Dietary total antioxidant capacity and head and neck cancer: a large case-control study in Iran

BackgroundData on the association between head and neck cancer (HNC) and dietary factors are inconclusive. No study has so far investigated the association between dietary total antioxidant capacity (dTAC) and HNC concerning interactions with other risk factors.MethodPathologically confirmed new diagnosed HNC patients were included in this study. The control group was healthy hospital visitors who were frequently matched with patients on age (5 years interval), gender, and province of residence. Trained interviewers administered a validated Food Frequency Questionnaire (FFQ) to assess the participants’ food intake 1 year before the cancer diagnosis. Data on TAC scores of foods was collected by Ferric Reducing Antioxidant Power (FRAP) and Total Radical-trapping Antioxidant Parameters (TRAP) from published data. We applied logistic regression adjusted for age, sex, energy intake, socioeconomic status, province, opium use, alcohol use, physical activity, and dental health. We also studied the interaction of dTAC with tobacco smoking status, and opium use on the risk of HNC.ResultsWe recruited 876 HNC patients and 3,409 healthy controls. We observed a significant decrease in the odds of HNC with increasing dTAC scores. The OR of HNC for the third vs. the first tertile was 0.49 (95%CI 0.39–0.61) for FRAP and 0.49 (95%CI 0.39–0.62) for TRAP. Both dTAC scores were inversely associated with lip and oral (T3 ver. T1 OR = 0.51; 95%CI 0.36–0.71 for FRAP and OR = 0.59; 95% CI 0.44–0.82 for TRAP) and larynx (T3 ver. T1 OR = 0.43; 95%CI 0.31–0.61 for FRAP and OR = 0.38; 95% CI 0.26–0.55 for TRAP) cancers. There was no interaction between tobacco smoking, opium use; and TRAP or FRAP on the risk of HNC.ConclusionAn antioxidant-rich diet in terms of FRAP or TRAP could decrease the risk of HNC and its subtypes

Lung cancer occurrence in never-smokers: an analysis of 13 cohorts and 22 cancer registry studies

Background: Better information on lung cancer occurrence in lifelong nonsmokers is needed to understand gender and racial disparities and to examine how factors other than active smoking influence risk in different time periods and geographic regions. Methods and Findings: We pooled information on lung cancer incidence and/or death rates among self-reported never-smokers from 13 large cohort studies, representing over 630,000 and 1.8 million persons for incidence and mortality, respectively. We also abstracted population-based data for women from 22 cancer registries and ten countries in time periods and geographic regions where few women smoked. Our main findings were: (1) Men had higher death rates from lung cancer than women in all age and racial groups studied; (2) male and female incidence rates were similar when standardized across all ages 40+ y, albeit with some variation by age; (3) African Americans and Asians living in Korea and Japan (but not in the US) had higher death rates from lung cancer than individuals of European descent; (4) no temporal trends were seen when comparing incidence and death rates among US women age 40–69 y during the 1930s to contemporary populations where few women smoke, or in temporal comparisons of never-smokers in two large American Cancer Society cohorts from 1959 to 2004; and (5) lung cancer incidence rates were higher and more variable among women in East Asia than in other geographic areas with low female smoking. Conclusions: These comprehensive analyses support claims that the death rate from lung cancer among never-smokers is higher in men than in women, and in African Americans and Asians residing in Asia than in individuals of European descent, but contradict assertions that risk is increasing or that women have a higher incidence rate than men. Further research is needed on the high and variable lung cancer rates among women in Pacific Rim countries

Association between Adult Height and Risk of Colorectal, Lung, and Prostate Cancer:Results from Meta-analyses of Prospective Studies and Mendelian Randomization Analyses

Background: Observational studies examining associations between adult height and risk of colorectal, prostate, and lung cancers have generated mixed results. We conducted meta-analyses using data from prospective cohort studies and further carried out Mendelian randomization analyses, using height-associated genetic variants identified in a genome-wide association study (GWAS), to evaluate the association of adult height with these cancers. Methods and Findings: A systematic review of prospective studies was conducted using the PubMed, Embase, and Web of Science databases. Using meta-analyses, results obtained from 62 studies were summarized for the association of a 10-cm increase in height with cancer risk. Mendelian randomization analyses were conducted using summary statistics obtained for 423 genetic variants identified from a recent GWAS of adult height and from a cancer genetics consortium study of multiple cancers that included 47,800 cases and 81,353 controls. For a 10-cm increase in height, the summary relative risks derived from the meta-analyses of prospective studies were 1.12 (95% CI 1.10, 1.15), 1.07 (95% CI 1.05, 1.10), and 1.06 (95% CI 1.02, 1.11) for colorectal, prostate, and lung cancers, respectively. Mendelian randomization analyses showed increased risks of colorectal (odds ratio [OR] = 1.58, 95% CI 1.14, 2.18) and lung cancer (OR = 1.10, 95% CI 1.00, 1.22) associated with each 10-cm increase in genetically predicted height. No association was observed for prostate cancer (OR = 1.03, 95% CI 0.92, 1.15). Our meta-analysis was limited to published studies. The sample size for the Mendelian randomization analysis of colorectal cancer was relatively small, thus affecting the precision of the point estimate. Conclusions: Our study provides evidence for a potential causal association of adult height with the risk of colorectal and lung cancers and suggests that certain genetic factors and biological pathways affecting adult height may also affect the risk of these cancers.</p

Association between Adult Height and Risk of Colorectal, Lung, and Prostate Cancer: Results from Meta-analyses of Prospective Studies and Mendelian Randomization Analyses.

BACKGROUND: Observational studies examining associations between adult height and risk of colorectal, prostate, and lung cancers have generated mixed results. We conducted meta-analyses using data from prospective cohort studies and further carried out Mendelian randomization analyses, using height-associated genetic variants identified in a genome-wide association study (GWAS), to evaluate the association of adult height with these cancers. METHODS AND FINDINGS: A systematic review of prospective studies was conducted using the PubMed, Embase, and Web of Science databases. Using meta-analyses, results obtained from 62 studies were summarized for the association of a 10-cm increase in height with cancer risk. Mendelian randomization analyses were conducted using summary statistics obtained for 423 genetic variants identified from a recent GWAS of adult height and from a cancer genetics consortium study of multiple cancers that included 47,800 cases and 81,353 controls. For a 10-cm increase in height, the summary relative risks derived from the meta-analyses of prospective studies were 1.12 (95% CI 1.10, 1.15), 1.07 (95% CI 1.05, 1.10), and 1.06 (95% CI 1.02, 1.11) for colorectal, prostate, and lung cancers, respectively. Mendelian randomization analyses showed increased risks of colorectal (odds ratio [OR] = 1.58, 95% CI 1.14, 2.18) and lung cancer (OR = 1.10, 95% CI 1.00, 1.22) associated with each 10-cm increase in genetically predicted height. No association was observed for prostate cancer (OR = 1.03, 95% CI 0.92, 1.15). Our meta-analysis was limited to published studies. The sample size for the Mendelian randomization analysis of colorectal cancer was relatively small, thus affecting the precision of the point estimate. CONCLUSIONS: Our study provides evidence for a potential causal association of adult height with the risk of colorectal and lung cancers and suggests that certain genetic factors and biological pathways affecting adult height may also affect the risk of these cancers.US NIH (Grant ID: R37CA070867), Ingram Professorship, Anne Potter Wilson , National Institutes of Health (Grant IDs: R25CA160056-03, U19CA148065, U19CA148107, U19CA148127, U19CA148537, Cancer Research UK, Prostate Cancer UK, The Institute of Cancer Research, Royal Marsden Biomedical Research Centre, National Institute of Health Research (Grant ID: C5047/A17528)This is the final version of the article. It first appeared from the Public Library of Science via http://dx.doi.org/10.1371/journal.pmed.100211

第809回千葉医学会例会・第一外科教室談話会 64.

<p>RR, relative risk.</p

Table_1_Dietary total antioxidant capacity and head and neck cancer: a large case-control study in Iran.pdf

BackgroundData on the association between head and neck cancer (HNC) and dietary factors are inconclusive. No study has so far investigated the association between dietary total antioxidant capacity (dTAC) and HNC concerning interactions with other risk factors.MethodPathologically confirmed new diagnosed HNC patients were included in this study. The control group was healthy hospital visitors who were frequently matched with patients on age (5 years interval), gender, and province of residence. Trained interviewers administered a validated Food Frequency Questionnaire (FFQ) to assess the participants’ food intake 1 year before the cancer diagnosis. Data on TAC scores of foods was collected by Ferric Reducing Antioxidant Power (FRAP) and Total Radical-trapping Antioxidant Parameters (TRAP) from published data. We applied logistic regression adjusted for age, sex, energy intake, socioeconomic status, province, opium use, alcohol use, physical activity, and dental health. We also studied the interaction of dTAC with tobacco smoking status, and opium use on the risk of HNC.ResultsWe recruited 876 HNC patients and 3,409 healthy controls. We observed a significant decrease in the odds of HNC with increasing dTAC scores. The OR of HNC for the third vs. the first tertile was 0.49 (95%CI 0.39–0.61) for FRAP and 0.49 (95%CI 0.39–0.62) for TRAP. Both dTAC scores were inversely associated with lip and oral (T3 ver. T1 OR = 0.51; 95%CI 0.36–0.71 for FRAP and OR = 0.59; 95% CI 0.44–0.82 for TRAP) and larynx (T3 ver. T1 OR = 0.43; 95%CI 0.31–0.61 for FRAP and OR = 0.38; 95% CI 0.26–0.55 for TRAP) cancers. There was no interaction between tobacco smoking, opium use; and TRAP or FRAP on the risk of HNC.ConclusionAn antioxidant-rich diet in terms of FRAP or TRAP could decrease the risk of HNC and its subtypes.</p

Association between Adult Height and Risk of Colorectal, Lung, and Prostate Cancer: Results from Meta-analyses of Prospective Studies and Mendelian Randomization Analyses

Background: Observational studies examining associations between adult height and risk of colorectal, prostate, and lung cancers have generated mixed results. We conducted meta-analyses using data from prospective cohort studies and further carried out Mendelian randomization analyses, using height-associated genetic variants identified in a genome-wide association study (GWAS), to evaluate the association of adult height with these cancers. Methods and Findings: A systematic review of prospective studies was conducted using the PubMed, Embase, and Web of Science databases. Using meta-analyses, results obtained from 62 studies were summarized for the association of a 10-cm increase in height with cancer risk. Mendelian randomization analyses were conducted using summary statistics obtained for 423 genetic variants identified from a recent GWAS of adult height and from a cancer genetics consortium study of multiple cancers that included 47,800 cases and 81,353 controls. For a 10-cm increase in height, the summary relative risks derived from the meta-analyses of prospective studies were 1.12 (95% CI 1.10, 1.15), 1.07 (95% CI 1.05, 1.10), and 1.06 (95% CI 1.02, 1.11) for colorectal, prostate, and lung cancers, respectively. Mendelian randomization analyses showed increased risks of colorectal (odds ratio [OR] = 1.58, 95% CI 1.14, 2.18) and lung cancer (OR = 1.10, 95% CI 1.00, 1.22) associated with each 10-cm increase in genetically predicted height. No association was observed for prostate cancer (OR = 1.03, 95% CI 0.92, 1.15). Our meta-analysis was limited to published studies. The sample size for the Mendelian randomization analysis of colorectal cancer was relatively small, thus affecting the precision of the point estimate. Conclusions: Our study provides evidence for a potential causal association of adult height with the risk of colorectal and lung cancers and suggests that certain genetic factors and biological pathways affecting adult height may also affect the risk of these cancers.</p

Association between Adult Height and Risk of Colorectal, Lung, and Prostate Cancer: Results from Meta-analyses of Prospective Studies and Mendelian Randomization Analyses

Background: Observational studies examining associations between adult height and risk of colorectal, prostate, and lung cancers have generated mixed results. We conducted meta-analyses using data from prospective cohort studies and further carried out Mendelian randomization analyses, using height-associated genetic variants identified in a genome-wide association study (GWAS), to evaluate the association of adult height with these cancers. Methods and Findings: A systematic review of prospective studies was conducted using the PubMed, Embase, and Web of Science databases. Using meta-analyses, results obtained from 62 studies were summarized for the association of a 10-cm increase in height with cancer risk. Mendelian randomization analyses were conducted using summary statistics obtained for 423 genetic variants identified from a recent GWAS of adult height and from a cancer genetics consortium study of multiple cancers that included 47,800 cases and 81,353 controls. For a 10-cm increase in height, the summary relative risks derived from the meta-analyses of prospective studies were 1.12 (95% CI 1.10, 1.15), 1.07 (95% CI 1.05, 1.10), and 1.06 (95% CI 1.02, 1.11) for colorectal, prostate, and lung cancers, respectively. Mendelian randomization analyses showed increased risks of colorectal (odds ratio [OR] = 1.58, 95% CI 1.14, 2.18) and lung cancer (OR = 1.10, 95% CI 1.00, 1.22) associated with each 10-cm increase in genetically predicted height. No association was observed for prostate cancer (OR = 1.03, 95% CI 0.92, 1.15). Our meta-analysis was limited to published studies. The sample size for the Mendelian randomization analysis of colorectal cancer was relatively small, thus affecting the precision of the point estimate. Conclusions: Our study provides evidence for a potential causal association of adult height with the risk of colorectal and lung cancers and suggests that certain genetic factors and biological pathways affecting adult height may also affect the risk of these cancers

Forest plot for prospective studies of adult height and prostate cancer.

<p>Overall prostate cancer (A); aggressive prostate cancer (B). RR, relative risk.</p

PRISMA flow chart for studies included in the meta-analysis.

<p>PRISMA flow chart for studies included in the meta-analysis.</p