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| 2. |
- Berndt, Sonja I, et al.
(författare)
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Large-scale fine mapping of the HNF1B locus and prostate cancer risk
- 2011
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Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 20:16, s. 3322-3329
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Tidskriftsartikel (refereegranskat)abstract
- Previous genome-wide association studies have identified two independent variants in HNF1B as susceptibility loci for prostate cancer risk. To fine-map common genetic variation in this region, we genotyped 79 single nucleotide polymorphisms (SNPs) in the 17q12 region harboring HNF1B in 10 272 prostate cancer cases and 9123 controls of European ancestry from 10 case-control studies as part of the Cancer Genetic Markers of Susceptibility (CGEMS) initiative. Ten SNPs were significantly related to prostate cancer risk at a genome-wide significance level of P < 5 × 10(-8) with the most significant association with rs4430796 (P = 1.62 × 10(-24)). However, risk within this first locus was not entirely explained by rs4430796. Although modestly correlated (r(2)= 0.64), rs7405696 was also associated with risk (P = 9.35 × 10(-23)) even after adjustment for rs4430769 (P = 0.007). As expected, rs11649743 was related to prostate cancer risk (P = 3.54 × 10(-8)); however, the association within this second locus was stronger for rs4794758 (P = 4.95 × 10(-10)), which explained all of the risk observed with rs11649743 when both SNPs were included in the same model (P = 0.32 for rs11649743; P = 0.002 for rs4794758). Sequential conditional analyses indicated that five SNPs (rs4430796, rs7405696, rs4794758, rs1016990 and rs3094509) together comprise the best model for risk in this region. This study demonstrates a complex relationship between variants in the HNF1B region and prostate cancer risk. Further studies are needed to investigate the biological basis of the association of variants in 17q12 with prostate cancer.
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| 4. |
- Maurichi, A, et al.
(författare)
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Reply to E. Hindié
- 2020
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Ingår i: Journal of clinical oncology : official journal of the American Society of Clinical Oncology. - 1527-7755. ; 38:27, s. 3238-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 5. |
- Yeager, Meredith, et al.
(författare)
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Identification of a new prostate cancer susceptibility locus on chromosome 8q24.
- 2009
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Ingår i: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 41:10, s. 1055-7
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Tidskriftsartikel (refereegranskat)abstract
- We report a genome-wide association study in 10,286 cases and 9,135 controls of European ancestry in the Cancer Genetic Markers of Susceptibility (CGEMS) initiative. We identify a new association with prostate cancer risk on chromosome 8q24 (rs620861, P = 1.3 x 10(-10), heterozygote OR = 1.17, 95% CI 1.10-1.24; homozygote OR = 1.33, 95% CI 1.21-1.45). This defines a new locus associated with prostate cancer susceptibility on 8q24.
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| 6. |
- Bailey-Wilson, Joan E, et al.
(författare)
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Analysis of Xq27-28 linkage in the international consortium for prostate cancer genetics (ICPCG) families
- 2012
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Ingår i: BMC Medical Genetics. - London : BioMed Central. - 1471-2350. ; 13, s. 46-
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Tidskriftsartikel (refereegranskat)abstract
- Background: Genetic variants are likely to contribute to a portion of prostate cancer risk. Full elucidation of the genetic etiology of prostate cancer is difficult because of incomplete penetrance and genetic and phenotypic heterogeneity. Current evidence suggests that genetic linkage to prostate cancer has been found on several chromosomes including the X; however, identification of causative genes has been elusive.Methods: Parametric and non-parametric linkage analyses were performed using 26 microsatellite markers in each of 11 groups of multiple-case prostate cancer families from the International Consortium for Prostate Cancer Genetics (ICPCG). Meta-analyses of the resultant family-specific linkage statistics across the entire 1,323 families and in several predefined subsets were then performed.Results: Meta-analyses of linkage statistics resulted in a maximum parametric heterogeneity lod score (HLOD) of 1.28, and an allele-sharing lod score (LOD) of 2.0 in favor of linkage to Xq27-q28 at 138 cM. In subset analyses, families with average age at onset less than 65 years exhibited a maximum HLOD of 1.8 (at 138 cM) versus a maximum regional HLOD of only 0.32 in families with average age at onset of 65 years or older. Surprisingly, the subset of families with only 2-3 affected men and some evidence of male-to-male transmission of prostate cancer gave the strongest evidence of linkage to the region (HLOD = 3.24, 134 cM). For this subset, the HLOD was slightly increased (HLOD = 3.47 at 134 cM) when families used in the original published report of linkage to Xq27-28 were excluded.Conclusions: Although there was not strong support for linkage to the Xq27-28 region in the complete set of families, the subset of families with earlier age at onset exhibited more evidence of linkage than families with later onset of disease. A subset of families with 2-3 affected individuals and with some evidence of male to male disease transmission showed stronger linkage signals. Our results suggest that the genetic basis for prostate cancer in our families is much more complex than a single susceptibility locus on the X chromosome, and that future explorations of the Xq27-28 region should focus on the subset of families identified here with the strongest evidence of linkage to this region.
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| 8. |
- Lu, Lingyi, et al.
(författare)
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Chromosomes 4 and 8 implicated in a genome wide SNP linkage scan of 762 prostate cancer families collected by the ICPCG
- 2012
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Ingår i: The Prostate. - : Wiley. - 0270-4137 .- 1097-0045. ; 72:4, s. 410-426
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND In spite of intensive efforts, understanding of the genetic aspects of familial prostate cancer (PC) remains largely incomplete. In a previous microsatellite-based linkage scan of 1,233 PC families, we identified suggestive evidence for linkage (i.e., LOD?=?1.86) at 5q12, 15q11, 17q21, 22q12, and two loci on 8p, with additional regions implicated in subsets of families defined by age at diagnosis, disease aggressiveness, or number of affected members. METHODS. In an attempt to replicate these findings and increase linkage resolution, we used the Illumina 6000 SNP linkage panel to perform a genome-wide linkage scan of an independent set of 762 multiplex PC families, collected by 11 International Consortium for Prostate Cancer Genetics (ICPCG) groups. RESULTS. Of the regions identified previously, modest evidence of replication was observed only on the short arm of chromosome 8, where HLOD scores of 1.63 and 3.60 were observed in the complete set of families and families with young average age at diagnosis, respectively. The most significant linkage signals found in the complete set of families were observed across a broad, 37cM interval on 4q13-25, with LOD scores ranging from 2.02 to 2.62, increasing to 4.50 in families with older average age at diagnosis. In families with multiple cases presenting with more aggressive disease, LOD cores over 3.0 were observed at 8q24 in the vicinity of previously identified common PC risk variants, as well as MYC, an important gene in PC biology. CONCLUSIONS. These results will be useful in prioritizing future susceptibility gene discovery efforts in thiscommon cancer. Prostate 72: 410-426, 2012. (C) 2011 Wiley Periodicals, Inc.
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| 9. |
- Raidén, A.B., et al.
(författare)
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Juggling work, family... and life in academia: The case of the "new" man
- 2012
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Ingår i: 28th Annual Conference of the Association of Researchers in Construction Management, ARCOM 2012; Edinburgh; United Kingdom; 3 September 2012 through 5 September 2012. - 9780955239069 ; 1, s. 273-283
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Konferensbidrag (refereegranskat)abstract
- Although the notion of the "new man" is gaining currency, there is very little research on how he manages to balance work and family. It is therefore timely to look moreclosely at this issue. We present preliminary results from an explorative pilot study onwork-life balance and "new men" in academia. Using an interprative approach, in-depth interviews were carried out with academics from construction-related universitydepartments in Britain and Sweden. Drawing on figures from the OECD and on Hofstede's masculine (Britain)/feminine (Sweden) dimension, we found that the smallpopulation of academic respondents studied struggled with the same kinds of workpressures and desires to achieve/perform according to the traditional norm of amasculine society. However, the Swedish men were more inclusive of the wholefamily life/circumstances in their accounts while the British men tended to be morefocused on themselves. Since the analysis of the data is still on-going, the findingsremain tentative. Early conclusions suggest that a satisfactory juggling of work-lifebalance for all these men is dependent on negotiations and re-negotiations ofresponsibilities between them and their partners. Some British men seemed to expectcompromise and sacrifice by their partners, while for all Swedish men there was anexpectation of compromise and sacrifice by both partners.
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| 10. |
- Sparén, Pär, et al.
(författare)
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Long term mortality after severe starvation during the siege of Leningrad : prospective cohort study
- 2004
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Ingår i: The BMJ. - 1756-1833. ; 328:7430, s. 11-14A
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Tidskriftsartikel (refereegranskat)abstract
- Objectives To determine whether starvation during periods of increased growth after birth have long term health consequences.Design Analysis of cardiovascular risk factors and mortality in a longitudinal follow up after the 1941-4 siege of Leningrad. Mortality measured from 1975 up to the end of 1999.Setting St Petersburg, Russia (formerly Leningrad).Participants 5000 men born 1916-35 who lived in Leningrad, randomly selected to take part in health examinations in 1975-7. Of the 3905 men who participated, a third had experienced the siege.Main outcome measures Relative risk of ischaemic heart disease and mortality from stroke by siege exposure. Odds ratios and means for several cardiovascular risk factors.Results Three to six decades after the siege, in men who experienced the siege around the age of puberty blood pressure was raised (mean difference in systolic 3.3 mm Hg, in diastolic 1.3 mm Hg) as was mortality from ischaemic heart disease (relative risk 1.39, 95% confidence interval 1.07 to 1.79) and stroke (1.67, 1.15 to 2.43), including haemorrhagic stroke (1.71, 0.90 to 3.22). The effect on mortality was partly mediated via blood pressure but not by any other measured biological, behavioural, or social factor.Conclusions Starvation, or accompanying chronic stress, particularly at the onset of or during puberty, may increase vulnerability to later cardiovascular disease.
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