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1.
Kraft P Pharoah P Chanock SJ Albanes D Kolonel LN Hayes RB Altshuler D Andriole G Berg C Boeing H Burtt NP Bueno-de-Mesquita B Calle EE Cann H Canzian F Chen YC Crawford DE Dunning AM Feigelson HS Freedman ML Gaziano JM Giovannucci E Gonzalez CA Haiman CA Hallmans G Henderson BE Hirschhorn JN Hunter DJ Kaaks R Key T Le Marchand L Ma J Overvad K Palli D Pike MC Riboli E Rodriguez C Setiawan WV Stampfer MJ Stram DO Thomas G Thun MJ Travis R Trichopoulou A Virtamo J Wacholder S 《PLoS genetics》2005,1(5):e68
Steroid hormones are believed to play an important role in prostate carcinogenesis, but epidemiological evidence linking prostate cancer and steroid hormone genes has been inconclusive, in part due to small sample sizes or incomplete characterization of genetic variation at the locus of interest. Here we report on the results of a comprehensive study of the association between HSD17B1 and prostate cancer by the Breast and Prostate Cancer Cohort Consortium, a large collaborative study. HSD17B1 encodes 17β-hydroxysteroid dehydrogenase 1, an enzyme that converts dihydroepiandrosterone to the testosterone precursor Δ5-androsterone-3β,17β-diol and converts estrone to estradiol. The Breast and Prostate Cancer Cohort Consortium researchers systematically characterized variation in HSD17B1 by targeted resequencing and dense genotyping; selected haplotype-tagging single nucleotide polymorphisms (htSNPs) that efficiently predict common variants in U.S. and European whites, Latinos, Japanese Americans, and Native Hawaiians; and genotyped these htSNPs in 8,290 prostate cancer cases and 9,367 study-, age-, and ethnicity-matched controls. We found no evidence that HSD17B1 htSNPs (including the nonsynonymous coding SNP S312G) or htSNP haplotypes were associated with risk of prostate cancer or tumor stage in the pooled multiethnic sample or in U.S. and European whites. Analyses stratified by age, body mass index, and family history of disease found no subgroup-specific associations between these HSD17B1 htSNPs and prostate cancer. We found significant evidence of heterogeneity in associations between HSD17B1 haplotypes and prostate cancer across ethnicity: one haplotype had a significant (p < 0.002) inverse association with risk of prostate cancer in Latinos and Japanese Americans but showed no evidence of association in African Americans, Native Hawaiians, or whites. However, the smaller numbers of Latinos and Japanese Americans in this study makes these subgroup analyses less reliable. These results suggest that the germline variants in HSD17B1 characterized by these htSNPs do not substantially influence the risk of prostate cancer in U.S. and European whites. 相似文献
2.
Large, rapidly evolving intergenic spacers in the mitochondrial DNA of the salamander family Ambystomatidae (Amphibia: Caudata) 总被引:3,自引:2,他引:3
We report the presence, in the mitochondrial DNA (mtDNA) of all of the
sexual species of the salamander family Ambystomatidae, of a shared 240- bp
intergenic spacer between tRNAThr and tRNAPro. We place the intergenic
spacer in context by presenting the sequence of 1,746 bp of mtDNA from
Ambystoma tigrinum tigrinum, describe the nucleotide composition of the
intergenic spacer in all of the species of Ambystomatidae, and compare it
to other coding and noncoding regions of Ambystoma and several other
vertebrate mtDNAs. The nucleotide substitution rate of the intergenic
spacer is approximately three times faster than the substitution rate of
the control region, as shown by comparisons among six Ambystoma
macrodactylum sequences and eight members of the Ambystoma tigrinum
complex. We also found additional inserts within the intergenic spacers of
five species that varied from 87-444 bp in length. The presence of the
intergenic spacer in all sexual species of Ambystomatidae suggests that it
arose at least 20 MYA and has been a stable component of the ambystomatid
mtDNA ever since. As such, it represents one of the few examples of a large
and persistent intergenic spacer in the mtDNA of any vertebrate clade.
相似文献
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Lindstrom S Schumacher F Siddiq A Travis RC Campa D Berndt SI Diver WR Severi G Allen N Andriole G Bueno-de-Mesquita B Chanock SJ Crawford D Gaziano JM Giles GG Giovannucci E Guo C Haiman CA Hayes RB Halkjaer J Hunter DJ Johansson M Kaaks R Kolonel LN Navarro C Riboli E Sacerdote C Stampfer M Stram DO Thun MJ Trichopoulos D Virtamo J Weinstein SJ Yeager M Henderson B Ma J Le Marchand L Albanes D Kraft P 《PloS one》2011,6(2):e17142
Genome-wide association studies (GWAS) have identified multiple single nucleotide polymorphisms (SNPs) associated with prostate cancer risk. However, whether these associations can be consistently replicated, vary with disease aggressiveness (tumor stage and grade) and/or interact with non-genetic potential risk factors or other SNPs is unknown. We therefore genotyped 39 SNPs from regions identified by several prostate cancer GWAS in 10,501 prostate cancer cases and 10,831 controls from the NCI Breast and Prostate Cancer Cohort Consortium (BPC3). We replicated 36 out of 39 SNPs (P-values ranging from 0.01 to 10−28). Two SNPs located near KLK3 associated with PSA levels showed differential association with Gleason grade (rs2735839, P = 0.0001 and rs266849, P = 0.0004; case-only test), where the alleles associated with decreasing PSA levels were inversely associated with low-grade (as defined by Gleason grade <8) tumors but positively associated with high-grade tumors. No other SNP showed differential associations according to disease stage or grade. We observed no effect modification by SNP for association with age at diagnosis, family history of prostate cancer, diabetes, BMI, height, smoking or alcohol intake. Moreover, we found no evidence of pair-wise SNP-SNP interactions. While these SNPs represent new independent risk factors for prostate cancer, we saw little evidence for effect modification by other SNPs or by the environmental factors examined. 相似文献
6.
V Gallo JP Mackenbach M Ezzati G Menvielle AE Kunst S Rohrmann R Kaaks B Teucher H Boeing MM Bergmann A Tjønneland SO Dalton K Overvad ML Redondo A Agudo A Daponte L Arriola C Navarro AB Gurrea KT Khaw N Wareham T Key A Naska A Trichopoulou D Trichopoulos G Masala S Panico P Contiero R Tumino HB Bueno-de-Mesquita PD Siersema PP Peeters S Zackrisson M Almquist S Eriksson G Hallmans G Skeie T Braaten E Lund AK Illner T Mouw E Riboli P Vineis 《PloS one》2012,7(7):e39013
Background
Socio-economic inequalities in mortality are observed at the country level in both North America and Europe. The purpose of this work is to investigate the contribution of specific risk factors to social inequalities in cause-specific mortality using a large multi-country cohort of Europeans.Methods
A total of 3,456,689 person/years follow-up of the European Prospective Investigation into Cancer and Nutrition (EPIC) was analysed. Educational level of subjects coming from 9 European countries was recorded as proxy for socio-economic status (SES). Cox proportional hazard model''s with a step-wise inclusion of explanatory variables were used to explore the association between SES and mortality; a Relative Index of Inequality (RII) was calculated as measure of relative inequality.Results
Total mortality among men with the highest education level is reduced by 43% compared to men with the lowest (HR 0.57, 95% C.I. 0.52–0.61); among women by 29% (HR 0.71, 95% C.I. 0.64–0.78). The risk reduction was attenuated by 7% in men and 3% in women by the introduction of smoking and to a lesser extent (2% in men and 3% in women) by introducing body mass index and additional explanatory variables (alcohol consumption, leisure physical activity, fruit and vegetable intake) (3% in men and 5% in women). Social inequalities were highly statistically significant for all causes of death examined in men. In women, social inequalities were less strong, but statistically significant for all causes of death except for cancer-related mortality and injuries.Discussion
In this European study, substantial social inequalities in mortality among European men and women which cannot be fully explained away by accounting for known common risk factors for chronic diseases are reported. 相似文献7.
Nina E. Berentzen Joline W. Beulens Marieke P. Hoevenaar-Blom Ellen Kampman H. Bas Bueno-de-Mesquita Dora Romaguera-Bosch Petra H. M. Peeters Anne M. May 《PloS one》2013,8(8)
Background
A healthy dietary pattern defined by international recommendations of the World Health Organisation (WHO) has been shown to reduce overall mortality risk. It is unknown whether this healthy dietary pattern is associated with overall cancer incidence.Design
In total 35,355 men and women within the Dutch European Prospective Investigation into Cancer and Nutrition-cohort were followed for cancer occurrence. Diet was assessed through a validated food-frequency questionnaire. We computed a dietary score for all participants based on the seven WHO dietary guidelines for the prevention of chronic diseases (Healthy Diet Indicator (HDI)). We used the existing HDI score based on the 1990 WHO guidelines, and adapted it to meet with the 2002 WHO guidelines. Multivariate-adjusted Cox proportional hazards analysis was used to examine the association between adherence to the HDI and subsequent overall cancer risk.Results
A number of 3,007 new cancers were identified during a mean follow-up of 12.7 years. Adherence to the HDI was not associated with a reduced overall cancer risk. The hazard ratio (HR) of overall cancer associated with a one-point increment of the HDI was 0.96 (95% CI 0.89–1.03) in men, and 1.00 (95% CI 0.96–1.04) in women. Adherence to the HDI was not associated with smoking-related cancer ((HR men: 0.94 (95% CI 0.84–1.04); HR women: 1.00 (95% CI 0.94–1.07)), or alcohol-related cancer ((HR men: 1.02 (95% CI 0.87–1.20); HR women: 1.03 (95% CI 0.98–1.08)).Conclusions
Greater adherence to the WHO’s Healthy Diet Indicator, a dietary pattern for prevention of chronic diseases, was not associated with reduced overall, smoking-related or alcohol-related cancer risk in men or women. 相似文献8.
Heidi P. Fransen Anne M. May Joline W. J. Beulens Ellen A. Struijk G. Ardine de Wit Jolanda M. A. Boer N. Charlotte Onland-Moret Jeljer Hoekstra Yvonne T. van der Schouw H. Bas Bueno-de-Mesquita Petra H. M. Peeters 《PloS one》2014,9(11)
The aim of our study was to relate four modifiable lifestyle factors (smoking status, body mass index, physical activity and diet) to health expectancy, using quality-adjusted life years (QALYs) in a prospective cohort study. Data of the prospective EPIC-NL study were used, including 33,066 healthy men and women aged 20–70 years at baseline (1993–7), followed until 31-12-2007 for occurrence of disease and death. Smoking status, body mass index, physical activity and adherence to a Mediterranean-style diet (excluding alcohol) were investigated separately and combined into a healthy lifestyle score, ranging from 0 to 4. QALYs were used as summary measure of healthy life expectancy, combining a person''s life expectancy with a weight for quality of life when having a chronic disease. For lifestyle factors analyzed separately the number of years living longer in good health varied from 0.12 year to 0.84 year, after adjusting for covariates. A combination of the four lifestyle factors was positively associated with higher QALYs (P-trend <0.0001). A healthy lifestyle score of 4 compared to a score of 0 was associated with almost a 2 years longer life in good health (1.75 QALYs [95% CI 1.37, 2.14]). 相似文献
9.
Braem MG Onland-Moret NC Schouten LJ Kruitwagen RF Lukanova A Allen NE Wark PA Tjønneland A Hansen L Braüner CM Overvad K Clavel-Chapelon F Chabbert-Buffet N Teucher B Floegel A Boeing H Trichopoulou A Adarakis G Plada M Rinaldi S Fedirko V Romieu I Pala V Galasso R Sacerdote C Palli D Tumino R Bueno-de-Mesquita HB Gram IT Gavrilyuk O Lund E Sánchez MJ Bonet C Chirlaque MD Larrañaga N Gurrea AB Quirós JR Idahl A Ohlson N Lundin E Jirström K Butt S Tsilidis KK Khaw KT Wareham N Riboli E Kaaks R 《PloS one》2012,7(5):e37141
While the risk of ovarian cancer clearly reduces with each full-term pregnancy, the effect of incomplete pregnancies is unclear. We investigated whether incomplete pregnancies (miscarriages and induced abortions) are associated with risk of epithelial ovarian cancer. This observational study was carried out in female participants of the European Prospective Investigation into Cancer and Nutrition (EPIC). A total of 274,442 women were followed from 1992 until 2010. The baseline questionnaire elicited information on miscarriages and induced abortions, reproductive history, and lifestyle-related factors. During a median follow-up of 11.5 years, 1,035 women were diagnosed with incident epithelial ovarian cancer. Despite the lack of an overall association (ever vs. never), risk of ovarian cancer was higher among women with multiple incomplete pregnancies (HR(≥4vs.0): 1.74, 95% CI: 1.20-2.70; number of cases in this category: n?=?23). This association was particularly evident for multiple miscarriages (HR(≥4vs.0): 1.99, 95% CI: 1.06-3.73; number of cases in this category: n?=?10), with no significant association for multiple induced abortions (HR(≥4vs.0): 1.46, 95% CI: 0.68-3.14; number of cases in this category: n?=?7). Our findings suggest that multiple miscarriages are associated with an increased risk of epithelial ovarian cancer, possibly through a shared cluster of etiological factors or a common underlying pathology. These findings should be interpreted with caution as this is the first study to show this association and given the small number of cases in the highest exposure categories. 相似文献
10.
Petra G.A. van Boeckel Hendriek C. Boshuizen Peter D. Siersema Alina Vrieling Anton E. Kunst Weimin Ye Malin Sund Dominique S. Michaud Valentina Gallo Elizabeth A. Spencer Antonia Trichopoulou Vasiliki Benetou Philippos Orfanos Lluis Cirera Eric J. Duell Sabine Rohrmann Silke Hemann Giovanni Masala Jonas Manjer Amalia Mattiello B. Bueno-de-Mesquita 《Cancer epidemiology》2010,34(6):696-701
Introduction: Until now, studies examining the relationship between socioeconomic status and pancreatic cancer incidence have been inconclusive. Aim: To prospectively investigate to what extent pancreatic cancer incidence varies according to educational level within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Methods: In the EPIC study, socioeconomic status at baseline was measured using the highest level of education attained. Hazard ratios by educational level and a summary index, the relative indices of inequality (RII), were estimated using Cox regression models stratified by age, gender, and center and adjusted for known risk factors. In addition, we conducted separate analyses by age, gender and geographical region. Results: Within the source population of 407, 944 individuals at baseline, 490 first incident primary pancreatic adenocarcinoma cases were identified in 9 European countries. The crude difference in risk of pancreatic cancer according to level of education was small and not statistically significant (RII = 1.14, 95% CI 0.80–1.62). Adjustment for known risk factors reduced the inequality estimates to only a small extent. In addition, no statistically significant associations were observed for age groups (adjusted RII≤ 60 years = 0.85, 95% CI 0.44–1.64, adjusted RII>60 years = 1.18, 95% CI 0.73–1.90), gender (adjusted RIImale = 1.20, 95% CI 0.68–2.10, adjusted RIIfemale = 0.96, 95% CI 0.56–1.62) or geographical region (adjusted RIINorthern Europe = 1.14, 95% CI 0.81–1.61, adjusted RIIMiddle Europe = 1.72, 95% CI 0.93–3.19, adjusted RIISouthern Europe = 0.75, 95% CI 0.32–1.80). Conclusion: Despite large educational inequalities in many risk factors within the EPIC study, we found no evidence for an association between educational level and the risk of developing pancreatic cancer in this European cohort. 相似文献