PDF file - 54K, Summary of Inflammation subpathways, genes and SNP's in Illumina chip

Supplementary Data from Lung Cancer in Never Smokers: Clinical Epidemiology and Environmental Risk Factors

Abstract Background: Case–control studies conducted in North America, Europe, and Asia provided evidence of increased lung cancer risk due to radon in homes. Here, the association between residential radon and lung cancer mortality was examined in a large-scale cohort study. Methods: Nearly 1.2 million Cancer Prevention Study-II participants were recruited in 1982. Mean county-level residential radon concentrations were linked to study participants according to ZIP code information at enrollment [mean (SD) = 53.5 Bq/m3 (38.0)]. Cox proportional hazards regression models were used to obtain adjusted HR and 95% CI for lung cancer mortality associated with radon. Potential effect modification by cigarette smoking, ambient sulfate concentrations, and other risk factors was assessed on both the additive and multiplicative scales. Results: Through 1988, 3,493 lung cancer deaths were observed among 811,961 participants included in the analysis. A significant positive linear trend was observed between categories of radon concentrations and lung cancer mortality (P = 0.02). A 15% (95% CI, 1–31) increase in the risk of lung cancer mortality was observed per 100 Bq/m3 increase in radon. Participants with mean radon concentrations above the EPA guideline value (148 Bq/m3) experienced a 34% (95% CI, 7–68) increase in risk for lung cancer mortality relative to those below the guideline value. Conclusions: This large prospective study showed positive associations between ecological indicators of residential radon and lung cancer. Impact: These results further support efforts to reduce radon concentrations in homes to the lowest possible level. Cancer Epidemiol Biomarkers Prev; 20(3); 438–48. ©2011 AACR.

Supplementary Methods from CYP19A1 Genetic Variation in Relation to Prostate Cancer Risk and Circulating Sex Hormone Concentrations in Men from the Breast and Prostate Cancer Cohort Consortium

Supplementary Tables 1-3 and Supplemenary Figure 1 from Radon and Lung Cancer in the American Cancer Society Cohort

Supplementary Table Legends from Refining the Prostate Cancer Genetic Association within the JAZF1 Gene on Chromosome 7p15.2

Supplementary Tables 1S-7S, Figure 1S from Haplotype Analysis of the HSD17B1 Gene and Risk of Breast Cancer: A Comprehensive Approach to Multicenter Analyses of Prospective Cohort Studies

Supplementary Methods and Tables 1-4 from Genetic Variation at the CYP19A1 Locus Predicts Circulating Estrogen Levels but not Breast Cancer Risk in Postmenopausal Women

Supplementary Table 1 from CYP19A1 Genetic Variation in Relation to Prostate Cancer Risk and Circulating Sex Hormone Concentrations in Men from the Breast and Prostate Cancer Cohort Consortium

Supplementary Table 2C from Refining the Prostate Cancer Genetic Association within the JAZF1 Gene on Chromosome 7p15.2

Tobacco and Cancer, pp. 129-156 (2022) No AccessChapter 5: Carcinogens and Toxicants in Smokeless Tobacco ProductsS. Jane Henley, Taylor Ellington, Stephen Stanfill, Kathi Mills, and Michael J. ThunS. Jane HenleyCenters for Disease Control and Prevention, Atlanta, GA, USA, Taylor EllingtonCenters for Disease Control and Prevention, Atlanta, GA, USA, Stephen StanfillCenters for Disease Control and Prevention, Atlanta, GA, USA, Kathi MillsCenters for Disease Control and Prevention, Atlanta, GA, USA, and Michael J. ThunEpidemiology Research Program, American Cancer Society, Atlanta, GA, USAhttps://doi.org/10.1142/9789811239533_0005Cited by:0 PreviousNext AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsRecommend to Library ShareShare onFacebookTwitterLinked InRedditEmail Abstract: The following sections are included: Introduction Types of Smokeless Tobacco A Brief History of Smokeless Tobacco Use in the United States Constituents of Smokeless Tobacco Products Research Links Smokeless Tobacco to Cancer Key Characteristics of Carcinogens in Smokeless Tobacco Products Scientific Basis on Which Smokeless Tobacco Is Classified as Carcinogenic to Humans Conclusion References The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention. FiguresReferencesRelatedDetails Tobacco and CancerMetrics History PDF download

Although many loci have been associated with height in European ancestry populations, very few have been identified in African ancestry individuals. Furthermore, many of the known loci have yet to be generalized to and fine-mapped within a large-scale African ancestry sample. We performed sex-combined and sex-stratified meta-analyses in up to 52,764 individuals with height and genome-wide genotyping data from the African Ancestry Anthropometry Genetics Consortium (AAAGC). We additionally combined our African ancestry meta-analysis results with published European genome-wide association study (GWAS) data. In the African ancestry analyses, we identified three novel loci (SLC4A3, NCOA2, ECD/FAM149B1) in sex-combined results and two loci (CRB1, KLF6) in women only. In the African plus European sex-combined GWAS, we identified an additional three novel loci (RCCD1, G6PC3, CEP95) which were equally driven by AAAGC and European results. Among 39 genome-wide significant signals at known loci, conditioning index SNPs from European studies identified 20 secondary signals. Two of the 20 new secondary signals and none of the 8 novel loci had minor allele frequencies (MAF) < 5%. Of 802 known European height signals, 643 displayed directionally consistent associations with height, of which 205 were nominally significant (p < 0.05) in the African ancestry sex-combined sample. Furthermore, 148 of 241 loci contained ≤20 variants in the credible sets that jointly account for 99% of the posterior probability of driving the associations. In summary, trans-ethnic meta-analyses revealed novel signals and further improved fine-mapping of putative causal variants in loci shared between African and European ancestry populations.

BACKGROUND:Previous studies showed a higher incidence of lung cancer among young women than among young men in the United States. Whether this pattern has continued in contemporary birth cohorts and, if so, whether it can be fully explained by sex differences in smoking behaviors are unknown. METHODS:We examined the nationwide population-based incidence of lung cancer according to sex, race or ethnic group, age group (30 to 34, 35 to 39, 40 to 44, 45 to 49, and 50 to 54 years), year of birth (1945 to 1980), and calendar period of diagnosis (1995-1999, 2000-2004, 2005-2009, and 2010-2014), and we calculated female-to-male incidence rate ratios. We also examined the prevalence of cigarette smoking, using data from the National Health Interview Survey from 1970 to 2016. RESULTS:Over the past two decades, the age-specific incidence of lung cancer has generally decreased among both men and women 30 to 54 years of age in all races and ethnic groups, but the declines among men have been steeper. Consequently, among non-Hispanic whites, the female-to-male incidence rate ratios increased, exceeding 1.0 in the age groups of 30 to 34, 35 to 39, 40 to 44, and 45 to 49 years. For example, the female-to-male incidence rate ratio among whites 40 to 44 years of age increased from 0.88 (95% confidence interval [CI], 0.84 to 0.92) during the 1995-1999 period to 1.17 (95% CI, 1.11 to 1.23) during the 2010-2014 period. The crossover in sex-specific rates occurred among non-Hispanic whites born since 1965. Sex-specific incidence rates converged among non-Hispanic blacks, Hispanics, and non-Hispanic Asians and Pacific Islanders but crossed over from a higher incidence among men to a higher incidence among women only among Hispanics. The prevalence of cigarette smoking among women born since 1965 has approached, but generally not exceeded, the prevalence among men. CONCLUSIONS:The patterns of historically higher incidence rates of lung cancer among men than among women have reversed among non-Hispanic whites and Hispanics born since the mid-1960s, and they are not fully explained by sex differences in smoking behaviors. Future studies are needed to identify reasons for the higher incidence of lung cancer among young women. (Funded by the American Cancer Society.).

The worldwide increase in the number of people affected by cancer and the costs of cancer care has increased the urgency of efforts to translate knowledge about the causes of cancer into effective preventive interventions. A wide range of interventions has proven to be effective for cancer prevention, either by reducing exposure to known causes of human cancer or by disrupting the multistage progression of tumors. Examples of progress include the up to 40% decrease in the age-standardized lung cancer incidence rate among men in high- and middle-income countries due to tobacco control; the 30% decrease in colorectal cancer incidence in the United States from widespread screening and the removal of precursor adenomatous tumors; the decreased prevalence of chronic hepatitis B virus (HBV) infection in East Asia due to neonatal vaccination; and protection against excessive sun exposure and decreased incidence of melanoma and keratinocytic carcinomas in Australia.

Primary prevention has enormous potential to reduce the human, social, and economic costs of cancer worldwide. The following sections discuss the development and application of preventive interventions in six broad areas of public health: tobacco control, the prevention of obesity and physical inactivity, prevention of infection-related cancers, protection against excessive exposure to ultraviolet light, preventive drug therapies (chemoprevention), and the regulation of carcinogenic exposures. All of these areas affect multiple types of cancer and massive numbers of people. Different interventions are at varying stages of development. For example, effective, evidence-based approaches have been developed over several decades to reduce tobacco use, prevent chronic infection with hepatitis B virus, protect children from excessive sun exposure, regulate exposures in high-income countries, and reduce breast cancer incidence and recurrence in high-risk women. More recent efforts are seeking to identify upstream measures to prevent excessive weight gain, reduce caloric intake, and increase physical activity.

Background:The 2014 US Surgeon General's report noted research gaps necessary to determine a causal relationship between active cigarette smoking and invasive breast cancer risk, including the role of alcohol consumption, timing of exposure, modification by menopausal status and heterogeneity by oestrogen receptor (ER) status. Methods:To address these issues, we pooled data from 14 cohort studies contributing 934 681 participants (36 060 invasive breast cancer cases). Cox proportional hazard regression models were used to calculate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). Results:Smoking duration before first birth was positively associated with risk ( P -value for trend = 2 × 10 -7 ) with the highest HR for initiation >10 years before first birth (HR = 1.18, CI 1.12-1.24). Effect modification by current alcohol consumption was evident for the association with smoking duration before first birth ( P -value=2×10 -4 ); compared with never-smoking non-drinkers, initiation >10 years before first birth was associated with risk in every category of alcohol intake, including non-drinkers (HR = 1.15, CI 1.04-1.28) and those who consumed at least three drinks per day (1.85, 1.55-2.21). Associations with smoking before first birth were limited to risk of ER+ breast cancer ( P -value for homogeneity=3×10 -3 ). Other smoking timing and duration characteristics were associated with risk even after controlling for alcohol, but were not associated with risk in non-drinkers. Effect modification by menopause was not evident. Conclusions:Smoking, particularly if initiated before first birth, was modestly associated with ER+ breast cancer risk that was not confounded by amount of adult alcohol intake. Possible links with breast cancer provide additional motivation for young women to not initiate smoking.