SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Ahlbom Anders) srt2:(2015-2019)"

Sökning: WFRF:(Ahlbom Anders) > (2015-2019)

  • Resultat 1-10 av 10
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Björk, Jonas, et al. (författare)
  • Commonly used estimates of the genetic contribution to disease are subject to the same fallacies as bad luck estimates
  • 2019
  • Ingår i: European Journal of Epidemiology. - Springer. - 0393-2990. ; 34:11, s. 987-992
  • Tidskriftsartikel (refereegranskat)abstract
    • The scientific debate following the initial formulation of the “bad luck” hypothesis in cancer development highlighted how measures based on analysis of variance are inappropriately used for risk communication. The notion of “explained” variance is not only used to quantify randomness, but also to quantify genetic and environmental contribution to disease in heritability coefficients. In this paper, we demonstrate why such quantifications are generally as problematic as bad luck estimates. We stress the differences in calculation and interpretation between the heritability coefficient and the population attributable fraction, the estimated fraction of all disease events that would not occur if an intervention could successfully prevent the excess genetic risk. We recommend using the population attributable fraction when communicating results regarding the genetic contribution to disease, as this measure is both more relevant from a public health perspective and easier to understand.
2.
  •  
3.
  • Alinaghizadeh, Hassan, Statistiker, 1961- (författare)
  • Radioactive fall-out from the Chernobyl nuclear power plant accident in 1986 and cancer rates in Sweden, a 25-year follow up
  • 2019
  • Licentiatavhandling (övrigt vetenskapligt)abstract
    • <p><strong><em>Aim:</em></strong><strong><em> </em></strong>The current research aimed to study the association between exposure to low-dose radiation fallout after the Chernobyl accident in 1986 and the incidence of cancer in Sweden.</p><p><strong><em>Methods:</em></strong><strong><em> </em></strong>A nationwide study population, selecting information from nine counties out of 21 in Sweden for the period from 1980 – 2010.</p><p>In the first study, an ecological design was defined for two closed cohorts from 1980 and 1986. A possible exposure response pattern between the exposure to <sup>137</sup>Cs on the ground and the cancer incidence after the Chernobyl nuclear power plant accident was investigated in the nine northernmost counties of Sweden (n=2.2 million). The <em>activity</em> of <sup>137</sup>Cs at the county, municipality and parish level in 1986 was retrieved from the <em>Swedish Radiation Safety Authority (</em>SSI) and used as a proxy for received dose of ionizing radiation. Information about diagnoses of cancer (ICD-7 code 140-209) from 1958 – 2009 were received from the Swedish Cancer Registry, National Board of Health and Welfare (368,244 cases were reported for the period 1958 to 2009). The incidence rate ratios were calculated by using Poisson Regression for pre-Chernobyl (1980 – 1986) and post-Chernobyl (1986 – 2009) using average deposition of <sup>137</sup>Cs at three geographical levels: county (n=9), municipality (n=95), and parish level (n=612). Also, a time trend analysis with age standardized cancer incidence in the study population and in the general Swedish population was drawn from 1980 – 2009.</p><p>In the second study, a closed cohort was defined as all individuals living in the three most contaminated counties in mid-Sweden in 1986. Fallout of <sup>137</sup>Cs was retrieved as a digital map from the Geological Survey of Sweden, demographic data from Statistics Sweden, and cancer diagnosis from the Swedish Cancer Registry, National Board of Health and Welfare. Individuals were assigned an annual <sup>137</sup>Cs exposure based on their place of residence (1986 through 1990), from which 5-year cumulative <sup>137</sup>Cs exposures were calculated, accounting for the physical decay of <sup>137</sup>Cs and changing residencies. Hazard ratios for having cancer during the follow-up period, adjusted for age, sex, rural/non-rural residence, and pre-Chernobyl total cancer incidence, were calculated.</p><p><strong><em>Results</em></strong><strong><em>: </em></strong>No obvious exposure-response pattern in the age-standardized total cancer incidence rate ratios could be seen in the first study. However, a spurious association between the fallout and cancer incidence was present, where areas with the lowest incidence of cancer before the accident coincidentally had the lowest fallout of cesium-137. Increasing the geographical resolution of exposure from the average values of nine counties to the average values of 612 parishes resulted in two to three times higher degree of variance explanation by regression model. There was a secular trend, with an increase in age standardized incidence of cancer from 1980 – 2009. This trend was stronger in the general Swedish population compared to the nine counties of the present study.</p><p>In the second study, 734,537 people identified were divided into three exposure categories: the first quartile was low exposure (0.0 to 45.4 kBq/m<sup>2</sup>), the second and third quartiles were intermediate exposure (45.41 to 118.8 kBq/m<sup>2</sup>), and the fourth quartile was highest exposure (118.81 to 564.71 kBq/m<sup>2</sup>). Between 1991 and 2010, 82,495 cancer cases were registered in the three counties. Adjusted HRs (95% CI) were 1.03 (1.01 to 1.05) for intermediate exposure, and 1.05 (1.03 to 1.07) for the highest exposure, when comparing to the reference exposure.</p><p><strong><em>Conclusion</em></strong><strong><em>: </em></strong>Using the ecological data, there was no exposure response trend; however, after refining the data to the individual level of exposure, there was an overall exposure response pattern. Nonetheless, due to the time dependency, these results were restricted to the age group of 25 – 49 among males. Using register-based data only, for determining the association between low-dose exposure to radiation and the risk of developing cancer, is difficult since we cannot control for other significant factors that are associated with cancer.</p>
  •  
4.
  • Fang, Fang, et al. (författare)
  • Amyotrophic lateral sclerosis among cross-country skiers in Sweden.
  • 2016
  • Ingår i: European Journal of Epidemiology. - 0393-2990 .- 1573-7284. ; 31:3, s. 247-253
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>A highly increased risk of amyotrophic lateral sclerosis (ALS) has been suggested among professional athletes. We aimed to examine whether long distance cross-country skiers have also a higher risk of ALS and whether the increased risk was modified by skiing performance. We followed 212,246 cross-country skiers in the Swedish Vasaloppet cohort and a random selection of 508,176 general Swedes not participating in the Vasaloppet during 1989-2010. The associations between cross-country skiing as well as skiing performance (i.e., type of race, finishing time and number of races) and the consequent risk of ALS were estimated through hazard ratios (HRs) derived from Cox model. During the study, 39 cases of ALS were ascertained among the skiers. The fastest skiers (100-150 % of winner time) had more than fourfold risk of ALS (HR 4.31, 95 % confidence interval [CI] 1.78-10.4), as compared to skiers that finished at &gt;180 % of winner time. Skiers who participated &gt;4 races during this period had also a higher risk (HR 3.13, 95 % CI 1.37-7.17) than those participated only one race. When compared to the non-skiers, the fastest skiers still had a higher risk (HR 2.08, 95 % CI 1.12-3.84), as skiers who had &gt;4 races (HR 1.88, 95 % CI 1.05-3.35), but those finishing at &gt;180 % of winner time had a lower risk (HR 0.46, 95 % CI 0.24-0.87). In conclusion, long distance cross-country skiing is associated with a higher risk of ALS, but only among the best skiers; recreational skiers appear to have a largely reduced risk.</p>
  •  
5.
  • Karampampa, Korinna, et al. (författare)
  • Declining incidence trends for hip fractures have not been accompanied by improvements in lifetime risk or post-fracture survival - A nationwide study of the Swedish population 60 years and older
  • 2015
  • Ingår i: Bone. - 8756-3282 .- 1873-2763. ; 78, s. 55-61
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: Hip fracture is a common cause of disability and mortality among the elderly. Declining incidence trends have been observed in Sweden. Still, this condition remains a significant public health problem since Sweden has one of the highest incidences worldwide. Yet, no Swedish lifetime risk or survival trends have been presented. By examining how hip fracture incidence, post-fracture survival, as well as lifetime risk have developed between 1995 and 2010 in Sweden, this study aims to establish how the burden hip fractures pose on the elderly changed over time, in order to inform initiatives for improvements of their health. Material and Methods: The entire Swedish population 60 years-old and above was followed between 1987 and 2010 in the National Patient Register and the Cause of Death Register. Annual age-specific hip fracture cumulative incidence was estimated using hospital admissions for hip fractures. Three-month and one-year survival after the first hip fracture were also estimated. Period life table was used to assess lifetime risk of hip fractures occuring from age 60 and above, and the expected mean age of the first hip fracture. Results: The age-specific hip fracture incidence decreased between 1995 and 2010 in all ages up to 94 years, on average by 1% per year. The lifetime risk remained almost stable, between 9% and 11% for men, and between 18% and 20% for women. The expected mean age of a first hip fracture increased by 2.5 years for men and by 2.2 years for women. No improvements over time were observed for the 3-month survival for men, while for women a 1% decrease per year was observed. The 1-year survival slightly increased over time for men (0.4% per year) while no improvement was observed for women. Conclusions: The age-specific hip fracture incidence has decreased overtime. Yet the lifetime risk of a hip fracture has not decreased because life expectancy in the population has increased in parallel. Overall, survival after hip fracture has not improved.</p>
  •  
6.
  • Modig, Karin, et al. (författare)
  • Stable or improved health status in the population 65 years and older in Stockholm, Sweden - an 8-year follow-up of self-reported health items
  • 2016
  • Ingår i: Scandinavian Journal of Public Health. - 1403-4948 .- 1651-1905. ; 44:5, s. 480-489
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: Previous studies have reached different conclusions about whether health is improving in the ageing population. More studies with narrow age groups analyzed separately for men and women will contribute to the literature. Aim: To describe trends in self-reported indicators of health and health-related quality of life between 2002 and 2010, focusing on differences between gender and age groups. A population-based survey of individuals 65+ in the Stockholm County was used. Results: Prevalence of health problems increased with age both among men and women. Men generally reported having no health problems to a larger extent than women, but the proportions reporting severe problems were similar. The larger picture is one of stability in health-related quality of life, even if several items developed for the better, especially among women. While the proportions reporting no health/functional problems increased for many items, the proportions reporting severe problems remained unchanged among men and improved only for two items among women. Conclusions: Overall, improvements were seen in many of the health-related quality of life items as well as for self-rated health among women. The proportions reporting long-term illness or persistent health problems increased, but fewer seem to be limited in their daily activities by these problems. The stable proportions of poor self-rated health indicates that while health and functioning seem to be improving for the majority of the older population, some groups may be lagging behind. Future studies should pay attention to changes both in the upper and lower ends of the health spectrum.</p>
  •  
7.
  • Sampson, Joshua N., et al. (författare)
  • Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
  • 2015
  • Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 107:12
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.</p>
  •  
8.
  • Sampson, Joshua N., et al. (författare)
  • Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
  • 2015
  • Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 107:12
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.</p><p>Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.</p><p>Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.</p><p>Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.</p>
  •  
9.
  • Torssander, Jenny, et al. (författare)
  • Four Decades of Educational Inequalities in Hospitalization and Mortality among Older Swedes
  • 2016
  • Ingår i: PLoS ONE. - 1932-6203 .- 1932-6203. ; 11:3
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background The inverse association between education and mortality has grown stronger the last decades in many countries. During the same period, gains in life expectancy have been concentrated to older ages; still, old-age mortality is seldom the focus of attention when analyzing trends in the education-mortality gradient. It is further unknown if increased educational inequalities in mortality are preceded by increased inequalities in morbidity of which hospitalization may be a proxy. Methods Using administrative population registers from 1971 and onwards, education-specific annual changes in the risk of death and hospital admission were estimated with complimentary log-log models. These risk changes were supplemented by estimations of the ages at which 25, 50, and 75% of the population had been hospitalized or died (after age 60). Results The mortality decline among older people increasingly benefitted the well-educated over the less well-educated. This inequality increase was larger for the younger old, and among men. Educational inequalities in the age of a first hospital admission generally followed the development of growing gaps, but at a slower pace than mortality and inequalities did not increase among the oldest individuals. Conclusions Education continues to be a significant predictor of health and longevity into old age. That the increase in educational inequalities is greater for mortality than for hospital admissions (our proxy of overall morbidity) may reflect that well-educated individuals gradually have obtained more possibilities or resources to survive a disease than less well-educated individuals have the last four decades.</p>
  •  
10.
  • Wang, Zhaoming, et al. (författare)
  • Further Confirmation of Germline Glioma Risk Variant rs78378222 in TP53 and Its Implication in Tumor Tissues via Integrative Analysis of TCGA Data
  • 2015
  • Ingår i: Human Mutation. - 1059-7794 .- 1098-1004. ; 36:7, s. 684-688
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>We confirmed strong association of rs78378222:A&gt;C (per allele odds ratio [OR] = 3.14; P = 6.48 x 10(-11)), a germline rare single-nucleotide polymorphism (SNP) in TP53, via imputation of a genome-wide association study of glioma (1,856 cases and 4,955 controls). We subsequently performed integrative analyses on the Cancer Genome Atlas (TCGA) data for GBM (glioblastoma multiforme) and LUAD (lung adenocarcinoma). Based on SNP data, we imputed genotypes for rs78378222 and selected individuals carrying rare risk allele (C). Using RNA sequencing data, we observed aberrant transcripts with approximate to 3 kb longer than normal for those individuals. Using exome sequencing data, we further showed that loss of haplotype carrying common protective allele (A) occurred somatically in GBM but not in LUAD. Our bioinformatic analysis suggests rare risk allele (C) disrupts mRNA termination, and an allelic loss of a genomic region harboring common protective allele (A) occurs during tumor initiation or progression for glioma.</p>
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 10
Åtkomst
fritt online (2)
Typ av publikation
tidskriftsartikel (9)
licentiatavhandling (1)
Typ av innehåll
refereegranskat (9)
övrigt vetenskapligt (1)
Författare/redaktör
Ahlbom, Anders (10)
Feychting, Maria (5)
Gapstur, Susan M (3)
Stevens, Victoria L (3)
Albanes, Demetrius (3)
Giles, Graham G (3)
visa fler...
Severi, Gianluca (3)
Glimelius, Bengt, (2)
Chang-Claude, Jenny (2)
Tjonneland, Anne (2)
Boutron-Ruault, Mari ... (2)
Boeing, Heiner (2)
Masala, Giovanna (2)
Krogh, Vittorio (2)
Chirlaque, Maria-Dol ... (2)
Khaw, Kay-Tee (2)
Riboli, Elio (2)
Liu, Li, (2)
Adami, Hans Olov (2)
Melbye, Mads (2)
Weiderpass, Elisabet ... (2)
Haiman, Christopher ... (2)
Berndt, Sonja I (2)
Cancel-Tassin, Geral ... (2)
Travis, Ruth C (2)
Kogevinas, Manolis (2)
Gago Dominguez, Manu ... (2)
Johansen, Christoffe ... (2)
Andersson, Tomas (2)
Huerta, José Maria (2)
Palli, Domenico (2)
Clavel-Chapelon, Fra ... (2)
Vineis, Paolo (2)
Trichopoulos, Dimitr ... (2)
Canzian, Federico (2)
Sund, Malin (2)
Jenab, Mazda (2)
Bueno-de-Mesquita, H ... (2)
Boffetta, Paolo (2)
Peeters, Petra H M (2)
Hallmans, Göran (2)
Gunter, Marc, (2)
Chen, Ying, (2)
Diver, W. Ryan (2)
Garcia-Closas, Monts ... (2)
Brinton, Louise (2)
Southey, Melissa C. (2)
Liu, Jianjun (2)
Li, Yuqing (2)
Andrulis, Irene L. (2)
visa färre...
Lärosäte
Uppsala universitet (4)
Stockholms universitet (3)
Umeå universitet (2)
Lunds universitet (1)
Karolinska Institutet (1)
Språk
Engelska (10)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (10)
Samhällsvetenskap (2)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy