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71.
  • Jayasekara, Harindra, et al. (författare)
  • Associations of alcohol intake, smoking, physical activity and obesity with survival following colorectal cancer diagnosis by stage, anatomic site and tumor molecular subtype
  • 2018
  • Ingår i: International Journal of Cancer. - 0020-7136. ; 142:2, s. 238-250
  • Tidskriftsartikel (refereegranskat)abstract
    • The influence of lifestyle factors on survival following a diagnosis of colorectal cancer (CRC) is not well established. We examined associations between lifestyle factors measured before diagnosis and CRC survival. The Melbourne Collaborative Cohort Study collected data on alcohol intake, cigarette smoking and physical activity, and body measurements at baseline (1990-1994) and wave 2 (2003-2007). We included participants diagnosed to 31 August 2015 with incident stages I-III CRC within 10-years post exposure assessment. Information on tumor characteristics and vital status was obtained. Tumor DNA was tested for microsatellite instability (MSI) and somatic mutations in oncogenes BRAF (V600E) and KRAS. We estimated hazard ratios (HRs) for associations between lifestyle factors and overall and CRC-specific mortality using Cox regression. Of 724 eligible CRC cases, 339 died (170 from CRC) during follow-up (average 9.0 years). Exercise (non-occupational/leisure-time) was associated with higher CRC-specific survival for stage II (HR=0.25, 95% CI: 0.10-0.60) but not stages I/III disease (p for interaction=0.01), and possibly for colon and KRAS wild-type tumors. Waist circumference was inversely associated with CRC-specific survival (HR=1.25 per 10 cm increment, 95% CI: 1.08-1.44), independent of stage, anatomic site and tumor molecular status. Cigarette smoking was associated with lower overall survival, with suggestive evidence of worse survival for BRAF mutated CRC, but not with CRC-specific survival. Alcohol intake was not associated with survival. Survival did not differ by MSI status. We have identified pre-diagnostic predictors of survival following CRC that may have clinical and public health relevance.
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72.
  • Jayasekara, Harindra, et al. (författare)
  • Is breast cancer risk associated with alcohol intake before first full-term pregnancy?
  • 2016
  • Ingår i: Cancer Causes and Control. - 0957-5243. ; 27:9, s. 1167-1174
  • Tidskriftsartikel (refereegranskat)abstract
    • PurposeIt is plausible that breast tissue is particularly susceptible to carcinogens, including ethanol, between menarche and the first full-term pregnancy (first pregnancy). There is some epidemiological evidence that intake before the first pregnancy is more closely associated with risk of breast cancer than is intake thereafter. We examined this association using lifetime alcohol consumption data from a prospective cohort study.MethodsWe calculated usual alcohol intake for age periods 15-19 years and for 10-year period from age 20 to current age (in grams per day) using recalled frequency and quantity of beverage-specific consumption for 13,630 parous women who had their first pregnancy at age 20 years or later, had no cancer history and were aged 40-69 years at enrollment. Cox regression was performed to estimate hazard ratios (HRs) and their 95 % confidence intervals (CIs).ResultsA total of 651 incident invasive adenocarcinomas of the breast were diagnosed during a mean follow-up of 16.1 years. Alcohol consumption was low overall with only a few drinking >= 40 g/day. Intake before the first pregnancy was markedly lower (mean intake: 2.5 g/day; abstention: 58.8 %) than intake thereafter (mean intake: 6.0 g/day; abstention: 33.6 %). Any alcohol intake before the first pregnancy was associated with an increased risk of breast cancer (HR 1.35, 95 % CI 1.10-1.66 for drinking compared with abstention), whereas any intake after the first pregnancy was not (HR 0.89, 95 % CI 0.72-1.09).ConclusionsLimiting alcohol intake before the first pregnancy might reduce women's risk of breast cancer.
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73.
  • Jayasekara, Harindra, et al. (författare)
  • Lifetime alcohol consumption and upper aero-digestive tract cancer risk in the Melbourne Collaborative Cohort Study
  • 2015
  • Ingår i: Cancer Causes and Control. - 0957-5243. ; 26:2, s. 297-301
  • Tidskriftsartikel (refereegranskat)abstract
    • Cohort studies have rarely examined the association between upper aero-digestive tract (UADT) cancer risk and lifetime alcohol intake. We examined the associations between incident squamous cell carcinoma of the UADT (oral cavity, pharynx, larynx, and esophagus) and alcohol intake for different periods in life using data from the Melbourne Collaborative Cohort Study. Usual alcohol intake for 10-year periods from age 20 was calculated using recalled frequency and quantity of beverage-specific consumption. Cox regression with age as the time axis was performed to estimate hazard ratios (HR) and 95 % confidence intervals (CI) for the associations of UADT cancer with alcohol intake for different periods in life compared with abstention. During a mean follow-up of 16.2 person-years, 98 incident cases of UADT cancer were identified. We observed a dose-dependent association between lifetime alcohol intake and the risk of UADT cancer (multivariable-adjusted HR 2.67, 95 % CI 1.27-5.60 for an intake of a parts per thousand yen40 g/day and multivariable-adjusted HR 1.16, 95 % CI 1.06-1.28 for a 10 g/day increment in intake). A positive association with baseline alcohol intake (multivariable-adjusted HR 1.12, 95 % CI 1.02-1.24 for a 10 g/day increment in intake) was found to be a slightly weaker predictor of risk than lifetime intake. Limiting alcohol intake from early adulthood may reduce UADT cancer risk.
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74.
  • Jayasekara, Harindra, et al. (författare)
  • Lifetime alcohol intake and pancreatic cancer incidence and survival : findings from the Melbourne Collaborative Cohort Study
  • 2019
  • Ingår i: Cancer Causes and Control. - 0957-5243. ; 30:4, s. 323-331
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose Pancreatic cancer has one of the worst prognoses with 5-year survival below 10%. There is some evidence that alcohol consumption might increase the risk of pancreatic cancer. We examined associations of pre-diagnostic alcohol intake with (i) incidence of pancreatic cancer, and (ii) overall survival following pancreatic cancer. Methods Usual alcohol intake was estimated at recruitment in 1990-1994 for 38,472 participants in the Melbourne Collaborative Cohort Study using recalled frequency and quantity of beverage-specific intake for 10-year periods from age 20. Pancreatic cancer incidence (C25 according to International Classification of Diseases for Oncology) and vital status were ascertained through to 30 September 2015. Cox regression was performed to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for associations with lifetime, age 20-29, and baseline alcohol intakes. Results By the end of follow-up (average 20.2 years), 239 incident cases of pancreatic cancer were diagnosed, of which 228 had died. No evidence of an association was observed between alcohol intake and risk of pancreatic cancer. Higher lifetime alcohol intake was associated with lower overall survival following a diagnosis of pancreatic cancer (mortality HR 1.09 per 10 g/day increment, 95% CI 1.00-1.19; p value=0.04). A similar finding was observed for age 20-29 intake (HR 1.09 per 10 g/day increment, 95% CI 1.02-1.18; p value=0.01) but not with baseline intake. Conclusions We observed an association between lower alcohol use from an early age and improved survival following pancreatic cancer, but this finding needs to be confirmed by other studies.
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75.
  • 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. ; 142:5, s. 919-926
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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76.
  • 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. ; 140:7, s. 1485-1493
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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77.
  • Jiao, Xiang, et al. (författare)
  • PHIP - a novel candidate breast cancer susceptibility locus on 6q14.1
  • 2017
  • Ingår i: OncoTarget. - IMPACT JOURNALS LLC. - 1949-2553 .- 1949-2553. ; 8:61, s. 102769-102782
  • Tidskriftsartikel (refereegranskat)abstract
    • Most non-BRCA1/2 breast cancer families have no identified genetic cause. We used linkage and haplotype analyses in familial and sporadic breast cancer cases to identify a susceptibility locus on chromosome 6q. Two independent genome-wide linkage analysis studies suggested a 3 Mb locus on chromosome 6q and two unrelated Swedish families with a LOD > 2 together seemed to share a haplotype in 6q14.1. We hypothesized that this region harbored a rare high-risk founder allele contributing to breast cancer in these two families. Sequencing of DNA and RNA from the two families did not detect any pathogenic mutations. Finally, 29 SNPs in the region were analyzed in 44,214 cases and 43,532 controls from BCAC, and the original haplotypes in the two families were suggested as low-risk alleles for European and Swedish women specifically. There was also some support for one additional independent moderate-risk allele in Swedish familial samples. The results were consistent with our previous findings in familial breast cancer and supported a breast cancer susceptibility locus at 6q14.1 around the PHIP gene.
78.
  • Kachuri, Linda, et al. (författare)
  • Fine mapping of chromosome 5p15.33 based on a targeted deep sequencing and high density genotyping identifies novel lung cancer susceptibility loci
  • 2016
  • Ingår i: Carcinogenesis. - 0143-3334. ; 37:1, s. 96-105
  • Tidskriftsartikel (refereegranskat)abstract
    • Chromosome 5p15.33 has been identified as a lung cancer susceptibility locus, however the underlying causal mechanisms were not fully elucidated. Previous fine-mapping studies of this locus have relied on imputation or investigated a small number of known, common variants. This study represents a significant advance over previous research by investigating a large number of novel, rare variants, as well as their underlying mechanisms through telomere length. Variants for this fine-mapping study were identified through a targeted deep sequencing (average depth of coverage greater than 4000x) of 576 individuals. Subsequently, 4652 SNPs, including 1108 novel SNPs, were genotyped in 5164 cases and 5716 controls of European ancestry. After adjusting for known risk loci, rs2736100 and rs401681, we identified a new, independent lung cancer susceptibility variant in LPCAT1: rs139852726 (OR = 0.46, P = 4.73x10(-9)), and three new adenocarcinoma risk variants in TERT: rs61748181 (OR = 0.53, P = 2.64x10(-6)), rs112290073 (OR = 1.85, P = 1.27x10(-5)), rs138895564 (OR = 2.16, P = 2.06x10(-5); among young cases, OR = 3.77, P = 8.41x10(-4)). In addition, we found that rs139852726 (P = 1.44x10(-3)) was associated with telomere length in a sample of 922 healthy individuals. The gene-based SKAT-O analysis implicated TERT as the most relevant gene in the 5p15.33 region for adenocarcinoma (P = 7.84x10(-7)) and lung cancer (P = 2.37x10(-5)) risk. In this largest fine-mapping study to investigate a large number of rare and novel variants within 5p15.33, we identified novel lung and adenocarcinoma susceptibility loci with large effects and provided support for the role of telomere length as the potential underlying mechanism.
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79.
  • Kar, Siddhartha P., et al. (författare)
  • The association between weight at birth and breast cancer risk revisited using Mendelian randomisation
  • 2019
  • Ingår i: European Journal of Epidemiology. - Springer. - 0393-2990. ; 34:6, s. 591-600
  • Tidskriftsartikel (refereegranskat)abstract
    • Observational studies suggest that higher birth weight (BW) is associated with increased risk of breast cancer in adult life. We conducted a two-sample Mendelian randomisation (MR) study to assess whether this association is causal. Sixty independent single nucleotide polymorphisms (SNPs) known to be associated at P < 5 × 10 −8 with BW were used to construct (1) a 41-SNP instrumental variable (IV) for univariable MR after removing SNPs with pleiotropic associations with other breast cancer risk factors and (2) a 49-SNP IV for multivariable MR after filtering SNPs for data availability. BW predicted by the 41-SNP IV was not associated with overall breast cancer risk in inverse-variance weighted (IVW) univariable MR analysis of genetic association data from 122,977 breast cancer cases and 105,974 controls (odds ratio = 0.86 per 500 g higher BW; 95% confidence interval 0.73–1.01). Sensitivity analyses using four alternative methods and three alternative IVs, including an IV with 59 of the 60 BW-associated SNPs, yielded similar results. Multivariable MR adjusting for the effects of the 49-SNP IV on birth length, adult height, adult body mass index, age at menarche, and age at menopause using IVW and MR-Egger methods provided estimates consistent with univariable analyses. Results were also similar when all analyses were repeated after restricting to estrogen receptor-positive or -negative breast cancer cases. Point estimates of the odds ratios from most analyses performed indicated an inverse relationship between genetically-predicted BW and breast cancer, but we are unable to rule out an association between the non-genetically-determined component of BW and breast cancer. Thus, genetically-predicted higher BW was not associated with an increased risk of breast cancer in adult life in our MR study.
80.
  • Khotyaintsev, Yuri V., et al. (författare)
  • Electron jet of asymmetric reconnection
  • 2016
  • Ingår i: Geophysical Research Letters. - 0094-8276 .- 1944-8007. ; 43:11, s. 5571-5580
  • Tidskriftsartikel (refereegranskat)abstract
    • We present Magnetospheric Multiscale observations of an electron-scale current sheet and electron outflow jet for asymmetric reconnection with guide field at the subsolar magnetopause. The electron jet observed within the reconnection region has an electron Mach number of 0.35 and is associated with electron agyrotropy. The jet is unstable to an electrostatic instability which generates intense waves with E-vertical bar amplitudes reaching up to 300mVm(-1) and potentials up to 20% of the electron thermal energy. We see evidence of interaction between the waves and the electron beam, leading to quick thermalization of the beam and stabilization of the instability. The wave phase speed is comparable to the ion thermal speed, suggesting that the instability is of Buneman type, and therefore introduces electron-ion drag and leads to braking of the electron flow. Our observations demonstrate that electrostatic turbulence plays an important role in the electron-scale physics of asymmetric reconnection.
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