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  • 1
    Keywords: CANCER ; EXPRESSION ; carcinoma ; CELL ; CELL LUNG-CANCER ; Germany ; POPULATION ; RISK ; GENE ; GENES ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; HEALTH ; PROMOTER ; case-control studies ; squamous cell carcinoma ; GASTRIC-CANCER ; EUROPE ; inflammation ; molecular epidemiology ; CYTOKINE ; CELL CARCINOMA ; ONCOLOGY ; case-control study ; RE ; INTERLEUKIN-1 ; PROMOTER POLYMORPHISM ; CYCLOOXYGENASE-2 ; case control studies ; methods ; INTERLEUKIN-8 ; oral cancer ; CANCERS ; ESOPHAGEAL CANCER ; SQUAMOUS-CELL ; INTERLEUKIN-8 PROMOTER ; larynx cancer ; pharynx cancer ; upper aerodigestive tract cancers
    Abstract: Objectives The purpose of this study was to investigate the role of polymorphisms of genes involved in inflammation in the risk of cancers of the upper aerodigestive tract (UADT). Methods We have evaluated the role of polymorphisms in key genes related to inflammation, namely IL1B (rs1143627), COX2/PTGS2 (rs5275), and IL8 (rs4073) in a large case-control study comprising 811 UADT cancer cases and 1,083 controls. Results An association was observed for squamous cell carcinoma of the pharynx for a polymorphism in the promoter of the IL1B gene, with an OR of 2.39 (95% CI = 1.19-4.81) for the homozygotes for the minor allele A promoter polymorphism of IL8 was associated with decreased risk of laryngeal cancer, with an OR of 0.70 (95% CI = 0.50-0.98) for carriers of the minor allele. Conclusions To our knowledge, this is the first report on the role of these polymorphisms with respect to UADT carcinogenesis. Our results suggest that inflammation-related polymorphisms play a role, albeit minor, in the risk of developing cancers of the upper aerodigestive tract
    Type of Publication: Journal article published
    PubMed ID: 17356794
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  • 2
    Keywords: CANCER ; LUNG ; DIAGNOSIS ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; EPIDEMIOLOGY ; incidence ; POPULATION ; RISK ; SITE ; SITES ; PATIENT ; primary ; PATTERNS ; NUMBER ; AGE ; smoking ; RATES ; cancer risk ; REGION ; FRANCE ; SQUAMOUS-CELL CARCINOMA ; HEAD ; ALCOHOL ; PREVALENCE ; TOBACCO SMOKING ; second cancer ; MULTICENTER ; NECK-CANCER ; ONCOLOGY ; REGISTRY ; RE ; PATTERN ; head and neck cancer ; cancer registries ; SURVIVORS ; analysis ; MALIGNANT-TUMORS ; cancer registry ; pooled analysis ; USA ; CANCER INCIDENCE ; CANCERS ; population-based ; CANCER-RISK ; NOV ; ORAL-CAVITY ; ALCOHOL-DRINKING ; EXCESS ; POOLED-ANALYSIS ; second primary ; YOUNG-PATIENTS
    Abstract: The objective of the study was to assess the risk of second primary cancers (SPCs) following a primary head and neck cancer (oral cavity, pharynx and larynx) and the risk of head and neck cancer as a PC. The present investigation is a multicenter study from 13 population-based cancer registries. The study population involved 99,257 patients with a first primary head and neck cancer and contributed 489,855 person-years of follow-up. To assess the excess risk of SPCs following head and neck cancers, we calculated standardized incidence ratios (SIRs) by dividing the observed numbers of SPCs by the expected number of cancers calculated from accumulated person-years and the age, sex- and calendar period-specific first primary cancer incidence rates in each of the cancer registries. During the observation period, there were 10,826 cases of SPCs after head and neck cancer. For all cancer sites combined, the SIR of SPCs was 1.86 (95% CI = 1.83-1.90) and the 20-year cumulative risk was 36%. Lung cancer contributed to the highest proportion of the SPCs with a 20-year cumulative risk of 13%. Excess second head and neck cancer risk was observed 10 years after diagnosis with lymphohaematopoietic cancers. The most common SPC following a first primary head and neck cancer was lung cancer. However, the highest excess of SPCs was in the head and neck region. These patterns were consistent with the notion that the pattern of cancer in survivors of head and neck cancer is dominated by the effect of tobacco smoking and alcohol drinking. (C) 2008 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18729183
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  • 3
    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; CELL ; LUNG ; LUNG-CANCER ; DEATH ; DISEASE ; RISK ; RISKS ; SITE ; GENE ; GENES ; GENOME ; PROTEIN ; TISSUE ; MARKER ; TISSUES ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; ACID ; COUNTRIES ; REGION ; FRANCE ; EPITHELIAL-CELLS ; RECEPTORS ; SMOKERS ; DEPENDENCE ; SNPs ; NEURONS ; CANDIDATE ; ENGLAND ; GENOME-WIDE ASSOCIATION ; NUCLEOTIDE ; FAGERSTROM TOLERANCE QUESTIONNAIRE ; HAPLOTYPE MAP
    Abstract: Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually(1). To identify genetic factors that modify disease risk, we conducted a genome- wide association study by analysing 317,139 single- nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer ( P= 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls ( P = 5 x 10(-20) overall), and it was found to account for 14%( attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits ( CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines(2,3), and they bind to N'- nitrosonornicotine and potential lung carcinogens(4). A non- synonymous variant of CHRNA5 that induces an amino acid substitution ( D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets(5)
    Type of Publication: Journal article published
    PubMed ID: 18385738
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  • 4
    Keywords: LUNG-CANCER ; SUSCEPTIBILITY LOCUS ; NECK-CANCER ; pooled analysis ; FAMILY-HISTORY ; ALCOHOL-DRINKING ; EPIDEMIOLOGY CONSORTIUM ; INTERNATIONAL HEAD ; SENSITIVITY PROTEIN MUS308 ; TOBACCO-RELATED CANCERS
    Abstract: Genome-wide association studies (GWAS) have been successful in identifying common genetic variation involved in susceptibility to etiologically complex disease. We conducted a GWAS to identify common genetic variation involved in susceptibility to upper aero-digestive tract (UADT) cancers. Genome-wide genotyping was carried out using the Illumina HumanHap300 beadchips in 2,091 UADT cancer cases and 3,513 controls from two large European multi-centre UADT cancer studies, as well as 4,821 generic controls. The 19 top-ranked variants were investigated further in an additional 6,514 UADT cancer cases and 7,892 controls of European descent from an additional 13 UADT cancer studies participating in the INHANCE consortium. Five common variants presented evidence for significant association in the combined analysis (p 〈= 5 x 10(-7)). Two novel variants were identified, a 4q21 variant (rs1494961, p = 1 x 10(-8)) located near DNA repair related genes HEL308 and FAM175A (or Abraxas) and a 12q24 variant (rs4767364, p = 2 x 10(-8)) located in an extended linkage disequilibrium region that contains multiple genes including the aldehyde dehydrogenase 2 (ALDH2) gene. Three remaining variants are located in the ADH gene cluster and were identified previously in a candidate gene study involving some of these samples. The association between these three variants and UADT cancers was independently replicated in 5,092 UADT cancer cases and 6,794 controls non-overlapping samples presented here (rs1573496-ADH7, p = 5 x 10(-8); rs1229984-ADH1B, p = 7 x 10(-9); and rs698-ADH1C, p = 0.02). These results implicate two variants at 4q21 and 12q24 and further highlight three ADH variants in UADT cancer susceptibility
    Type of Publication: Journal article published
    PubMed ID: 21437268
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  • 5
    Keywords: COHORT ; POPULATION ; POLYMORPHISMS ; HEALTH ; DIET ; TOBACCO ; exercise ; UPPER AERODIGESTIVE TRACT ; METAANALYSIS
    Abstract: Increasing evidence suggests that physical activity could prevent cancer, but scanty data is available on head and neck cancer (HNC). The aim of our study is to clarify the effect of recreational physical activity (rPA) on HNC. We analyzed data from four case-control studies, including 2,289 HNC cases and 5,580 controls. rPA was classified as: none/low (reference group), moderate and high. We calculated summary Odds Ratios (ORs) by pooling study-specific ORs. Overall, moderate rPA was associated with 22% lower risk of HNC compared to those with none or very low rPA levels [OR = 0.78, 95% Confidence Interval (95% CI): 0.66, 0.91]. Moderate rPA is associated with reduced risk of oral (OR = 0.74, 95% CI: 0.56, 0.97) and pharyngeal cancer (OR = 0.67, 95% CI: 0.53, 0.85), as well as high rPA levels (OR = 0.53, 95% CI: 0.32, 0.88 for oral cavity, OR = 0.58, 95% CI: 0.38, 0.89 for pharynx). High rPA levels, however, is associated with higher risk of laryngeal cancer (OR = 1.73, 95% CI: 1.04, 2.88). Stratified analyses showed that such inverse association between moderate rPA and HNC was more evident among males (OR = 0.75, 95% CI: 0.62, 0.90), subjects a parts per thousand yen45 years (OR = 0.78, 95% CI: 0.66, 0.93), and ever smokers and ever drinkers (OR = 0.72, 95% CI: 0.59, 0.88). High rPA significantly reduces HNC risk among subject a parts per thousand yen45 years (OR = 0.66, 95% CI: 0.48, 0.91). Promoting rPA might be inversely associated with HNC.
    Type of Publication: Journal article published
    PubMed ID: 21842237
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  • 6
    Keywords: CIGARETTE-SMOKING ; HUMAN-PAPILLOMAVIRUS ; ORAL-CANCER ; UPPER AERODIGESTIVE TRACT ; occupational exposures ; ALCOHOL-DRINKING ; SOCIOECONOMIC INEQUALITIES ; EPIDEMIOLOGY CONSORTIUM ; INTERNATIONAL HEAD ; OROPHARYNGEAL-CANCER
    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 behavioral 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 behaviors; and it remained elevated among never users of tobacco and nondrinkers (OR = 1.61; 95% CI = 1.13 - 2.31). More of the estimated education effect was not explained by cigarette smoking and alcohol behaviors: 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 versus 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 behavioral risk factors for these cancers and which varies across cancer sites, sexes, countries and country income inequality levels. What's new? Head and neck cancer is among the most common and increasing cancers in the world. Besides smoking, alcohol drinking, and human papilloma virus infections, low socioeconomic status has been implicated as one of the most important risk factors for this cancer type. This large multinational study authoritatively confirmed that lower education status and lower income are associated with increased risk for head and neck cancer development. Smoking and alcohol consumption could not entirely explain the risk associated with low socioeconomic factors, and therefore, as the authors argue, need to be more explicitly recognized in the etiology associated with head and neck cancer.
    Type of Publication: Journal article published
    PubMed ID: 24996155
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  • 7
    Keywords: RISK-FACTORS ; GASTRIC-CANCER ; UPPER AERODIGESTIVE TRACT ; pooled analysis ; PHARYNGEAL CANCER ; ALCOHOL-DRINKING ; EPIDEMIOLOGY CONSORTIUM ; INTERNATIONAL HEAD ; LARYNGEAL-CANCER ; BUCCAL POUCH CARCINOGENESIS
    Abstract: Scope: Only a few studies analyzed the role of allium vegetables with reference to head and neck cancers (HNC), with mixed results. We investigated the potential favorable role of garlic and onion within the International Head and Neck Cancer Epidemiology (INHANCE) Consortium. Methods and results: We analyzed pooled individual-level data from eight case-control studies, including 4590 cases and 7082 controls. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between garlic and onion intakes and HNC risk. Compared with no or low garlic use, the ORs of HNC were 0.95 (95% CI 0.71-1.27) for intermediate and 0.74 (95% CI 0.55-0.99) for high garlic use (p for trend = 0.02). The ORs of HNC for increasing categories of onion intake were 0.91 (95% CI 0.68-1.21) for 〉 1 to 〈= 3 portions per week, and 0.83 (95% CI 0.60-1.13) for 〉 3 portions per week (p for trend = 0.02), as compared to 〈1 portion per week. We found an inverse association between high onion intake and laryngeal cancer risk (OR = 0.69; 95% CI 0.54-0.88), but no significant association for other subsites. Conclusion: The results of this pooled-analysis support a possible moderate inverse association between garlic and onion intake and HNC risk.
    Type of Publication: Journal article published
    PubMed ID: 26018663
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  • 8
    Abstract: The International Head and Neck Cancer Epidemiology (INHANCE) consortium is a collaboration of research groups leading large epidemiology studies to improve the understanding of the causes and mechanisms of head and neck cancer. The consortium includes investigators of 35 studies who have pooled their data on 25 500 patients with head and neck cancer (i.e., cancers of the oral cavity, oropharynx, hypopharynx, and larynx) and 37 100 controls. The INHANCE analyses have confirmed that tobacco use and alcohol intake are key risk factors of these diseases and have provided precise estimates of risk and dose response, the benefit of quitting, and the hazard of smoking even a few cigarettes per day. Other risk factors include short height, lean body mass, low education and income, and a family history of head and neck cancer. Risk factors are generally similar for oral cavity, pharynx, and larynx, although the magnitude of risk may vary. Some major strengths of pooling data across studies include more precise estimates of risk and the ability to control for potentially confounding factors and to examine factors that may interact with each other. The INHANCE consortium provides evidence of the scientific productivity and discoveries that can be obtained from data pooling projects.
    Type of Publication: Journal article published
    PubMed ID: 25809224
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  • 9
    Keywords: CANCER ; carcinoma ; CELL ; LUNG ; PROSTATE ; DIAGNOSIS ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; DEATH ; EPIDEMIOLOGY ; incidence ; RISK ; FAMILY ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; MALIGNANCIES ; PATTERNS ; AGE ; ovarian cancer ; OVARIAN-CANCER ; WOMEN ; CIGARETTE-SMOKING ; MEN ; PROSTATE-CANCER ; adenocarcinoma ; EUROPE ; ONCOLOGY ; small cell lung carcinoma ; ASSOCIATIONS ; PATTERN ; METAANALYSIS ; development ; HORMONES ; CANCERS ; SQUAMOUS-CELL ; sex differences ; SPCs
    Abstract: BACKGROUND: Patterns of second primary cancers (SPCs) following first primary lung cancers (FPLCs) may provide aetiological insights into FPLC. METHODS: Cases of FPLCs in 13 cancer registries in Europe, Australia, Canada, and Singapore were followed up from the date of FPLC diagnosis to the date of SPC diagnosis, date of death, or end of follow-up. Standardised incidence ratios (SIRs) were calculated to estimate the magnitude of SPC development following squamous cell carcinoma (SCC), small cell lung carcinoma (SCLC), and adenocarcinoma (ADC). RESULTS: Among SCC patients, male SIR = 1.58 (95% confidence interval (CI) 1.50-1.66) and female SIR = 2.31 (1.94-2.72) for smoking-related SPC. Among SCLC patients, the respective ratios were 1.39 (1.20-1.60) and 2.28 (1.73-2.95), and among ADC patients, they were 1.73 (1.57-1.90) and 2.24 (1.91-2.61). We also observed associations between first primary lung ADC and second primary breast cancer in women (SIR = 1.25, 95% CI 1.05-1.48) and prostate cancer (1.56, 1.39-1.79) in men. CONCLUSION: The FPLC patients carried excess risks of smoking-related SPCs. An association between first primary lung ADC and second primary breast and ovarian cancer in women at younger age and prostate cancers in men may reflect an aetiological role of hormones in lung ADC. British Journal of Cancer (2010) 102, 1190-1195. doi:10.1038/sj.bjc.6605616 www.bjcancer.com (C) 2010 Cancer Research UK
    Type of Publication: Journal article published
    PubMed ID: 20354532
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  • 10
    Keywords: CANCER ; EPIDEMIOLOGY ; METABOLISM ; IMPACT ; ASSOCIATION ; SQUAMOUS-CELL CARCINOMA ; insulin ; MELLITUS ; ONCOLOGY ; ASSOCIATIONS ; UPPER AERODIGESTIVE TRACT ; MOLECULAR-MECHANISMS ; BLOOD-GLUCOSE ; BODY-MASS INDEX ; INCREASED RISK ; HUMAN-PAPILLOMAVIRUS INFECTION ; ORAL-CAVITY ; INHANCE CONSORTIUM
    Abstract: BACKGROUND: A history of diabetes is associated with an increased risk of several types of cancers. Whether diabetes is a risk factor for head and neck cancer (HNC) has received little attention. METHODS: We pooled data from 12 case-control studies including 6,448 cases and 13,747 controls, and estimated OR and 95% CI for the associations between diabetes and HNC, adjusted for age, education level, sex, race/ethnicity, study center, cigarette smoking, alcohol use, and body mass index. RESULTS: We observed a weak association between diabetes and the incidence of HNC overall (OR, 1.09; 95% CI: 0.95-1.24). However, we observed a modest association among never smokers (OR, 1.59; 95% CI: 1.22-2.07), and no association among ever smokers (OR, 0.96; 95% CI: 0.83-1.11); likelihood ratio test for interaction P = 0.001. CONCLUSION: A history of diabetes was weakly associated with HNC overall, but we observed evidence of effect modification by smoking status, with a positive association among those who never smoked cigarettes.Impact: This study suggests that glucose metabolism abnormalities may be a HNC risk factor in subgroups of the population. Prospective studies incorporating biomarkers are needed to improve our understanding of the relationship between diabetes and HNC risk, possibly providing new strategies in the prevention of HNC.
    Type of Publication: Journal article published
    PubMed ID: 22144496
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