Joshua E Muscat

Pennsylvania State University, University Park, Maryland, United States

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Publications (164)803.65 Total impact

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    ABSTRACT: Background: Polymorphisms in the hemochromatosis (HFE) gene are associated with excessive iron absorption from the diet, and pro-oxidant effects of iron accumulation are thought to be a risk factor for several types of cancer. Methods: The C282Y (rs1800562) and H63D (rs1799945) polymorphisms were genotyped in 301 oral cancer cases and 437 controls and analyzed in relation to oral cancer risk, and serum iron biomarker levels from a subset of 130 subjects. Results: Individuals with the C282Y allele had lower total iron binding capacity (TIBC) (321.2 ± 37.2 µg/dL vs. 397.7 ± 89.0 µg/dL, p = 0.007) and higher percent transferrin saturation (22.0 ± 8.7 vs. 35.6 ± 22.9, p = 0.023) than wild type individuals. Iron and ferritin levels approached significantly higher levels for the C282Y allele (p = 0.0632 and p = 0.0588, respectively). Conclusions: Iron biomarker levels were elevated by the C282Y allele, but neither (rs1800562) nor (rs1799945) was associated with oral cancer risk in blacks and whites.
    No preview · Article · Dec 2015 · Cancers
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    ABSTRACT: Cigarette smoke contains high concentrations of free radical components that induce oxidative stress. Smoking-induced oxidative stress is thought to contribute to chronic obstructive pulmonary disease, cardiovascular disease and lung cancer through degenerative processes in the lung and other tissues. It is uncertain however whether smoking cessation lowers the burden of oxidative stress. We used data from a randomized controlled cessation trial of 434 current smokers for a post-hoc examination of the effects of smoking cessation on blood plasma levels of total glutathione (tGSH), the most abundant endogenous antioxidant in cells, and total cysteine (tCys), an amino acid and constituent of glutathione. Smoking status was validated based on serum cotinine levels. Multivariate linear mixed models were fitted to examine the association of smoking cessation and change in cigarette consumption with tGSH and tCys. After 12 months follow-up, quitters (n=55) had significantly increased levels of tGSH compared to subjects who continued to smoke (P<0.01). No significant change in tGSH was found for subjects who continued to smoke but reduced their intensity of smoking. No significant effect of smoking cessation or reduction was observed on levels of tCys. These results suggest that smoking cessation but not smoking reduction reduces levels of oxidative stress.
    Full-text · Article · Dec 2015 · Free Radical Biology and Medicine
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    ABSTRACT: A strong association between smoking and SCLC is noted whereas the dose–response relationships are less clear. We demonstrate that cumulative smoking of the first 50 pack-years is associated with a sharper increase in SCLC risk. Moreover, although the relationship between smoking and COPD or COPD and SCLC is well-established, no study has investigated the causal pathway among smoking, COPD, and SCLC. Here we reveal the risks of smoking behaviors on SCLC which are partially mediated (up to 7.6%) through COPD. The findings warrant further experimental study to elucidate the mechanisms in this causal pathway.
    Full-text · Article · Sep 2015 · EBioMedicine
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    ABSTRACT: Most mouthwashes contain alcohol, a known cause of head and neck cancer (oral cavity, pharynx, larynx), likely through the carcinogenic activity of acetaldehyde, formed in the oral cavity from alcohol. We carried out a pooled analysis of 8981 cases of head and neck cancer and 10 090 controls from 12 case-control studies with comparable information on mouthwash use in the International Head and Neck Cancer Epidemiology Consortium. Logistic regression was used to assess the association of mouthwash use with cancers of the oral cavity, oropharynx, hypopharynx, and larynx, adjusting for study, age, sex, pack-years of tobacco smoking, number of alcoholic drinks/day, and education. Compared with never users of mouthwash, the odds ratio (OR) of all head and neck cancers was 1.01 [95% confidence interval (CI): 0.94-1.08] for ever users, based on 12 studies. The corresponding ORs of cancer of the oral cavity and oropharynx were 1.11 (95% CI: 1.00-1.23) and 1.28 (95% CI: 1.06-1.56), respectively. OR for all head and neck cancer was 1.15 (95% CI: 1.01-1.30) for use for more than 35 years, based on seven studies (P for linear trend=0.01), and OR 1.31 (95% CI: 1.09-1.58) for use more than one per day, based on five studies (P for linear trend <0.001). Although limited by the retrospective nature of the study and the limited ability to assess risks of mouthwash use in nonusers of tobacco and alcohol, this large investigation shows potential risks for head and neck cancer subsites and in long-term and frequent users of mouthwash. This pooled analysis provides the most precise estimate of the association between mouthwash use and head and neck cancer.
    No preview · Article · Aug 2015 · European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP)
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    ABSTRACT: Epidemiological evidence indicates that greater intakes of vitamin D may decrease the risk of colorectal cancer (CRC). Variants in the vitamin D receptor (VDR) gene have the potential to modify associations between vitamin D intake and CRC. Associations between intakes of vitamin D and CRC were studied in a large case-control study conducted in central and northeastern Pennsylvania including 1012 cases with histologically confirmed colorectal cancer and 1080 population-based controls. Associations between 35 tagSNPs encompassing the VDR gene and risk for CRC as well as gene-diet associations were also assessed among a subset of the population (770 controls, 710 cases). No significant trends were observed between vitamin D intake and CRC risk. After adjustment for multiple comparisons, none of the SNPs or haplotypes within the VDR gene were associated with CRC. There were also no interactions between dietary factors and variants in the entire VDR gene. Overall, results from this study suggest that vitamin D intake and variants in the VDR gene have little effect on risk for CRC. Increasing vitamin D intake from the diet may not result in decreasing the incidence of CRC. Copyright © 2015, American Association for Cancer Research.
    No preview · Article · Jul 2015 · Cancer Epidemiology Biomarkers & Prevention
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    ABSTRACT: Cigarette smoking is a major risk factor for head and neck cancer (HNC). To our knowledge, low cigarette smoking (<10 cigarettes per day) has not been extensively investigated in fine categories or among never alcohol drinkers. We conducted a pooled analysis of individual participant data from 23 independent case-control studies including 19 660 HNC cases and 25 566 controls. After exclusion of subjects using other tobacco products including cigars, pipes, snuffed or chewed tobacco and straw cigarettes (tobacco product used in Brazil), as well as subjects smoking more than 10 cigarettes per day, 4093 HNC cases and 13 416 controls were included in the analysis. The lifetime average frequency of cigarette consumption was categorized as follows: never cigarette users, >0-3, >3-5, >5-10 cigarettes per day. Smoking >0-3 cigarettes per day was associated with a 50% increased risk of HNC in the study population [odds ratio (OR) = 1.52, 95% confidence interval (CI): (1.21, 1.90). Smoking >3-5 cigarettes per day was associated in each subgroup from OR = 2.01 (95% CI: 1.22, 3.31) among never alcohol drinkers to OR = 2.74 (95% CI: 2.01, 3.74) among women and in each cancer site, particularly laryngeal cancer (OR = 3.48, 95% CI: 2.40, 5.05). However, the observed increased risk of HNC for low smoking frequency was not found among smokers with smoking duration shorter than 20 years. Our results suggest a public health message that low frequency of cigarette consumption contributes to the development of HNC. However, smoking duration seems to play at least an equal or a stronger role in the development of HNC. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    Full-text · Article · Jun 2015 · International Journal of Epidemiology
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    ABSTRACT: Lung cancer rates in Israeli Jews have remained stable over the last 5 decades and are much lower than in most developed countries despite high historical smoking rates. We compared lung cancer risk in Jews and non-Jews in Israel and in the US. Data were derived from a population-based, case-control study in Israel (638 cases, 496 controls) to estimate lung cancer risk associated with smoking. Data were also acquired from a case-control study in the US with information on religious affiliation (5093 cases, 4735 controls). Smoking was associated with lung cancer risk in all religion/gender groups in both studies. However, major differences in risk magnitude were noted between Jews and non-Jews; ever smoking was associated with a moderately elevated risk of lung cancer in Jewish men and women in Israel, (OR=4.61,2.90-7.31 and OR=2.10,1.36-3.24 respectively), and in Jewish men and women in the US (OR=7.63,5.34-10.90 and OR=8.50, 5.94-12.17) but were significantly higher in Israeli Non-Jewish men (OR=12.96, 4.83-34.76) and US non-Jewish men and women (OR=11.33,9.09-14.12 and OR=12.78,10.45-15.63). A significant interaction between smoking and religion was evident in light, moderate and heavy, male and female smokers. The differences in risk level between Israeli Jews and non-Jews could not be explained by lung cancer genetic risk variants which were identified in GWAS (genes in the CHRNA5, TERT and CLPTM1L regions). Data from the two studies support the notion of a reduced risk of lung cancer in Jewish compared to non-Jewish smokers in different areas of the world. This article is protected by copyright. All rights reserved. © 2015 UICC.
    No preview · Article · Apr 2015 · International Journal of Cancer
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    John P Richie · Joshua Muscat
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    ABSTRACT: Dear Dr. Rowland,Please accept our response to Dr. Frederick Guilford’s comments of November 17, 2014, regarding our recent article which appeared in your Journal [1].The main issue described by Dr. Guilford refers to a published paper [2] referenced in the discussion section of our paper (reference #68). We cited that paper as an example of an in vitro study where intact GSH was shown to be more effective than N-acetylcysteine in “restoring immune function in macrophages from HIV-infected individuals” [1]. Indeed, Dr. Guilford is correct in that the GSH preparation used in that study was a liposome encapsulated GSH obtained from his company as opposed to the non-encapsulated form used in our study. However, I would like to emphasize that our study was not designed to test the relative efficacy of different GSH preparations, including liposomal GSH, but rather to determine the impact of GSH supplementation alone on GSH levels in blood and exfoliated buccal cells.We disagree with Dr. Gu ...
    Preview · Article · Mar 2015 · European Journal of Nutrition
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    ABSTRACT: A critical component of the US Food and Drug Administration's new authority to regulate tobacco products is understanding communications and marketing of tobacco products and their perceived risks in different geographic, age, race, ethnic and socioeconomic groups. Such information might be particularly useful in subgroups of the population or geographic areas that experience high tobacco use and suffer a disproportionate burden from tobacco-related diseases. For certain populations, there may be additional cultural factors unique to the geographical region which may promote smoking behavior. The purpose of the present study was to examine the perceptions of tobacco-related media messages among a sample of rural Appalachian natives, a population with smoking rates higher than the national average and who are disproportionately affected by tobacco-related and other cancers. A series of four focus group sessions were conducted in a north-central area of Pennsylvania, in one of 52 counties in Pennsylvania designated as within the Appalachian region. Participants were recruited via direct mail letters, advertisements in a local newspaper, and recruiting flyers posted at the local library. The focus groups were moderated by trained professional staff from The Pennsylvania State University's Center for Survey Research (CSR). Focus group sessions sought to examine perceptions of tobacco-related media in an Appalachian region of Pennsylvania. The sessions were audiotaped and transcribed, and the data was analyzed using qualitative approaches. Participants reported that pro-tobacco ads and favorable messages were received through the internet, direct mail, convenience stores, billboards, movies, and other sources. Anti-tobacco messages were identified primarily from television and magazines. In general, participants concluded that quitting was a matter of choice and was not influenced by pro- or anti-tobacco media. These results indicate that both pro- and anti-tobacco messages from a variety of sources are highly recognized and remembered in detail in Appalachia, but the effectiveness of anti-tobacco messages is questionable within this group. It was found that, without exception, group members reported that no media messages - either pro- or anti-tobacco - had any meaningful impact on their current behavior. Group members did, however, recognize that media messages influenced their behavior at the time they were first starting to smoke. The failure of these messages to connect with this population may reflect the lack of specific tailoring of messages to fit the distinct culture and values of this Appalachian population.
    No preview · Article · Mar 2015 · Rural and remote health
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    ABSTRACT: Increasing incidence of head and neck cancer (HNC) in young adults has been reported. We aimed to compare the role of major risk factors and family history of cancer in HNC in young adults and older patients. We pooled data from 25 case-control studies and conducted separate analyses for adults ≤45 years old ('young adults', 2010 cases and 4042 controls) and >45 years old ('older adults', 17 700 cases and 22 704 controls). Using logistic regression with studies treated as random effects, we estimated adjusted odds ratios (ORs) and 95% confidence intervals (CIs). The young group of cases had a higher proportion of oral tongue cancer (16.0% in women; 11.0% in men) and unspecified oral cavity / oropharynx cancer (16.2%; 11.1%) and a lower proportion of larynx cancer (12.1%; 16.6%) than older adult cases. The proportions of never smokers or never drinkers among female cases were higher than among male cases in both age groups. Positive associations with HNC and duration or pack-years of smoking and drinking were similar across age groups. However, the attributable fractions (AFs) for smoking and drinking were lower in young when compared with older adults (AFs for smoking in young women, older women, young men and older men, respectively, = 19.9% (95% CI = 9.8%, 27.9%), 48.9% (46.6%, 50.8%), 46.2% (38.5%, 52.5%), 64.3% (62.2%, 66.4%); AFs for drinking = 5.3% (-11.2%, 18.0%), 20.0% (14.5%, 25.0%), 21.5% (5.0%, 34.9%) and 50.4% (46.1%, 54.3%). A family history of early-onset cancer was associated with HNC risk in the young [OR = 2.27 (95% CI = 1.26, 4.10)], but not in the older adults [OR = 1.10 (0.91, 1.31)]. The attributable fraction for family history of early-onset cancer was 23.2% (8.60% to 31.4%) in young compared with 2.20% (-2.41%, 5.80%) in older adults. Differences in HNC aetiology according to age group may exist. The lower AF of cigarette smoking and alcohol drinking in young adults may be due to the reduced length of exposure due to the lower age. Other characteristics, such as those that are inherited, may play a more important role in HNC in young adults compared with older adults. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    Full-text · Article · Jan 2015 · International Journal of Epidemiology

  • No preview · Article · Jan 2015 · Drug and Alcohol Dependence
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    ABSTRACT: The HFE (high iron) protein plays a key role in the regulation of body iron. HFE polymorphisms (H63D and C282Y) are the common genetic variants in Caucasians. Based on frequency data, both HFE polymorphisms have been associated with increased risk in a number of cancers. The prevalence of the two major HFE polymorphisms in a human brain tumor patient populations and the impact of HFE polymorphisms on survival have not been studied. In the present study, there is no overall difference in survival by HFE genotype. However, male GBM patients with H63D HFE (H63D) have poorer overall survival than wild type HFE (WT) male GBM (p = 0.03). In GBM patients with the C282Y HFE polymorphism (C282Y), female patients have poorer survival than male patients (p = 0.05). In addition, female metastatic brain tumor patients with C282Y have shorter survival times post diagnosis than WT patients (p = 0.02) or male metastatic brain tumor patients with C282Y (p = 0.02). There is a tendency toward a lower proportion of H63D genotype in GBM patients than a non-tumor control group (p = 0.09) or other subtypes of brain tumors. In conclusion, our study suggests that HFE genotype impacts survival of brain tumor patients in a gender specific manner. We previously reported that glioma and neuroblastoma cell lines with HFE polymorphisms show greater resistance to chemo and radiotherapy. Taken together, these data suggest HFE genotype is an important consideration for evaluating and planning therapeutic strategies in brain tumor patients.
    Preview · Article · Dec 2014 · Journal of Neuro-Oncology
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    ABSTRACT: The time to first cigarette of the day (TTFC) is a strong indicator of nicotine dependence behaviors such as nicotine uptake and quit success in young and older smokers. There are substantial differences in levels of nicotine dependence by race and ethnic group. Data from Wave III of the multiracial National Longitudinal Study of Adolescent Health were analyzed for young smokers between the ages of 21 and 28 (N = 1,425). Time to first cigarette data was compared between Hispanic, White, Black, Native American, and Asian smokers. Black smokers were significantly more likely to smoke within 5min of waking than White, Hispanic, and Asian smokers. Lower personal income predicted smoking within 5min of waking for both White and Black smokers. For White smokers, increased number of cigarettes per day and increased years of smoking also predicted smoking within 5min of waking. The number of days smoked or number of cigarettes per day did not predict smoking within 5min of waking among smokers. The higher prevalence of early TTFC among Blacks indicates increased nicotine and carcinogen exposure, and may help explain the increased lung cancer rates and failed cessation attempts among Black smokers. TTFC may be an important screening item, independent of cigarettes per day, for clinicians and interventions to identify those at highest risk for cessation failure and disease risk. © The Author 2014. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail:
    No preview · Article · Nov 2014 · Nicotine & Tobacco Research

  • No preview · Article · Nov 2014 · Epidemiology (Cambridge, Mass.)

  • No preview · Article · Oct 2014 · Cancer Research
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    ABSTRACT: Background: Type 2 diabetes mellitus has been associated with an excess risk of pancreatic cancer, but the magnitude of the risk and the time-risk relationship are unclear, and there is limited information on the role of antidiabetic medications. Patients and methods: We analyzed individual-level data from 15 case-control studies within the Pancreatic Cancer Case-Control Consortium, including 8305 cases and 13 987 controls. Pooled odds ratios (ORs) were estimated from multiple logistic regression models, adjusted for relevant covariates. Results: Overall, 1155 (15%) cases and 1087 (8%) controls reported a diagnosis of diabetes 2 or more years before cancer diagnosis (or interview, for controls), corresponding to an OR of 1.90 (95% confidence interval, CI, 1.72-2.09). Consistent risk estimates were observed across strata of selected covariates, including body mass index and tobacco smoking. Pancreatic cancer risk decreased with duration of diabetes, but a significant excess risk was still evident 20 or more years after diabetes diagnosis (OR 1.30, 95% CI 1.03-1.63). Among diabetics, long duration of oral antidiabetic use was associated with a decreased pancreatic cancer risk (OR 0.31, 95% CI 0.14-0.69, for ≥15 years). Conversely, insulin use was associated with a pancreatic cancer risk in the short term (OR 5.60, 95% CI 3.75-8.35, for <5 years), but not for longer duration of use (OR 0.95, 95% CI 0.53-1.70, for ≥15 years). Conclusion: This study provides the most definitive quantification to date of an excess risk of pancreatic cancer among diabetics. It also shows that a 30% excess risk persists for more than two decades after diabetes diagnosis, thus supporting a causal role of diabetes in pancreatic cancer. Oral antidiabetics may decrease the risk of pancreatic cancer, whereas insulin showed an inconsistent duration-risk relationship.
    Full-text · Article · Jul 2014 · Annals of Oncology
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    ABSTRACT: Low socioeconomic status has been reported to be associated with head and neck cancer risk. However, previous studies have been too small to examine the associations by cancer subsite, age, sex, global region, and calendar time, and to explain the association in terms of behavioural risk factors. Individual participant data of 23,964 cases with head and neck cancer and 31,954 controls from 31 studies in 27 countries pooled with random effects models. Overall, low education was associated with an increased risk of head and neck cancer (OR = 2·50; 95%CI 2·02- 3·09). Overall one-third of the increased risk was not explained by differences in the distribution of cigarette smoking and alcohol behaviours; and it remained elevated among never users of tobacco and non-drinkers (OR = 1·61; 95%CI 1·13 - 2·31). More of the estimated education effect was not explained by cigarette smoking and alcohol behaviours: in women than in men, in older than younger groups, in the oropharynx than in other sites, in South/Central America than in Europe/North America, and was strongest in countries with greater income inequality. Similar findings were observed for the estimated effect of low vs high household income. The lowest levels of income and educational attainment were associated with more than 2-fold increased risk of head and neck cancer, which is not entirely explained by differences in the distributions of behavioural risk factors for these cancers, and which varies across cancer sites, sexes, countries, and country income inequality levels. © 2014 Wiley Periodicals, Inc.
    Full-text · Article · Jul 2014 · International Journal of Cancer
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    ABSTRACT: UDP-glucuronosyltransferases (UGTs) play an important role in the phase II metabolism of exogenous and endogenous compounds. As colorectal cancer (CRC) etiology is thought to involve the biotransformation of dietary factors, UGT polymorphisms may affect CRC risk by altering levels of exposure. Genotyping of over 1800 Caucasian subjects was completed to identify the role of genetic variation in nine UGT1A and five UGT2B genes on CRC risk. Unconditional logistic regression and haplotype analyses were conducted to identify associations with CRC risk and potential gene-environment interactions. UGT1A haplotype analysis found that the T-G haplotype in UGT1A10 exon 1 (block 2: rs17864678, rs10929251) decreased cancer risk for the colon [proximal (OR = 0.28, 95% CI = 0.11–0.69) and for the distal colon (OR = 0.32, 95% CI = 0.12–0.91)], and that the C-T-G haplotype in the 3′ region flanking the UGT1A shared exons (block 11: rs7578153, rs10203853, rs6728940) increased CRC risk in males (OR = 2.56, 95% CI = 1.10–5.95). A haplotype in UGT2B15 containing a functional variant (rs4148269, K523T) and an intronic SNP (rs6837575) was found to affect rectal cancer risk overall (OR = 2.57, 95% CI = 1.21–5.04) and in females (OR = 3.08, 95% CI = 1.08–8.74). An interaction was found between high NSAID use and the A-G-T haplotype (block 10: rs6717546, rs1500482, rs7586006) in the UGT1A shared exons that decreased CRC risk. This suggests that UGT genetic variation alters CRC risk differently by anatomical sub-site and gender and that polymorphisms in the UGT1A shared exons may have a regulatory effect on gene expression that allows for the protective effect of NSAIDs on CRC risk.
    No preview · Article · Jun 2014 · Genes Chromosomes and Cancer
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    ABSTRACT: The tobacco-specific nitrosamine NNK is a potent carcinogen found in tobacco smoke and implicated in the development of lung cancer. The major route of NNK metabolism is carbonyl reduction by AKR1C1, AKR1C2, CBR1, and 11β-HSD1 to form NNAL. This study investigated the potential role of variants in this pathway on lung cancer risk by examining 53 tag-SNPs representing the common variations in AKR1C1, AKR1C2, CBR1, and HSD11B1 in 456 lung cancer cases and 807 controls. One SNP in CBR1 (rs2835267) was significantly associated with overall risk of lung cancer, but did not pass multiple testing adjustment (OR: 0.76 95% CI: 0.58-0.99, P = 0.048, FDR P = 0.20). After stratification and multiple testing correction, three SNPs showed significance. One SNP (rs2835267) in CBR1 showed a significant decreased risk for smokers with a high pack-years (OR: 0.3595% CI: 0.17-0.69, P = 0.018) and in SCC (OR: 0.4895% CI: 0.29-0.76, P = 0.018). Another SNP located in CBR1 (rs3787728) also showed a significant decreased risk in SCC (OR: 0.4695% CI: 0.26-0.80, P = 0.024) and small cell carcinoma (only in current smokers) (OR: 0.06895% CI: 0.01-0.42, P = 0.028). The HSD11B1 SNP (rs4844880) showed a significant increased risk for adenocarcinoma within former smokers (OR: 3.9495% CI: 1.68-9.22, P = 0.011). Haplotype analysis found significance with six haplotypes and lung cancer risk. These findings indicate that select variants in genes in the carbonyl reduction pathway of NNK may alter the risk of lung cancer. © 2014 Wiley Periodicals, Inc.
    No preview · Article · Jun 2014 · Molecular Carcinogenesis
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    ABSTRACT: Glutathione (GSH), the most abundant endogenous antioxidant, is a critical regulator of oxidative stress and immune function. While oral GSH has been shown to be bioavailable in laboratory animal models, its efficacy in humans has not been established. Our objective was to determine the long-term effectiveness of oral GSH supplementation on body stores of GSH in healthy adults. A 6-month randomized, double-blinded, placebo-controlled trial of oral GSH (250 or 1,000 mg/day) on GSH levels in blood, erythrocytes, plasma, lymphocytes and exfoliated buccal mucosal cells was conducted in 54 non-smoking adults. Secondary outcomes on a subset of subjects included a battery of immune markers. GSH levels in blood increased after 1, 3 and 6 months versus baseline at both doses. At 6 months, mean GSH levels increased 30-35 % in erythrocytes, plasma and lymphocytes and 260 % in buccal cells in the high-dose group (P < 0.05). GSH levels increased 17 and 29 % in blood and erythrocytes, respectively, in the low-dose group (P < 0.05). In most cases, the increases were dose and time dependent, and levels returned to baseline after a 1-month washout period. A reduction in oxidative stress in both GSH dose groups was indicated by decreases in the oxidized to reduced glutathione ratio in whole blood after 6 months. Natural killer cytotoxicity increased >twofold in the high-dose group versus placebo (P < 0.05) at 3 months. These findings show, for the first time, that daily consumption of GSH supplements was effective at increasing body compartment stores of GSH.
    Full-text · Article · May 2014 · European Journal of Nutrition

Publication Stats

6k Citations
803.65 Total Impact Points


  • 2006-2015
    • Pennsylvania State University
      • • Department of Biobehavioral Health
      • • Department of Nutritional Sciences
      • • Department of Public Health Sciences
      University Park, Maryland, United States
  • 2005-2015
    • Penn State Hershey Medical Center and Penn State College of Medicine
      • • Public Health Sciences
      • • Department of Health Evaluation Sciences
      هرشي، بنسيلفانيا, Pennsylvania, United States
    • Boston University
      • Department of Epidemiology
      Boston, MA, United States
  • 2008-2014
    • William Penn University
      Worcester, Massachusetts, United States
    • University of South Carolina
      Columbia, South Carolina, United States
  • 2012
    • Samuel Lunenfeld Research Institute
      Toronto, Ontario, Canada
  • 2007
    • University of Milan
      Milano, Lombardy, Italy
  • 2001-2004
    • Columbia University
      • Department of Epidemiology
      New York, New York, United States
  • 2000
    • Memorial Sloan-Kettering Cancer Center
      New York, New York, United States
  • 1997
    • Moore Orthopaedics
      Лексингтон, South Carolina, United States
  • 1991
    • Inter American Foundation for Clinical Research, New York
      New York, New York, United States