American Cancer Society

About: American Cancer Society is a nonprofit organization based out in Atlanta, Georgia, United States. It is known for research contribution in the topics: Cancer & Population. The organization has 1339 authors who have published 3700 publications receiving 688166 citations. The organization is also known as: American Cancer Society, ACS & American Society for the Control of Cancer.

Pathway analysis of genome-wide association study data highlights pancreatic development genes as susceptibility factors for pancreatic cancer

Abstract: Four loci have been associated with pancreatic cancer through genome-wide association studies (GWAS) Pathway-based analysis of GWAS data is a complementary approach to identify groups of genes or biological pathways enriched with disease-associated single-nucleotide polymorphisms (SNPs) whose individual effect sizes may be too small to be detected by standard single-locus methods We used the adaptive rank truncated product method in a pathway-based analysis of GWAS data from 3851 pancreatic cancer cases and 3934 control participants pooled from 12 cohort studies and 8 case-control studies (PanScan) We compiled 23 biological pathways hypothesized to be relevant to pancreatic cancer and observed a nominal association between pancreatic cancer and five pathways (P < 005), ie pancreatic development, Helicobacter pylori lacto/neolacto, hedgehog, Th1/Th2 immune response and apoptosis (P = 20 × 10(-6), 16 × 10(-5), 00019, 0019 and 0023, respectively) After excluding previously identified genes from the original GWAS in three pathways (NR5A2, ABO and SHH), the pancreatic development pathway remained significant (P = 83 × 10(-5)), whereas the others did not The most significant genes (P < 001) in the five pathways were NR5A2, HNF1A, HNF4G and PDX1 for pancreatic development; ABO for Hpylori lacto/neolacto; SHH for hedgehog; TGFBR2 and CCL18 for Th1/Th2 immune response and MAPK8 and BCL2L11 for apoptosis Our results provide a link between inherited variation in genes important for pancreatic development and cancer and show that pathway-based approaches to analysis of GWAS data can yield important insights into the collective role of genetic risk variants in cancer

The Association between Cigarette Smoking and Risk of Colorectal Cancer in a Large Prospective Cohort from the United States

Abstract: Background: Many studies have reported a 20% to 60% increase in risk of colorectal cancer associated with active smoking. However, neither the U.S. Surgeon General nor the IARC have classified the relationship as causal because of concern about residual confounding. Methods: In a prospective study of 184,187 people followed from 1992 to 2005, we used Cox proportional hazard models to examine the relationship of cigarette smoking to incident colorectal cancer, controlling for screening and multiple known and putative risk factors. Information on smoking and time-varying covariates was updated in 1997, 1999, 2001, and 2003. Results: The incidence of colorectal cancer was significantly higher in current [hazard ratios (HR), 1.27; 95% confidence intervals (CI), 1.06-1.52] and former smokers (HR, 1.23; 95% CI, 1.11-1.36) compared with lifelong nonsmokers in analyses that controlled for 13 covariates, including screening. The relative risk was greatest among current smokers with at least 50 years of smoking (HR, 1.38; 95% CI, 1.04-1.84). Among former smokers, risk of colorectal cancer decreased with greater time since cessation ( P trend = 0.0003), and also decreased with earlier age at cessation ( P trend = 0.0014). No association was seen among former smokers who had quit before age of 40 years or abstained for 31 years or more. Conclusions: Long-term cigarette smoking is associated with colorectal cancer, even after controlling for screening and multiple other risk factors. (Cancer Epidemiol Biomarkers Prev 2009;18(12):3362–7)

Maternal fumonisin exposure as a risk factor for neural tube defects.

Abstract: Fumonisins are mycotoxins produced by the fungus F. verticillioides, a common contaminant of maize (corn) worldwide. Maternal consumption of fumonisin B1‐contaminated maize during early pregnancy has recently been associated with increased risk for neural tube defects (NTDs) in human populations that rely heavily on maize as a dietary staple. Experimental administration of purified fumonisin to mice early in gestation also results in an increased incidence of NTDs in exposed offspring. Fumonisin inhibits the enzyme ceramide synthase in de novo sphingolipid biosynthesis, resulting in an elevation of free sphingoid bases and depletion of downstream glycosphingolipids. Increased sphingoid base metabolites (i.e., sphinganine‐1‐phosphate) may perturb signaling cascades involved in embryonic morphogenesis by functioning as ligands for sphingosine‐1‐P (S1P) receptors, a family of G‐protein‐coupled receptors that regulate key biological processes such as cell survival/proliferation, differentiation and migration. Fumonisin‐induced depletion of glycosphingolipids impairs expression and function of the GPI‐anchored folate receptor (Folr1), which may also contribute to adverse pregnancy outcomes. NTDs appear to be multifactorial in origin, involving complex gene‐nutrient‐environment interactions. Vitamin supplements containing folic acid have been shown to reduce the occurrence of NTDs, and may help protect the developing fetus from environmental teratogens. Fumonisins appear to be an environmental risk factor for birth defects, although other aspects of maternal nutrition and genetics play interactive roles in determining pregnancy outcome. Minimizing exposures to mycotoxins through enhanced agricultural practices, identifying biomarkers of exposure, characterizing mechanisms of toxicity, and improving maternal nutrition are all important strategies for reducing the NTD burden in susceptible human populations.

Fine-mapping identifies multiple prostate cancer risk loci at 5p15, one of which associates with TERT expression

Abstract: Associations between single nucleotide polymorphisms (SNPs) at 5p15 and multiple cancer types have been reported. We have previously shown evidence for a strong association between prostate cancer (PrCa) risk and rs2242652 at 5p15, intronic in the telomerase reverse transcriptase (TERT) gene that encodes TERT. To comprehensively evaluate the association between genetic variation across this region and PrCa, we performed a fine-mapping analysis by genotyping 134 SNPs using a custom Illumina iSelect array or Sequenom MassArray iPlex, followed by imputation of 1094 SNPs in 22 301 PrCa cases and 22 320 controls in The PRACTICAL consortium. Multiple stepwise logistic regression analysis identified four signals in the promoter or intronic regions of TERT that independently associated with PrCa risk. Gene expression analysis of normal prostate tissue showed evidence that SNPs within one of these regions also associated with TERT expression, providing a potential mechanism for predisposition to disease.

Deaths Due to Cigarette Smoking for 12 Smoking-Related Cancers in the United States

Abstract: Deaths Due to Cigarette Smoking for 12 Smoking-Related Cancers in the United States The 2014 US Surgeon General’s Report provided the estimated annual number of smoking-attributable deaths during 2005 to 2009 from cancer overall and lung cancer specifically but not separately for the 11 other cancers found to be caused by smoking.1 Current estimates of smokingattributable mortality for specific c ancer sites are based on data from 2000 to 2004.2 Updated estimates are needed because smoking patterns and the magnitude of the association between smoking and cancer death have changed in the past decade. From 2000 to 2012, smoking prevalence decreased from 23.2% to 18.1%.3 In contrast to this favorable trend, recently published data revealed that the risk of cancer death among smokers can increase over time.4 Therefore, we estimated the number and proportion of deaths in the United States in 2011 attributable to cigarette smoking for 12 cancers caused by smoking.