SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(English Dallas R.) ;srt2:(2015-2019)"

Sökning: WFRF:(English Dallas R.) > (2015-2019)

  • Resultat 11-16 av 16
  • Föregående 1[2]
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
11.
  • Jayasekara, Harindra, et al. (författare)
  • Lifetime alcohol intake and risk of non-Hodgkin lymphoma : Findings from the Melbourne Collaborative Cohort Study
  • 2018
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 142:5, s. 919-926
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Cohort studies have reported inconsistent evidence regarding alcohol intake and risk of non-Hodgkin lymphoma (NHL), mostly based on alcohol intake assessed close to study enrolment. We examined this association using alcohol intake measured from age 20 onwards. We calculated usual alcohol intake for 10-year periods from age 20 using recalled frequency and quantity of beverage-specific consumption for 37,990 participants aged 40-69 years from the Melbourne Collaborative Cohort Study. Cox regression was performed to derive hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between alcohol intake (g/day) and NHL risk. After a mean follow-up of 19.3 years, 538 NHL cases were diagnosed. Approximately 80% of participants were either lifetime abstainers or consumed below 20 g of ethanol/day. All categories of lifetime alcohol intake were associated with about 20% lower incidence of NHL compared with lifetime abstention, but there was no evidence of a trend by amount consumed (HR=0.97 per 10 g/day increment in intake, 95% CI: 0.92-1.03; p value=0.3). HRs for beer, wine and spirits were 0.91 (95% CI: 0.83-1.00; p value=0.05), 1.03 (95% CI: 0.94-1.12; p value=0.6), and 1.06 (95% CI: 0.83-1.37; p value=0.6), respectively, per 10 g/day increment in lifetime intake. There were no significant differences in associations between NHL subtypes. In this low-drinking cohort, we did not detect a dose-dependent association between lifetime alcohol intake and NHL risk.</p>
  •  
12.
  • Jayasekara, Harindra, et al. (författare)
  • Lifetime alcohol intake is associated with an increased risk of KRAS plus and BRAF-/KRAS- but not BRAF plus colorectal cancer
  • 2017
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 140:7, s. 1485-1493
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Ethanol in alcoholic beverages is a causative agent for colorectal cancer. Colorectal cancer is a biologically heterogeneous disease, and molecular subtypes defined by the presence of somatic mutations in BRAF and KRAS are known to exist. We examined associations between lifetime alcohol intake and molecular and anatomic subtypes of colorectal cancer. We calculated usual alcohol intake for 10-year periods from age 20 using recalled frequency and quantity of beverage-specific consumption for 38,149 participants aged 40-69 years from the Melbourne Collaborative Cohort Study. Cox regression was performed to derive hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between lifetime alcohol intake and colorectal cancer risk. Heterogeneity in the HRs across subtypes of colorectal cancer was assessed. A positive dose-dependent association between lifetime alcohol intake and overall colorectal cancer risk (mean follow-up=14.6 years; n=596 colon and n=326 rectal cancer) was observed (HR=1.08, 95% CI: 1.04-1.12 per 10 g/day increment). The risk was greater for rectal than colon cancer (p(homogeneity)=0.02). Alcohol intake was associated with increased risks of KRAS+ (HR=1.07, 95% CI: 1.00-1.15) and BRAF-/KRAS- (HR=1.05, 95% CI: 1.00-1.11) but not BRAF+ tumors (HR=0.89, 95% CI: 0.78-1.01; p(homogeneity)=0.01). Alcohol intake is associated with an increased risk of KRAS+ and BRAF-/KRAS- tumors originating via specific molecular pathways including the traditional adenoma-carcinoma pathway but not with BRAF+ tumors originating via the serrated pathway. Therefore, limiting alcohol intake from a young age might reduce colorectal cancer originating via the traditional adenoma-carcinoma pathway.</p>
  •  
13.
  • Jayasekara, Harindra, et al. (författare)
  • Long-Term Alcohol Consumption and Breast, Upper Aero-Digestive Tract and Colorectal Cancer Risk : A Systematic Review and Meta-Analysis
  • 2016
  • Ingår i: Alcohol and Alcoholism. - 0735-0414 .- 1464-3502. ; 51:3, s. 315-330
  • Forskningsöversikt (refereegranskat)abstract
    • <p>Cancers of female breast, upper aero-digestive tract (UADT) (oral cavity, pharynx, larynx, oesophagus) and colorectum are causally related to alcohol consumption. Although alcohol consumption is likely to vary during life, the few studies that have explicitly measured lifetime consumption or intake over time have not been summarised. We therefore conducted a systematic review and meta-analysis. Studies were identified by searching the Medline, CINAHL (Cumulative Index to Nursing and Allied Health Literature) and Scopus databases through January 2015 using broad search criteria. Studies reporting relative risks (RR) for quantitatively defined categories of alcohol consumption over time for breast, UADT or colorectal cancer were eligible. A two-stage random-effects meta-analysis was used to estimate a dose-response relationship between alcohol intake and each cancer site. RRs were also calculated for the highest relative to the lowest intake category. Sixteen articles for breast, 16 for UADT and 7 for colorectal cancer met the eligibility criteria. We observed a weak non-linear dose-response relationship for breast cancer and positive linear dose-response relationships for UADT and colorectal cancer. The pooled RRs were 1.28 (95% confidence interval, CI: 1.07, 1.52) for breast, 2.83 (95% CI: 1.73, 4.62) for UADT, 4.84 (95% CI: 2.51, 9.32) for oral cavity and pharynx, 2.25 (95% CI: 1.49, 3.42) for larynx, 6.71 (95% CI: 4.21, 10.70) for oesophageal and 1.49 (95% CI: 1.27, 1.74) for colorectal cancer. Our findings confirm dose-dependent associations between long-term alcohol intake and breast, UADT and colorectal cancer.</p>
  •  
14.
  • Jiang, Heng, et al. (författare)
  • Temporal Associations of Alcohol and Tobacco Consumption With Cancer Mortality
  • 2018
  • Ingår i: Jama Network Open. - 2574-3805. ; 1:3
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>IMPORTANCE Understanding whether the population-level consumption of alcohol and tobacco is associated with cancer mortality is a crucial question for public health policy that has not been answered by previous studies. OBJECTIVE To examine temporal associations of alcohol and tobacco consumption with overall cancer mortality in the Australian population, looking across different sex and age groups. DESIGN, SETTING, AND PARTICIPANTS This population-based cohort study conducted a time series analysis (autoregressive integrated moving average models) using aggregate-level annual time series data from multiple sources. Data on alcohol consumption and tobacco consumption per capita between 1935 and 2014 among the Australian population aged 15 years and older were collected from the Australian Bureau of Statistics and Cancer Council Victoria. Analysis was conducted from June 1, 2017, to October 30, 2017. EXPOSURES Sex- and age-specific cancer mortality rates from 1968 to 2014 were collected from the Australian Institute Health and Welfare. MAIN OUTCOMES AND MEASURES Population-level cancer mortality in different sex and age groups in Australia, controlling for the effects of health expenditure. RESULTS Among the Australian total population aged 15 years and older in this study, 50.5% were women. Cancer death rates per 100 000 persons increased from 199 in 1968 to 214 in 1989 and then decreased steadily to 162 in 2014. Taking into account lagged effects, 1-L decreases in alcohol consumption per capita were associated with a decline of 3.9% in overall cancer mortality over a 20-year period, and 1-kg decreases in tobacco consumption per capita were associated with a 16% reduction. Alcohol consumption per capita was significantly associated with overall cancer mortality among men aged 50 to 69 years and women aged 50 years and older. Tobacco consumption per capita was found to be significantly associated with overall cancer mortality only among men aged 50 years and older. CONCLUSIONS AND RELEVANCE In this study, alcohol consumption per capita was positively associated with overall cancer mortality among older men and women, and tobacco consumption per capita was positively associated with overall cancer mortality among older men over a 20-year period. This study provides evidence that a decrease in population-level drinking and tobacco smoking could lead to a reduction in cancer mortality.</p>
  •  
15.
  • O'Reilly, Éilis J, et al. (författare)
  • Prediagnostic body size and risk of amyotrophic lateral sclerosis death in 10 studies
  • 2018
  • Ingår i: Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration. - 2167-8421 .- 2167-9223. ; 19:5-6, s. 396-406
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>OBJECTIVES AND METHODS:</strong> Using pooled multivariable-adjusted rate ratios (RR), we explored relationships between prediagnostic body-mass-index (BMI), waist-to-hip-ratio (WHR), and weight-gain during adulthood, and ALS in 419,894 women and 148,166 men from 10 community-based cohorts in USA, Europe, and Australia; 428 ALS deaths were documented in women and 204 in men.</p><p><strong>RESULTS:</strong> , limiting power. Weight-gain during adulthood was strongly associated with lower ALS; for an additional 1kg gain in weight/year, the RR = 0.43 (95% CI: 0.28-0.65; p &lt; 0.001). Associations persisted when adjusted for diabetes at enrollment, restricted to never-smokers, and ALS deaths in the 5 years after enrollment were excluded (accounting for recent weight loss).</p><p><strong>CONCLUSIONS:</strong> These findings confirm somewhat conflicting, underpowered evidence that adiposity is inversely associated with ALS. We newly demonstrate that weight-gain during adulthood is strongly predictive of lower ALS risk.</p>
16.
  • Watts, Eleanor L., et al. (författare)
  • The associations of anthropometric, behavioural and sociodemographic factors with circulating concentrations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 in a pooled analysis of 16,024 men from 22 studies
  • 2019
  • Ingår i: International Journal of Cancer. - WILEY. - 0020-7136 .- 1097-0215. ; 145:12, s. 3244-3256
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Insulin-like growth factors (IGFs) and insulin-like growth factor binding proteins (IGFBPs) have been implicated in the aetiology of several cancers. To better understand whether anthropometric, behavioural and sociodemographic factors may play a role in cancer risk via IGF signalling, we examined the cross-sectional associations of these exposures with circulating concentrations of IGFs (IGF-I and IGF-II) and IGFBPs (IGFBP-1, IGFBP-2 and IGFBP-3). The Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset includes individual participant data from 16,024 male controls (i.e. without prostate cancer) aged 22-89 years from 22 prospective studies. Geometric means of protein concentrations were estimated using analysis of variance, adjusted for relevant covariates. Older age was associated with higher concentrations of IGFBP-1 and IGFBP-2 and lower concentrations of IGF-I, IGF-II and IGFBP-3. Higher body mass index was associated with lower concentrations of IGFBP-1 and IGFBP-2. Taller height was associated with higher concentrations of IGF-I and IGFBP-3 and lower concentrations of IGFBP-1. Smokers had higher concentrations of IGFBP-1 and IGFBP-2 and lower concentrations of IGFBP-3 than nonsmokers. Higher alcohol consumption was associated with higher concentrations of IGF-II and lower concentrations of IGF-I and IGFBP-2. African Americans had lower concentrations of IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 and Hispanics had lower IGF-I, IGF-II and IGFBP-3 than non-Hispanic whites. These findings indicate that a range of anthropometric, behavioural and sociodemographic factors are associated with circulating concentrations of IGFs and IGFBPs in men, which will lead to a greater understanding of the mechanisms through which these factors influence cancer risk.</p>
Skapa referenser, mejla, bekava och länka
  • Resultat 11-16 av 16
  • Föregående 1[2]
 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy