Joshua E Muscat

Pennsylvania State University, University Park, Maryland, United States

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Publications (180)

  • Nicolle M. Krebs · Allshine Chen · Junjia Zhu · [...] · Joshua E. Muscat
    [Show abstract] [Hide abstract] ABSTRACT: The role of inhalation behaviors as predictors of nicotine uptake was examined in the Pennsylvania Adult Smoking Study (2012–2014), a study of 332 adults whose cigarette smoking was measured in a naturalistic environment (e.g., at home) with portable handheld topography devices. Piecewise regression analyses showed that levels of salivary cotinine, trans-3′-hydroxycotinine, and total salivary nicotine metabolites (cotinine + trans-3′-hydroxycotinine) increased linearly up to a level of about 1 pack per day (20 cigarettes per day (CPD)) (P < 0.01). Total daily puff volume (TDPV; in mL) (P < 0.05) and total daily number of puffs (P < 0.05), but not other topographical measures, increased linearly with CPD up to a level of about 1 pack per day. The mean level of cotinine per cigarette did not change above 20 CPD and was 36% lower in heavy smokers (≥20 CPD) than in lighter smokers (<20 CPD) (15.6 ng/mL vs. 24.5 ng/mL, respectively; P < 0.01). Mediation models showed that TDPV accounted for 43%–63% of the association between CPD and nicotine metabolites for smokers of <20 CPD. TDPV was the best predictor of nicotine metabolite levels in light-to-moderate smokers (1–19 CPD). In contrast, neither CPD, total daily number of puffs, nor TDPV predicted nicotine metabolite levels above 20 CPD (up to 40 CPD). Finally, although light smokers are traditionally considered less dependent on nicotine, these findings suggest that they are exposed to more nicotine per cigarette than are heavy smokers due to more frequent, intensive puffing.
    Article · Jun 2016 · American Journal of Epidemiology
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    Nathan R Jones · Joseph H Ashmore · Sang Y Lee · [...] · Joshua E Muscat
    [Show abstract] [Hide abstract] 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.
    Full-text Article · Dec 2015 · Cancers
  • Young H Lee · Thomas P Scharnitz · Joshua Muscat · [...] · Joslyn S Kirby
    [Show abstract] [Hide abstract] ABSTRACT: Importance Oral isotretinoin has been associated with several adverse effects, but evidence-based estimates of laboratory changes during isotretinoin therapy in large patient samples are limited.Objective To develop estimates of the laboratory changes that occur during isotretinoin therapy for acne using extant data and meta-analytic methods.Data Sources A comprehensive search strategy using Ovid/MEDLINE, EMBASE, and gray literature was conducted (1960-August 1, 2013) to identify all relevant studies of isotretinoin use in acne vulgaris. Terms related to acne treatment, isotretinoin, and diagnostic procedures were searched with all available synonyms.Study Selection Inclusion criteria consisted of clinical trials using oral isotretinoin, doses of 40 mg/d or more, duration of at least 4 weeks, patients aged 9 to 35 years with acne vulgaris, and 10 or more participants. Studies from all countries published in any language were included. Exclusion criteria were use of modified isotretinoin products, isotretinoin therapy for conditions other than acne vulgaris, and concomitant acne therapy. The initial search yielded 342 records; 116 of these were screened for full-text examination.Data Extraction and Synthesis Two authors independently reviewed the publications to determine eligibility, and disagreements were resolved by a third author. Generated weighted means and 99% CIs were calculated using the reported means (SDs or SEs). A random effects model was created, and statistical heterogeneity was quantified. Data were analyzed from August 25, 2014, to December 4, 2015.Main Outcomes and Measures Laboratory values for lipid levels, hepatic function, and complete blood cell count were evaluated.Results Data from 61 of the 116 studies were evaluated; 26 studies (1574 patients) were included in the meta-analysis. The mean (99% CI) values during treatment (nonbaseline) for triglycerides was 119.98 mg/dL (98.58-141.39 mg/dL); for total cholesterol, 184.74 mg/dL (178.17-191.31 mg/dL); for low-density lipoprotein cholesterol, 109.23 mg/dL (103.68-114.79 mg/dL); for high-density lipoprotein cholesterol, 42.80 mg/dL (39.84-45.76 mg/dL); for aspartate aminotransferase, 22.67 U/L (19.94-25.41 U/L); for alanine aminotransferase, 21.77 U/L (18.96-24.59 U/L); for alkaline phosphatase, 88.35 U/L (58.94-117.76 U/L); and for white blood cell count, 6890/µL (5700/µL-8030/µL). This meta-analysis showed that (1) isotretinoin is associated with a statistically significant change in the mean value of several laboratory tests (white blood cell count and hepatic and lipid panels), yet (2) the mean changes across a patient group did not meet a priori criteria for high-risk and (3) the proportion of patients with laboratory abnormalities was low.Conclusions and Relevance The evidence from this study does not support monthly laboratory testing for use of standard doses of oral isotretinoin for the standard patient with acne.
    Article · Dec 2015
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    Ute Mons · Joshua E Muscat · Jennifer Modesto · [...] · Hermann Brenner
    [Show abstract] [Hide abstract] 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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    [Show abstract] [Hide abstract] ABSTRACT: The high relapse and mortality rate of small-cell lung cancer (SCLC) fuels the need for epidemiologic study to aid in its prevention. Methods We included 24 studies from the ILCCO collaboration. Random-effects panel logistic regression and cubic spline regression were used to estimate the effects of smoking behaviors on SCLC risk and explore their non-linearity. Further, we explored whether the risk of smoking on SCLC was mediated through COPD. Findings Significant dose–response relationships of SCLC risk were observed for all quantitative smoking variables. Smoking pack-years were associated with a sharper increase of SCLC risk for pack-years ranged 0 to approximately 50. The former smokers with longer cessation showed a 43%quit_for_5–9 years to 89%quit_for_≥ 20 years declined SCLC risk vs. subjects who had quit smoking < 5 years. Compared with non-COPD subjects, smoking behaviors showed a significantly higher effect on SCLC risk among COPD subjects, and further, COPD patients showed a 1.86-fold higher risk of SCLC. Furthermore, smoking behaviors on SCLC risk were significantly mediated through COPD which accounted for 0.70% to 7.55% of total effects. Interpretation This is the largest pooling study that provides improved understanding of smoking on SCLC, and further demonstrates a causal pathway through COPD that warrants further experimental study. Abbreviations COPD, chronic obstructive pulmonary disease; CPG, cigarettes per day; ILCCO, International Lung Cancer Consortium; MeSH, medical subject headings; NSCLC, non-small cell lung cancer; OR, odds ratio; SCLC, small cell lung cancer.
    Full-text Article · Nov 2015 · EBioMedicine
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    [Show abstract] [Hide abstract] ABSTRACT: Background: The high relapse and mortality rate of small-cell lung cancer (SCLC) fuels the need for epidemiologic study to aid in its prevention. Methods: We included 24 studies from the ILCCO collaboration. Random-effects panel logistic regression and cubic spline regression were used to estimate the effects of smoking behaviors on SCLC risk and explore their non-linearity. Further, we explored whether the risk of smoking on SCLC was mediated through COPD. Findings: Significant dose–response relationships of SCLC risk were observed for all quantitative smoking variables. Smoking pack-years were associated with a sharper increase of SCLC risk for pack-years ranged 0 to approximately 50. The former smokers with longer cessation showed a 43%quit_for_5–9 years to 89%quit_for_≥20 years declined SCLC risk vs. subjects who had quit smoking
    Full-text Article · Sep 2015 · EBioMedicine
  • [Show abstract] [Hide abstract] 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.
    Article · Aug 2015 · European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP)
  • [Show abstract] [Hide abstract] 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.
    Article · Jul 2015 · Cancer Epidemiology Biomarkers & Prevention
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    [Show abstract] [Hide abstract] 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
  • Gad Rennert · Ran Kremer · Hedy S Rennert · [...] · Joshua E Muscat
    [Show abstract] [Hide abstract] 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.
    Article · Apr 2015 · International Journal of Cancer
  • John P Richie · Joshua Muscat
    [Show abstract] [Hide abstract] 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 ...
    Article · Mar 2015 · European Journal of Nutrition
  • [Show abstract] [Hide abstract] 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.
    Article · Mar 2015 · Rural and remote health
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    [Show abstract] [Hide abstract] 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
  • Article · Jan 2015 · Drug and Alcohol Dependence
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    [Show abstract] [Hide abstract] 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.
    Full-text Article · Dec 2014 · Journal of Neuro-Oncology
  • [Show abstract] [Hide abstract] 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: journals.permissions@oup.com.
    Article · Nov 2014 · Nicotine & Tobacco Research
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    Full-text Article · Nov 2014 · Epidemiology (Cambridge, Mass.)
  • Article · Oct 2014 · Cancer Research
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    C Bosetti · V Rosato · D Li · [...] · C La Vecchia
    [Show abstract] [Hide abstract] 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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    [Show abstract] [Hide abstract] 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

Publication Stats

6k Citations

Institutions

  • 2006-2015
    • Pennsylvania State University
      University Park, Maryland, United States
  • 2013
    • William Penn University
      Hershey, Pennsylvania, United States
  • 2005
    • Boston University
      • Department of Epidemiology
      Boston, MA, United States
  • 2004
    • Columbia University
      • Department of Epidemiology
      New York, New York, United States
    • The University of Tampa
      Tampa, Florida, United States
  • 2002
    • University of South Florida
      Tampa, Florida, United States
  • 2000
    • Memorial Sloan-Kettering Cancer Center
      New York, New York, United States
  • 1997
    • Moore Orthopaedics
      Лексингтон, South Carolina, United States