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    Keywords: RECEPTOR ; CANCER ; tumor ; Germany ; MODEL ; MODELS ; CT ; DEATH ; RISK ; GENE ; GENES ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; ACID ; NUMBER ; colorectal cancer ; COLORECTAL-CANCER ; COLON-CANCER ; LINKAGE DISEQUILIBRIUM ; FATTY-ACIDS ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; nutrition ; ARACHIDONIC-ACID ; PPAR-GAMMA ; signaling ; ONCOLOGY ; REGRESSION ; FRAMEWORK ; VARIANT ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; HAPLOTYPE ; prospective ; fish consumption ; GENOME-WIDE ASSOCIATION ; GENETIC-VARIATION ; Genetic ; POPULATION STRATIFICATION ; COMMON POLYMORPHISMS ; single nucleotide ; ASPIRIN-INTOLERANT ASTHMA ; METABOLIZING GENES ; PROSTAGLANDIN-E
    Abstract: Colorectal cancer (CRC) is the third most common malignant tumor and the fourth leading cause of cancer death worldwide. The crucial role of fatty acids for a number of important biological processes suggests a more in-depth analysis of inter-individual differences in fatty acid metabolizing genes as contributing factor to colon carcinogenesis. We examined the association between genetic variability in 43 fatty acid metabolism-related genes and colorectal risk in 1225 CRC cases and 2032 controls participating in the European Prospective Investigation into Cancer and Nutrition study. Three hundred and ninety two single-nucleotide polymorphisms were selected using pairwise tagging with an r(2) cutoff of 0.8 and a minor allele frequency of 〉 5%. Conditional logistic regression models were used to estimate odds ratios and corresponding 95% confidence intervals. Haplotype analysis was performed using a generalized linear model framework. On the genotype level, hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD), phospholipase A2 group VI (PLA2G6) and transient receptor potential vanilloid 3 were associated with higher risk for CRC, whereas prostaglandin E receptor 2 (PTGER2) was associated with lower CRC risk. A significant inverse association (P 〈 0.006) was found for PTGER2 GGG haplotype, whereas HPGD AGGAG and PLA2G3 CT haplotypes were significantly (P 〈 0.001 and P = 0.003, respectively) associated with higher risk of CRC. Based on these data, we present for the first time the association of HPGD variants with CRC risk. Our results support the key role of prostanoid signaling in colon carcinogenesis and suggest a relevance of genetic variation in fatty acid metabolism-related genes and CRC risk
    Type of Publication: Journal article published
    PubMed ID: 20042636
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  • 2
    Keywords: DISEASE ; RISK ; prognosis ; polymorphism ; SUSCEPTIBILITY LOCUS ; VARIANTS ; smoking ; GENOME-WIDE ASSOCIATION ; NICOTINE DEPENDENCE ; POPULATION STRATIFICATION ; CHRNA5
    Abstract: The single-nucleotide polymorphisms (SNPs) rs402710 (5p15.33), rs16969968 and rs8034191 (15q25.1) have been consistently identified by genome-wide association studies (GWAS) as significant predictors of lung cancer risk, while rs4324798 (6p22.1) was previously found to influence survival time in small-cell lung cancer (SCLC) patients. Using the same population of one of the original GWAS, we investigated whether the selected SNPs and 31 others (also identified in GWAS) influence survival time, assuming an additive model. The effect of each polymorphism on all cause survival was estimated in 1094 lung cancer patients, and lung cancer-specific survival in 763 patients, using Cox regression adjusted for a priori confounders and competing causes of death where appropriate. Overall, after 1558 person-years of post-diagnostic follow-up, 874 deaths occurred from all causes, including 690 from lung cancer. In the lung cancer-specific survival analysis (1102 person-years), only rs7452888 (6q27) and rs2710994 (7p15.3) modified survival, with adjusted hazard ratios of 1.19 (P = 0.009) and 1.32 (P = 0.011) respectively, taking competing risks into account. Some weak associations were identified in subgroup analysis for rs16969968 and rs8034191 (15q25.1) and rs4324798 (6p22.1) and survival in never-smokers, as well as for rs402710 in current smokers and SCLC patients. In conclusion, rs402710 (5p15.33), rs16969968 and rs8034191 (both 15q25.1) and rs4324798 (6p22.1) were found to be unrelated to survival times in this large cohort of lung cancer patients, regardless of whether the cause of death was from lung cancer or not. However, rs7452888 (6q27) was identified as a possible candidate SNP to influence lung cancer survival, while stratified analysis hinted at a possible role for rs8034191, rs16969968 (15q25.1) and rs4324798 (6p22.1) in influencing survival time in lung cancer patients who were never-smokers, based on a small sample
    Type of Publication: Journal article published
    PubMed ID: 21750227
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