronegative women, though most also develop HPV infections. (c) 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
    AIDS (London, England) 09/2014; 28(17). DOI:10.1097/QAD.0000000000000455 · 6.56 Impact Factor
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    ABSTRACT: Objective Circulating free insulin-like growth factor (IGF)-I and its binding proteins, most notably, IGFBP-1 and IGFBP-2, have been prospectively associated with incident type 2 diabetes in women. However, little is known regarding the factors that may influence these IGF-axis protein levels. To study the relation of IGF-axis protein levels with adipocytokines, macronutrient consumption, and other factors related to diabetes. Design Fasting plasma from 558 controls enrolled in a nested case-control study within the Nurses’ Health Study of incident type 2 diabetes in women were tested for: IGF-axis proteins (free and total IGF-I, IGFBP-1, IGFBP-2, IGFBP-3), adipocytokines (leptin, adiponectin, resistin), soluble leptin receptor (sOB-R), inflammatory factors (IL-18 and C-reactive protein (CRP)), insulin, and glycated hemoglobin (HbA1C). Results In multivariate models, each 1% increase in sOB-R (mean 34.9 ng/mL, standard deviation (SD) ± 11.3) was associated with -0.20% total IGF-I (P = 0.0003) and -0.42% free IGF-I (P = 0.002), as well as 0.73% higher IGFBP-1 (P < 0.0001) and 0.27% IGFBP-2 (P = 0.003). For example, a one SD change from the mean sOB-R level was associated with 11% lower free IGF-I. Insulin levels (mean 6.8 μU/mL ± 5.3) were inversely and adiponectin (mean 18.3 μg/mL ± 7.4) positively associated with IGFBP-1 and IGFBP-2 (all P < 0.01). Consumption of dairy protein, monounsaturated fats, and saturated fats, was also correlated with IGF-axis protein levels (all P < 0.05). Conclusions Several molecular factors and macronutrients were independently associated with plasma IGF-axis protein levels. Which of these, if any, reflect biologic relationships that can be intervened upon to influence IGF-axis protein concentrations warrants further investigation.
    Growth Hormone & IGF Research 08/2014; DOI:10.1016/j.ghir.2014.04.006 · 1.33 Impact Factor
  • AIDS (London, England) 07/2014; 28(11):1696-1698. DOI:10.1097/QAD.0000000000000285 · 6.56 Impact Factor
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    ABSTRACT: OBJECTIVE: Obesity is an established risk factor for development of endometrial cancer. We hypothesized that obesity might also be associated with an earlier age at endometrial cancer diagnosis, because mechanisms that drive the obesity-endometrial cancer association might also accelerate tumorigenesis. METHODS: A retrospective chart review was conducted of all cases of endometrial cancer diagnosed from 1999 to 2009 at a large medical center in New York City. The association of body mass index (BMI) with age at endometrial cancer diagnosis, comorbidities, stage, grade, and radiation treatment was examined using analysis of variance and linear regression. Overall survival by BMI category was assessed using Kaplan-Meier method and the log-rank test. RESULTS: A total of 985 cases of endometrial cancer were identified. The mean age at endometrial cancer diagnosis was 67.1 years (+/- 11.9 standard deviation) in women with a normal BMI, whereas it was 56.3 years (+/- 10.3 standard deviation) in women with a BMI greater than 50. Age at diagnosis of endometrioid-type cancer decreased linearly with increasing BMI (y=67.89-1.86x, R-2=0.049, P<.001). This association persisted after multivariable adjustment (R-2=0.181, P=.02). A linear association between BMI and age of nonendometrioid cancers was not found (P=.12). There were no differences in overall survival by BMI category. CONCLUSIONS: Obesity is associated with earlier age at diagnosis of endometrioid-type endometrial cancers. Similar associations were not, however, observed with nonendometrioid cancers, consistent with different pathways of tumorigenesis.
    Obstetrics and Gynecology 07/2014; 124(2). DOI:10.1097/AOG.0000000000000381 · 4.37 Impact Factor

Publication Stats

4k Citations
1,099.77 Total Impact Points

Institutions

  • 1999–2015
    • Albert Einstein College of Medicine
      • • Department of Epidemiology & Population Health
      • • Division of Epidemiology
      New York, New York, United States
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
  • 2014
    • Regional Alliance for Sustainable Development (RASD Rwanda)
      Kigale, Kigali, Rwanda
  • 2013
    • Cook County Health and Hospitals System
      Chicago, Illinois, United States
  • 1998–2013
    • Johns Hopkins Bloomberg School of Public Health
      • Department of Epidemiology
      Baltimore, Maryland, United States
    • NCI-Frederick
      Фредерик, Maryland, United States
    • National Institutes of Health
      Maryland, United States
  • 1999–2012
    • University of California, San Francisco
      San Francisco, California, United States
  • 2011
    • Montefiore Medical Center
      New York, New York, United States
  • 2009
    • University of Illinois Springfield
      Спрингфилд, Florida, United States
  • 2008
    • Yeshiva University
      • Department of Epidemiology & Population Health
      New York City, New York, United States
  • 2007
    • University of Pittsburgh
      • Department of Medicine
      Pittsburgh, Pennsylvania, United States
    • Southern Illinois University School of Medicine
      • Department of Obstetrics and Gynecology
      Springfield, IL, United States
    • University of Texas Southwestern Medical Center
      • Division of Epidemiology
      Dallas, TX, United States
  • 2004–2007
    • University of Southern California
      • • Department of Pediatrics
      • • Keck School of Medicine
      Los Angeles, CA, United States
    • Lincoln Hospital
      New York, United States
    • Johns Hopkins University
      Baltimore, Maryland, United States
    • Cook County Hospital
      Chicago, Illinois, United States
  • 2006
    • State University of New York Downstate Medical Center
      • Department of Obstetrics and Gynecology
      Brooklyn, NY, United States
  • 2005
    • Cornell University
      Итак, New York, United States
  • 1994–2003
    • National Cancer Institute (USA)
      • • Division of Cancer Epidemiology and Genetics
      • • Epidemiology and Biostatistics
      Bethesda, MD, United States
  • 1995–1997
    • Northern Inyo Hospital
      BIH, California, United States